236 research outputs found

    All at Once: Transient Pulsations, Spin-down, and a Glitch from the Pulsating Ultraluminous X-Ray Source M82 X-2

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    The first pulsating ultraluminous X-ray source (PULX) to be identified is M82 X-2. After the discovery in 2014, NuSTAR observed the M82 field 15 times throughout 2015 and 2016. In this paper, we report the results of pulsation searches in all of these data sets and find only one new detection. This new detection allows us to refine the orbital period of the source and measure an average spin-down rate between 2014 and 2016 of ∼-6 × 10-11 Hz s-1, which is in contrast to the strong spin-up seen during the 2014 observations, representing the first detection of spin-down in a PULX system. Thanks to the improved orbital solution allowed by this new detection, we are also able to detect pulsations in additional segments of the original 2014 data set. We find a glitch superimposed on the very strong and variable spin-up already reported - the first positive glitch identified in a PULX system. We discuss the new findings in the context of current leading models for PULXs

    A dust-enshrouded tidal disruption event with a resolved radio jet in a galaxy merger

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    Tidal disruption events (TDEs) are transient flares produced when a star is ripped apart by the gravitational field of a supermassive black hole (SMBH). We have observed a transient source in the western nucleus of the merging galaxy pair Arp 299 that radiated >1.5 × 10 erg at infrared and radio wavelengths but was not luminous at optical or x-ray wavelengths. We interpret this as a TDE with much of its emission reradiated at infrared wavelengths by dust. Efficient reprocessing by dense gas and dust may explain the difference between theoretical predictions and observed luminosities of TDEs. The radio observations resolve an expanding and decelerating jet, probing the jet formation and evolution around a SMBH. Copyright © 2018, American Association for the Advancement of ScienceS.M. acknowledges financial support from the Academy of Finland (pmject 8120503). The research leading to these mats has received funding from the European.. Commission Seventh Framework Programme (FP/2007-2013) under grant agreement number & 227290, 283393 (RadioNc-t) and 60725 (HELP). AA., M.P.-T., N.R.-O. and R.H.T. acknowledge support from the Spanish MINECO through grants AYA2012-38491-002-02 and AYA2015 63939 C2 1 P. P.G.J. acknowledges support from European Research Council Consolidator Grant 647208. C.R.-C. acknowledges support by the Ministry of Economy, Development and Tourism's Millennium Science Initiative through grant 10120009, awarded to The Millennium. Institute of Astrophysics, MAS Chile, and from CONICYT through FONDECYT grant 3150238 and China-CON1CYT fund CAS160313. P.M. and M.A.A. acknowledge support from the ERC research grant CAMAP-250276, and partial support from the Spanish MINECO grant AYA2015-66889C2-1P Lard the local Valencia government ghat PROMETE0-11-2014069. FIE. acknowledges support from a Science Foundation Ireland-Royal Society University Research Fellowship. D.L.C. acknowledges support from grants ST/0001901/4 ST/J001368/1, ST/ K001051/1, and st/N0001138/1. P.V. acknowledges support from the National Research Foundation of South Africa.. J.H. acknowledges financial support tom the Finis h ChAth ral Fouridation and the Virile), YIP and Kahle Vais8I8 Foundation. J.K. acknowledges financial support from the Academy of Finland (grant 311138)

    Histone hyperacetylation disrupts core gene regulatory architecture in rhabdomyosarcoma

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    Core regulatory transcription factors (CR TFs) orchestrate the placement of super-enhancers (SEs) to activate transcription of cell-identity specifying gene networks, and are critical in promoting cancer. Here, we define the core regulatory circuitry of rhabdomyosarcoma and identify critical CR TF dependencies. These CR TFs build SEs that have the highest levels of histone acetylation, yet paradoxically the same SEs also harbor the greatest amounts of histone deacetylases. We find that hyperacetylation selectively halts CR TF transcription. To investigate the architectural determinants of this phenotype, we used absolute quantification of architecture (AQuA) HiChIP, which revealed erosion of native SE contacts, and aberrant spreading of contacts that involved histone acetylation. Hyperacetylation removes RNA polymerase II (RNA Pol II) from core regulatory genetic elements, and eliminates RNA Pol II but not BRD4 phase condensates. This study identifies an SE-specific requirement for balancing histone modification states to maintain SE architecture and CR TF transcription

    Spi-OPS : Spitzer and CHEOPS confirm the near-polar orbit of MASCARA-1 b and reveal a hint of dayside reflection

