Stephan's Quintet: The X-ray Anatomy of a Multiple Galaxy Collision

Chandra observations of the compact galaxy group known as Stephan's Quintet (SQ) are presented. The major morphological features that were discovered with the ROSAT HRI are now imaged with higher resolution and S/N. The large scale shock (1.5', ~40kpc if at 85 Mpc) is resolved into a narrow NS feature embedded in more extended diffuse emission (D>=3'). The NS structure is somewhat clumpy, more sharply bounded on the W side and prominent only in the soft band (energies below ~2 keV). Its observational properties are best explained as a shock produced by a high velocity encounter between NGC7318b, a ``new intruder'', and the intergalactic medium in SQ. The shock conditions near the high speed intruder suggest that a bow shock is propagating into a pre-existing HI cloud and heating the gas to a temperature of ~0.5 keV. The low temperature in the shock is a problem unless we postulate an oblique shock. One member, NGC7319, hosts a Seyfert 2 nucleus, with an intrinsic luminosity Lx=10^43 erg/s, embedded in a region of more diffuse emission with 10'' radius extent. The nuclear spectrum can be modeled with a strongly absorbed power-law typical of this class of sources. Several additional compact sources are detected including three in foreground NGC7320. Some of these sources are very luminous and could be related to the ultraluminous X-ray sources found in nearby galaxies.Comment: Accepted for publication in Astronomy & Astrophysics Quality of figures has been degraded to fit in the astroph requirements; fig12 could not be inserted in the tex and is given as a jpe

Gene expression response in target organ and whole blood varies as a function of target organ injury phenotype

Histopathology, clinical chemistry, hematology and gene expression data were collected from the rat liver and blood after treatment with eight known hepatotoxins

The contribution of X-linked coding variation to severe developmental disorders

Over 130 X-linked genes have been robustly associated with developmental disorders, and X-linked causes have been hypothesised to underlie the higher developmental disorder rates in males. Here, we evaluate the burden of X-linked coding variation in 11,044 developmental disorder patients, and find a similar rate of X-linked causes in males and females (6.0% and 6.9%, respectively), indicating that such variants do not account for the 1.4-fold male bias. We develop an improved strategy to detect X-linked developmental disorders and identify 23 significant genes, all of which were previously known, consistent with our inference that the vast majority of the X-linked burden is in known developmental disorder-associated genes. Importantly, we estimate that, in male probands, only 13% of inherited rare missense variants in known developmental disorder-associated genes are likely to be pathogenic. Our results demonstrate that statistical analysis of large datasets can refine our understanding of modes of inheritance for individual X-linked disorders