Erratum: Corrigendum to “Development and initial validation of the Role Strain Questionnaire for Junior Athletes (RSQ-JA)” (Psychology of Sport and Exercise (2016) 24 (168–178)(S146902921630022X)(10.1016/j.psychsport.2016.02.004))

The authors regret to let us know that there is an authorship change in the article. The authors would like add another author to the article namely Fiona Chun Man Ling, as they believe that she has made a substantial intellectual contribution to this work and is deserving authorship. As such, they would like to change the reference of the article to: Fleur E.C.A. van Rens a, *, Erika Borkoles b, Damian Farrow a, c, Thomas Curran d, Fiona Chun Man Ling a, Remco C.J. Polman e The authors would like to apologise for any inconvenience caused

Antarctic ice sheet discharge driven by atmosphere-ocean feedbacks at the Last Glacial Termination

Reconstructing the dynamic response of the Antarctic ice sheets to warming during the Last Glacial Termination (LGT; 18,000–11,650 yrs ago) allows us to disentangle ice-climate feedbacks that are key to improving future projections. Whilst the sequence of events during this period is reasonably well-known, relatively poor chronological control has precluded precise alignment of ice, atmospheric and marine records, making it difficult to assess relationships between Antarctic ice-sheet (AIS) dynamics, climate change and sea level. Here we present results from a highly-resolved ‘horizontal ice core’ from the Weddell Sea Embayment, which records millennial-scale AIS dynamics across this extensive region. Counterintuitively, we find AIS mass-loss across the full duration of the Antarctic Cold Reversal (ACR; 14,600–12,700 yrs ago), with stabilisation during the subsequent millennia of atmospheric warming. Earth-system and ice-sheet modelling suggests these contrasting trends were likely Antarctic-wide, sustained by feedbacks amplified by the delivery of Circumpolar Deep Water onto the continental shelf. Given the anti-phase relationship between inter-hemispheric climate trends across the LGT our findings demonstrate that Southern Ocean-AIS feedbacks were controlled by global atmospheric teleconnections. With increasing stratification of the Southern Ocean and intensification of mid-latitude westerly winds today, such teleconnections could amplify AIS mass loss and accelerate global sea-level rise

Post-Newtonian SPH calculations of binary neutron star coalescence. I. Method and first results

We present the first results from our Post-Newtonian (PN) Smoothed Particle Hydrodynamics (SPH) code, which has been used to study the coalescence of binary neutron star (NS) systems. The Lagrangian particle-based code incorporates consistently all lowest-order (1PN) relativistic effects, as well as gravitational radiation reaction, the lowest-order dissipative term in general relativity. We test our code on sequences of single NS models of varying compactness, and we discuss ways to make PN simulations more relevant to realistic NS models. We also present a PN SPH relaxation procedure for constructing equilibrium models of synchronized binaries, and we use these equilibrium models as initial conditions for our dynamical calculations of binary coalescence. Though unphysical, since tidal synchronization is not expected in NS binaries, these initial conditions allow us to compare our PN work with previous Newtonian results. We compare calculations with and without 1PN effects, for NS with stiff equations of state, modeled as polytropes with $\Gamma=3$. We find that 1PN effects can play a major role in the coalescence, accelerating the final inspiral and causing a significant misalignment in the binary just prior to final merging. In addition, the character of the gravitational wave signal is altered dramatically, showing strong modulation of the exponentially decaying waveform near the end of the merger. We also discuss briefly the implications of our results for models of gamma-ray bursts at cosmological distances.Comment: RevTeX, 37 pages, 17 figures, to appear in Phys. Rev. D, minor corrections onl

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

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

Genetic and Functional Analyses of SHANK2 Mutations Suggest a Multiple Hit Model of Autism Spectrum Disorders

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