Electron Population Aging Models for Wide-Angle Tails

Color-color diagrams have been useful in studying the spectral shapes in radio galaxies. At the workshop we presented color-color diagrams for two wide-angle tails, 1231+674 and 1433+553, and found that the standard aging models do not adequately represent the observed data. Although the JP and KP models can explain some of the observed points in the color-color diagram, they do not account for those found near the power-law line. This difficulty may be attributable to several causes. Spectral tomography has been previously used to discern two separate electron populations in these sources. The combination spectra from two such overlying components can easily resemble a range of power-laws. In addition, any non-uniformity in the magnetic field strength can also create a power-law-like spectrum. We will also discuss the effects that angular resolution has on the shape of the spectrum.Comment: 4 pages, 1 figure, proceedings from 1999 'Life Cycles of Radio Galaxies' workshop at STScI in Baltimore, M

Survival Probability of a Ballistic Tracer Particle in the Presence of Diffusing Traps

We calculate the survival probability P_S(t) up to time t of a tracer particle moving along a deterministic trajectory in a continuous d-dimensional space in the presence of diffusing but mutually noninteracting traps. In particular, for a tracer particle moving ballistically with a constant velocity c, we obtain an exact expression for P_S(t), valid for all t, for d<2. For d \geq 2, we obtain the leading asymptotic behavior of P_S(t) for large t. In all cases, P_S(t) decays exponentially for large t, P_S(t) \sim \exp(-\theta t). We provide an explicit exact expression for the exponent \theta in dimensions d \leq 2, and for the physically relevant case, d=3, as a function of the system parameters.Comment: RevTeX, 4 page

Persistence properties of a system of coagulating and annihilating random walkers

We study a d-dimensional system of diffusing particles that on contact either annihilate with probability 1/(q-1) or coagulate with probability (q-2)/(q-1). In 1-dimension, the system models the zero temperature Glauber dynamics of domain walls in the q-state Potts model. We calculate P(m,t), the probability that a randomly chosen lattice site contains a particle whose ancestors have undergone exactly (m-1) coagulations. Using perturbative renormalization group analysis for d < 2, we show that, if the number of coagulations m is much less than the typical number M(t), then P(m,t) ~ m^(z/d) t^(-theta), with theta=d Q + Q(Q-1/2) epsilon + O(epsilon^2), z=(2Q-1) epsilon + (2 Q-1) (Q-1)(1/2+A Q) epsilon^2 +O(epsilon^3), where Q=(q-1)/q, epsilon =2-d and A =-0.006. M(t) is shown to scale as t^(d/2-delta), where delta = d (1 -Q)+(Q-1)(Q-1/2) epsilon+ O(epsilon^2). In two dimensions, we show that P(m,t) ~ ln(t)^(Q(3-2Q)) ln(m)^((2Q-1)^2) t^(-2Q) for m << t^(2 Q-1). The 1-dimensional results corresponding to epsilon=1 are compared with results from Monte Carlo simulations.Comment: 12 pages, revtex, 5 figure

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