Spitzer Observations of 3C Quasars and Radio Galaxies: Mid-Infrared Properties of Powerful Radio Sources

We have measured mid-infrared radiation from an orientation-unbiased sample of 3CRR galaxies and quasars at redshifts 0.4 < z < 1.2 with the IRS and MIPS instruments on the Spitzer Space Telescope. Powerful emission (L_24micron > 10^22.4 W/Hz/sr) was detected from all but one of the sources. We fit the Spitzer data as well as other measurements from the literature with synchrotron and dust components. The IRS data provide powerful constraints on the fits. At 15 microns, quasars are typically four times brighter than radio galaxies with the same isotropic radio power. Based on our fits, half of this difference can be attributed to the presence of non-thermal emission in the quasars but not the radio galaxies. The other half is consistent with dust absorption in the radio galaxies but not the quasars. Fitted optical depths are anti-correlated with core dominance, from which we infer an equatorial distribution of dust around the central engine. The median optical depth at 9.7 microns for objects with core-dominance factor R > 10^-2 is approximately 0.4; for objects with R < 10^-2, it is 1.1. We have thus addressed a long-standing question in the unification of FR II quasars and galaxies: quasars are more luminous in the mid-infrared than galaxies because of a combination of Doppler-boosted synchrotron emission in quasars and extinction in galaxies, both orientation-dependent effects.Comment: 42 pages, 14 figures plus two landscape tables. Accepted for publication in Ap

The galaxy-halo connection from a joint lensing, clustering and abundance analysis in the CFHTLenS/VIPERS field

We present new constraints on the relationship between galaxies and their host dark matter halos, measured from the location of the peak of the stellar-to-halo mass ratio (SHMR), up to the most massive galaxy clusters at redshift $z\sim0.8$ and over a volume of nearly 0.1~Gpc$^3$. We use a unique combination of deep observations in the CFHTLenS/VIPERS field from the near-UV to the near-IR, supplemented by $\sim60\,000$ secure spectroscopic redshifts, analysing galaxy clustering, galaxy-galaxy lensing and the stellar mass function. We interpret our measurements within the halo occupation distribution (HOD) framework, separating the contributions from central and satellite galaxies. We find that the SHMR for the central galaxies peaks at $M_{\rm h, peak} = 1.9^{+0.2}_{-0.1}\times10^{12} M_{\odot}$ with an amplitude of $0.025$, which decreases to $\sim0.001$ for massive halos ($M_{\rm h} > 10^{14} M_{\odot}$). Compared to central galaxies only, the total SHMR (including satellites) is boosted by a factor 10 in the high-mass regime (cluster-size halos), a result consistent with cluster analyses from the literature based on fully independent methods. After properly accounting for differences in modelling, we have compared our results with a large number of results from the literature up to $z=1$: we find good general agreement, independently of the method used, within the typical stellar-mass systematic errors at low to intermediate mass (${M}_{\star} < 10^{11} M_{\odot}$) and the statistical errors above. We have also compared our SHMR results to semi-analytic simulations and found that the SHMR is tilted compared to our measurements in such a way that they over- (under-) predict star formation efficiency in central (satellite) galaxies.Comment: 31 pages, 18 figures, 4 table. Accepted for publication in MNRAS. Online material available at http://www.cfhtlens.or

The galaxy-halo connection from a joint lensing, clustering and abundance analysis in the CFHTLenS/VIPERS field

We present new constraints on the relationship between galaxies and their host dark matter haloes, measured from the location of the peak of the stellar-to-halo mass ratio (SHMR), up to the most massive galaxy clusters at redshift z∼0.8 and over a volume of nearly 0.1Gpc3. We use a unique combination of deep observations in the CFHTLenS/VIPERS field from the near-UV to the near-IR, supplemented by ∼60 000 secure spectroscopic redshifts, analysing galaxy clustering, galaxy-galaxy lensing and the stellar mass function. We interpret our measurements within the halo occupation distribution (HOD) framework, separating the contributions from central and satellite galaxies. We find that the SHMR for the central galaxies peaks at $M_{\rm h, peak} = 1.9^{+0.2}_{-0.1}\times 10^{12}{\,{\rm M}_{{\odot }}}$ with an amplitude of 0.025, which decreases to ∼0.001 for massive haloes (${{{M}_{\rm h}}}> 10^{14} {\,{\rm M}_{{\odot }}}$). Compared to central galaxies only, the total SHMR (including satellites) is boosted by a factor of 10 in the high-mass regime (cluster-size haloes), a result consistent with cluster analyses from the literature based on fully independent methods. After properly accounting for differences in modelling, we have compared our results with a large number of results from the literature up to z=1: we find good general agreement, independently of the method used, within the typical stellar-mass systematic errors at low to intermediate mass (${{{M}_{\rm \star }}}<10^{11} {\,{\rm M}_{{\odot }}}$) and the statistical errors above. We have also compared our SHMR results to semi-analytic simulations and found that the SHMR is tilted compared to our measurements in such a way that they over- (under-) predict star formation efficiency in central (satellite) galaxie

