Formation and Evolution of Supermassive Black Holes

The correlation between the mass of supermassive black holes in galaxy nuclei and the mass of the galaxy spheroids or bulges (or more precisely their central velocity dispersion), suggests a common formation scenario for galaxies and their central black holes. The growth of bulges and black holes can commonly proceed through external gas accretion or hierarchical mergers, and are both related to starbursts. Internal dynamical processes control and regulate the rate of mass accretion. Self-regulation and feedback are the key of the correlation. It is possible that the growth of one component, either BH or bulge, takes over, breaking the correlation, as in Narrow Line Seyfert 1 objects. The formation of supermassive black holes can begin early in the universe, from the collapse of Population III, and then through gas accretion. The active black holes can then play a significant role in the re-ionization of the universe. The nuclear activity is now frequently invoked as a feedback to star formation in galaxies, and even more spectacularly in cooling flows. The growth of SMBH is certainly there self-regulated. SMBHs perturb their local environment, and the mergers of binary SMBHs help to heat and destroy central stellar cusps. The interpretation of the X-ray background yields important constraints on the history of AGN activity and obscuration, and the census of AGN at low and at high redshifts reveals the downsizing effect, already observed for star formation. History appears quite different for bright QSO and low-luminosity AGN: the first grow rapidly at high z, and their number density decreases then sharply, while the density of low-luminosity objects peaks more recently, and then decreases smoothly.Comment: 31 pages, 13 figures, review paper for Astrophysics Update

Detection of paralytic shellfish toxins in mussels and oysters using the qualitative neogen lateral-flow immunoassay: an interlaboratory study

Paralytic shellfish toxins (PSTs) in bivalve molluscs represent a public health risk and are controlled via compliance with a regulatory limit of 0.8 mg saxitoxin (STX)center dot 2HCl equivalents per kilogram of shellfish meat (eq/kg). Shellfish industries would benefit from the use of rapid immunological screening tests for PSTs to be used for regulation, but to date none have been fully validated. An interlaboratory study involving 16 laboratories was performed to determine the suitability of the Neogen test to detect PSTs in mussels and oysters. Participants performed the standard protocol recommended by the manufacturer and a modified protocol with a conversion step to improve detection of gonyautoxin 1&4. The statistical analysis showed that the protocols had good homogeneity across all laboratories, with satisfactory repeatability, laboratory, and reproducibility variation near the regulatory level. The mean probability of detection (POD) at 0.8 mg STX center dot 2HCl eq/kg using the standard protocol in mussels and oysters was 0.966 and 0.997, respectively, and 0.968 and 0.966 using the modified protocol. The estimated LOD in mussels was 0.316 mg STX center dot 2HCl eq/kg with the standard and 0.682 mg STX center dot 2HCl eq/kg with the modified protocol, and 0.710 and 0.734 mg STX center dot 2HCl eq/kg for oysters, respectively. The Neogen test may be acceptable for regulatory purposes for oysters in accordance with European Commission directives in which the standard protocol provides, at the regulatory level, a probability of a negative response of 0.033 on 95% of occasions. Its use for mussels is less consistent at the regulatory level due to the wide prediction interval around the POD

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

Defining Essential Regions of the Human Genome

There is a longstanding interest in identifying the subset of our genome that is the most essential to life and normal development. Such regions should be under the highest purifying selection, and therefore, exhibit lower nucleotide diversity. In the case of protein-coding genes, especially strong "constraint" should be observed against protein-altering (i.e., missense, stop-gain, frameshift, etc.) variants. Prior studies have attempted to identify constrained genes, but have been unable to identify focal regions of constraint within each gene: in other words, which specific regions of protein genes are most intolerant, and therefore most likely to cause disease when mutated? To address this question, Quinlan and colleagues studied genetic variation detected among >120,000 human exomes to reveal focal coding regions that lack variation in healthy individuals. These "constrained coding regions" (CCRs) are inferred to be under strong purifying selection and are enriched for known pathogenic variants. Perhaps the most intriguing aspect of this map of CCRs is the fact than many of the most constrained regions lie within genes that lacked prior disease association. Thus, these regions hold the promise of new disease gene discovery in the context of developmental disorders and are used to prioritize mutations in rare human diseases

Towards an archaeology of religion

Available from British Library Document Supply Centre- DSC:DX183070 / BLDSC - British Library Document Supply CentreSIGLEGBUnited Kingdo

Towards an archaeology of religion

Available from British Library Document Supply Centre- DSC:DX183070 / BLDSC - British Library Document Supply CentreSIGLEGBUnited Kingdo