Constraining the electric charges of some astronomical bodies in Reissner-Nordstrom spacetimes and generic r^-2-type power-law potentials from orbital motions

We put model-independent, dynamical constraints on the net electric charge Q of some astronomical and astrophysical objects by assuming that their exterior spacetimes are described by the Reissner-Nordstroem metric, which induces an additional potential U_RN \propto Q^2 r^-2. Our results extend to other hypothetical power-law interactions inducing extra-potentials U_pert = r^-2 as well (abridged).Comment: LaTex2e, 16 pages, 3 figures, no tables, 128 references. Version matching the one at press in General Relativity and Gravitation (GRG). arXiv admin note: substantial text overlap with arXiv:1112.351

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

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

The effect of verb semantic class and verb frequency (entrenchment) on children's and adults' graded judgements of argument-structure overgeneralization errors

Item does not contain fulltextParticipants (aged 5-6 yrs, 9-10 yrs and adults) rated (using a five-point scale) grammatical (intransitive) and overgeneralized (transitive causative)(1) uses of a high frequency, low frequency and novel intransitive verb from each of three semantic classes [Pinker, S. (1989a). Learnability and cognition: The acquisition of argument structure. Cambridge, MA: MIT Press]: "directed motion" (fall, tumble), "going out of existence" (disappear, vanish) and "semivoluntary expression of emotion" (laugh, giggle). In support of Pinker's semantic verb class hypothesis, participants' preference for grammatical over overgeneralized uses of novel (and English) verbs increased between 5-6 yrs and 9-10 yrs, and was greatest for the latter class, which is associated with the lowest degree of direct external causation (the prototypical meaning of the transitive causative construction). In support of Braine and Brooks's [Braine, M.D.S., & Brooks, P.J. (1995). Verb argument strucure and the problem of avoiding an overgeneral grammar. In M. Tomasello & W. E. Merriman (Eds.), Beyond names for things: Young children's acquisition of verbs (pp. 352-376). Hillsdale, NJ: Erlbaum] entrenchment hypothesis, all participants showed the greatest preference for grammatical over ungrammatical uses of high frequency verbs, with this preference smaller for low frequency verbs, and smaller again for novel verbs. We conclude that both the formation of semantic verb classes and entrenchment play a role in children's retreat from argument-structure overgeneralization errors.43 p

Stratospheric ozone depletion

Solar ultraviolet radiation creates an ozone layer in the atmosphere which in turn completely absorbs the most energetic fraction of this radiation. This process both warms the air, creating the stratosphere between 15 and 50 km altitude, and protects the biological activities at the Earth's surface from this damaging radiation. In the last half-century, the chemical mechanisms operating within the ozone layer have been shown to include very efficient catalytic chain reactions involving the chemical species HO, HO(2), NO, NO(2), Cl and ClO. The NO(X) and ClO(X) chains involve the emission at Earth's surface of stable molecules in very low concentration (N(2)O, CCl(2)F(2), CCl(3)F, etc.) which wander in the atmosphere for as long as a century before absorbing ultraviolet radiation and decomposing to create NO and Cl in the middle of the stratospheric ozone layer. The growing emissions of synthetic chlorofluorocarbon molecules cause a significant diminution in the ozone content of the stratosphere, with the result that more solar ultraviolet-B radiation (290–320 nm wavelength) reaches the surface. This ozone loss occurs in the temperate zone latitudes in all seasons, and especially drastically since the early 1980s in the south polar springtime—the ‘Antarctic ozone hole’. The chemical reactions causing this ozone depletion are primarily based on atomic Cl and ClO, the product of its reaction with ozone. The further manufacture of chlorofluorocarbons has been banned by the 1992 revisions of the 1987 Montreal Protocol of the United Nations. Atmospheric measurements have confirmed that the Protocol has been very successful in reducing further emissions of these molecules. Recovery of the stratosphere to the ozone conditions of the 1950s will occur slowly over the rest of the twenty-first century because of the long lifetime of the precursor molecules