Jet and torus orientations in high redshift radio galaxies

We examine the relative orientation of radio jets and dusty tori surrounding the active galactic nucleus (AGN) in powerful radio galaxies at z &gt; 1. The radio core dominance R = Pcore 20GHz/P extended 500MHz serves as an orientation indicator, measuring the ratio between the anisotropic Doppler-beamed core emission and the isotropic lobe emission. Assuming a fixed cylindrical geometry for the hot, dusty torus, we derive its inclination i by fitting optically-thick radiative transfer models to spectral energy distributions obtained with the Spitzer Space Telescope. We find a highly significant anti-correlation (p &lt; 0.0001) between R and i in our sample of 35 type 2 AGN combined with a sample of 18 z ~ 1 3CR sources containing both type 1 and 2 AGN. This analysis provides observational evidence both for the Unified scheme of AGN and for the common assumption that radio jets are in general perpendicular to the plane of the torus. The use of inclinations derived from mid-infrared photometry breaks several degeneracies which have been problematic in earlier analyses. We illustrate this by deriving the core Lorentz factor G from the R-i anti-correlation, Γ ≳ 1.3

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

Early versus delayed endocrine treatment of pN1-3 M0 prostate cancer without local treatment of the primary tumor: results of European Organisation for the Research and Treatment of Cancer 30846--a phase III study

The timing of endocrine treatment for prostate cancer remains controversial. The issue is addressed in protocol 30846 of the European Organisation for Research and Treatment of Cancer for patients with lymph node positive cancer without local treatment of the primary tumor. A total of 302 patients with metastatic regional lymph nodes who had not received local treatment for the primary tumor were included in the trial, of whom 234 were randomized to immediate vs delayed endocrine treatment. Endocrine treatment consisted of an luteinizing hormone-releasing hormone agonist and 1 month of antiandrogen treatment or surgical castration. The main end point of the trial was overall survival. Analysis followed the intent to treat principle. At a median followup of 9.6 years (8.7 in the randomized sample) 190 patients (62.9%) had died, including 76% of prostate cancer. In the randomized sample the HR for survival on delayed vs immediate treatment was 1.23 (95% CI 0.88 to 1.71), indicating a 23% nonsignificant trend in favor of early treatment. However, the wide CI showed that results remained compatible with true effects, ranging from a 12% benefit in favor of delayed treatment to a 71% detriment for the same treatment approach. While this study suggests an advantage for early treatment, it is under powered to show equivalence or superiority for the early or delayed approach. When dealing with individual patients, the potential survival advantage on early treatment must be balanced against potential advantages in quality of life on delayed treatmen

Early versus delayed endocrine treatment of T2-T3 pN1-3 M0 prostate cancer without local treatment of the primary tumour: final results of European Organisation for the Research and Treatment of Cancer protocol 30846 after 13 years of follow-up (a randomised controlled trial)

The timing of endocrine treatment (ET) for prostate cancer (PCa) remains controversial. The issue is addressed in European Organisation for the Research and Treatment of Cancer (EORTC) protocol 30846 for patients with lymph node-positive (pN1-3) cancer without local treatment of the primary tumour. To evaluate the effect of early versus delayed treatment in pN1-3 PCa. Two hundred thirty-four patients with histologically proven PCa and nodal metastases (pN1-3) were randomized to immediate versus delayed ET without treatment of the primary tumour. ET consisted of a depot luteinising hormone-releasing hormone (LHRH) agonist and 1 mo of an anti-androgen or surgical castration. The trial's main objective was to show non-inferiority of delayed ET to immediate ET by ruling out a hazard ratio (HR) of 1.50 for overall survival (OS), with 85% power at one-sided alpha=5%. All but three patients were treated as randomized. The median follow-up is 13 yr. The median protocol treatment duration was 2.7 yr in the delayed and 3.2 yr in the immediate ET groups. Overall, 193 patients (82.5%) have died (97 on delayed ET and 96 on immediate ET), 59.4% of them as a result of PCa. The intention-to-treat analysis shows a 22% increase in the hazard of death of those randomized to delayed treatment (HR=1.22, 95% confidence interval [CI]: 0.92, 1.62). The difference is not statistically significant, but non-inferiority is also not proved. The median OS on immediate ET is 7.6 yr (95% CI, 6.3-8.3 yr) versus 6.1 yr (95% CI, 5.7-7.3 yr) in the delayed ET group. The 10-yr cumulative incidence of death resulting from PCa was 55.6% in the delayed ET group versus 52.1% with immediate ET group. Similar conclusions hold for PCa-specific survival. After 13 years of follow-up, survival or PCa-specific survival between immediate and delayed ET appear similar, but the trial is underpowered to reach its goal of showing non-inferiorit