The hot gas content of fossil galaxy clusters

We investigate the properties of the hot gas in four fossil galaxy systems detected at high significance in the Planck Sunyaev-Zeldovich (SZ) survey. XMM-Newton observations reveal overall temperatures of kT ~ 5-6 keV and yield hydrostatic masses M500,HE > 3.5 x 10e14 Msun, confirming their nature as bona fide massive clusters. We measure the thermodynamic properties of the hot gas in X-rays (out to beyond R500 in three cases) and derive their individual pressure profiles out to R ~ 2.5 R500 with the SZ data. We combine the X-ray and SZ data to measure hydrostatic mass profiles and to examine the hot gas content and its radial distribution. The average Navarro-Frenk-White (NFW) concentration parameter, c500 = 3.2 +/- 0.4, is the same as that of relaxed `normal' clusters. The gas mass fraction profiles exhibit striking variation in the inner regions, but converge to approximately the cosmic baryon fraction (corrected for depletion) at R500. Beyond R500 the gas mass fraction profiles again diverge, which we interpret as being due to a difference in gas clumping and/or a breakdown of hydrostatic equilibrium in the external regions. Overall our observations point to considerable radial variation in the hot gas content and in the gas clumping and/or hydrostatic equilibrium properties in these fossil clusters, at odds with the interpretation of their being old, evolved and undisturbed. At least some fossil objects appear to be dynamically young.Comment: 4 pages, 2 figures. Accepted for publication in A&

Pion photoproduction off the proton in a gauge-invariant chiral unitary framework

We investigate pion photoproduction off the proton in a manifestly gauge-invariant chiral unitary extension of chiral perturbation theory. In a first step, we consider meson-baryon scattering taking into account all next-to-leading order contact interactions. The resulting low-energy constants are determined by a fit to s-wave pion-nucleon scattering and the low-energy data for the reaction pi- p --> eta n. To assess the theoretical uncertainty, we perform two different fit strategies. Having determined the low-energy constants, we then analyse the data on the s-wave multipole amplitudes E0+ of pion and eta photoproduction. These are parameter-free predictions, as the two new low-energy constants are determined by the neutron and proton magnetic moments.Comment: 23 pages, 17 figure

The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates

Degeneration of nigrostriatal dopaminergic neurons is the primary histopathological feature of Parkinson's disease. The neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induces a neurological syndrome in man and non-human primates very similar to idiopathic Parkinson's disease by selectively destroying dopaminergic nigrostriatal neurons. This gives rise to the hypothesis that Parkinson's disease may be caused by endogenous or environmental toxins. Endogenous excitatory amino acids (EAAs) such as L-glutamate could be involved in neurodegenerative disorders including Parkinson's disease. We report in this study that the competitive NMDA antagonist CPP (3-((+/-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid) protects nigral tyrosine hydroxylase (TH) positive neurons from degeneration induced by systemic treatment with MPTP in common marmosets. This indicates that EAAs are involved in the pathophysiological cascade of MPTP-induced neuronal cell death and that EAA antagonists may offer a neuroprotective therapy for Parkinson's disease

Association of acute coronary syndrome-induced posttraumatic stress disorder symptoms with self-reported sleep

Background Symptoms of posttraumatic stress disorder (PTSD) after acute coronary syndrome (ACS) are associated with recurrent ACS events and mortality. Poor sleep may be a mechanism, but the association between PTSD and sleep after ACS is unknown. Purpose This study aims to estimate the association between ACS-induced PTSD symptoms and self-reported sleep. Methods ACS-induced PTSD symptoms were assessed 1-month post-ACS in 188 adults using the Impact of Events Scale-Revised. Sleep was assessed using the Pittsburgh Sleep Quality Index. Linear and logistic regression models were used to determine whether PTSD symptoms were associated with self-reported sleep, independent of sociodemographic and clinical covariates. Results In adjusted models, ACS-induced PTSD symptoms were associated with worse overall sleep (β = 0.22, p = 0.003) and greater impairment in six of seven components of sleep (all p values <0.05). Conclusions ACS-induced PTSD symptoms may be associated with poor sleep, which may explain why PTSD confers increased cardiovascular risk after ACS

Posttraumatic stress disorder and risk for coronary heart disease: A meta-analytic review

Objective The aim of this study was to estimate the association of posttraumatic stress disorder (PTSD) with risk for incident coronary heart disease (CHD). Design A systematic review and meta-analysis were used as study designs. Data Sources Articles were identified by searching Ovid MEDLINE, PsycINFO, Scopus, Cochrane Library, PILOTS database, and PubMed Related Articles and through a manual search of reference lists (1948-present). Study Selection All studies that assessed PTSD in participants initially free of CHD and subsequently assessed CHD/cardiac-specific mortality were included. Data Extraction Two investigators independently extracted estimates of the association of PTSD with CHD, as well as study characteristics. Odds ratios were converted to hazard ratios (HRs), and a random-effects model was used to pool results. A secondary analysis including only studies that reported estimates adjusted for depression was conducted. Results Six studies met our inclusion criteria (N = 402,274); 5 of these included depression as a covariate. The pooled HR for the magnitude of the relationship between PTSD and CHD was 1.55 (95% CI 1.34-1.79) before adjustment for depression. The pooled HR estimate for the 5 depression-adjusted estimates (N = 362,950) was 1.27 (95% CI 1.08-1.49). Conclusion Posttraumatic stress disorder is independently associated with increased risk for incident CHD, even after adjusting for depression and other covariates. It is common in both military veterans and civilian trauma survivors, and these results suggest that it may be a modifiable risk factor for CHD. Future research should identify the mechanisms of this association and determine whether PTSD treatment offsets CHD risk