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    A.C.C. and T.G.W. acknowledge support from STFC consolidated grant number ST/M001296/1.Context. The light curves of tidally locked hot Jupiters transiting fast-rotating, early-type stars are a rich source of information about both the planet and star, with full-phase coverage enabling a detailed atmospheric characterisation of the planet. Although it is possible to determine the true spin–orbit angle Ψ – a notoriously difficult parameter to measure – from any transit asymmetry resulting from gravity darkening induced by the stellar rotation, the correlations that exist between the transit parameters have led to large disagreements in published values of Ψ for some systems. Aims. We aimed to study these phenomena in the light curves of the ultra-hot Jupiter MASCARA-1 b, which is characteristically similar to well-studied contemporaries such as KELT-9 b and WASP-33 b. Methods. We obtained optical CHaracterising ExOPlanet Satellite (CHEOPS) transit and occultation light curves of MASCARA-1 b, and analysed them jointly with a Spitzer/IRAC 4.5 μm full-phase curve to model the asymmetric transits, occultations, and phase-dependent flux modulation. For the latter, we employed a novel physics-driven approach to jointly fit the phase modulation by generating a single 2D temperature map and integrating it over the two bandpasses as a function of phase to account for the differing planet–star flux contrasts. The reflected light component was modelled using the general ab initio solution for a semi-infinite atmosphere. Results. When fitting the CHEOPS and Spitzer transits together, the degeneracies are greatly diminished and return results consistent with previously published Doppler tomography. Placing priors informed by the tomography achieves even better precision, allowing a determination of Ψ = 72.1−2.4+2.5 deg. From the occultations and phase variations, we derived dayside and nightside temperatures of 3062−68+66 K and 1720 ± 330 K, respectively.Our retrieval suggests that the dayside emission spectrum closely follows that of a blackbody. As the CHEOPS occultation is too deep to be attributed to blackbody flux alone, we could separately derive geometric albedo Ag = 0.171−0.068+0.066 and spherical albedo As = 0.266−0.100+0.097 from the CHEOPS data, and Bond albedoAB = 0.057−0.101+0.083 from the Spitzer phase curve.Although small, the Ag and As indicate that MASCARA-1 b is more reflective than most other ultra-hot Jupiters, where H− absorption is expected to dominate. Conclusions. Where possible, priors informed by Doppler tomography should be used when fitting transits of fast-rotating stars, though multi-colour photometry may also unlock an accurate measurement of Ψ. Our approach to modelling the phase variations at different wavelengths provides a template for how to separate thermal emission from reflected light in spectrally resolved James Webb Space Telescope phase curve data.Publisher PDFPeer reviewe

    The genetic architecture of the human cerebral cortex

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    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

    Reproducibility in the absence of selective reporting : An illustration from large-scale brain asymmetry research

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    Altres ajuts: Max Planck Society (Germany).The problem of poor reproducibility of scientific findings has received much attention over recent years, in a variety of fields including psychology and neuroscience. The problem has been partly attributed to publication bias and unwanted practices such as p-hacking. Low statistical power in individual studies is also understood to be an important factor. In a recent multisite collaborative study, we mapped brain anatomical left-right asymmetries for regional measures of surface area and cortical thickness, in 99 MRI datasets from around the world, for a total of over 17,000 participants. In the present study, we revisited these hemispheric effects from the perspective of reproducibility. Within each dataset, we considered that an effect had been reproduced when it matched the meta-analytic effect from the 98 other datasets, in terms of effect direction and significance threshold. In this sense, the results within each dataset were viewed as coming from separate studies in an "ideal publishing environment," that is, free from selective reporting and p hacking. We found an average reproducibility rate of 63.2% (SD = 22.9%, min = 22.2%, max = 97.0%). As expected, reproducibility was higher for larger effects and in larger datasets. Reproducibility was not obviously related to the age of participants, scanner field strength, FreeSurfer software version, cortical regional measurement reliability, or regional size. These findings constitute an empirical illustration of reproducibility in the absence of publication bias or p hacking, when assessing realistic biological effects in heterogeneous neuroscience data, and given typically-used sample sizes

    ENIGMA and global neuroscience: A decade of large-scale studies of the brain in health and disease across more than 40 countries

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    This review summarizes the last decade of work by the ENIGMA (Enhancing NeuroImaging Genetics through Meta Analysis) Consortium, a global alliance of over 1400 scientists across 43 countries, studying the human brain in health and disease. Building on large-scale genetic studies that discovered the first robustly replicated genetic loci associated with brain metrics, ENIGMA has diversified into over 50 working groups (WGs), pooling worldwide data and expertise to answer fundamental questions in neuroscience, psychiatry, neurology, and genetics. Most ENIGMA WGs focus on specific psychiatric and neurological conditions, other WGs study normal variation due to sex and gender differences, or development and aging; still other WGs develop methodological pipelines and tools to facilitate harmonized analyses of "big data" (i.e., genetic and epigenetic data, multimodal MRI, and electroencephalography data). These international efforts have yielded the largest neuroimaging studies to date in schizophrenia, bipolar disorder, major depressive disorder, post-traumatic stress disorder, substance use disorders, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, autism spectrum disorders, epilepsy, and 22q11.2 deletion syndrome. More recent ENIGMA WGs have formed to study anxiety disorders, suicidal thoughts and behavior, sleep and insomnia, eating disorders, irritability, brain injury, antisocial personality and conduct disorder, and dissociative identity disorder. Here, we summarize the first decade of ENIGMA's activities and ongoing projects, and describe the successes and challenges encountered along the way. We highlight the advantages of collaborative large-scale coordinated data analyses for testing reproducibility and robustness of findings, offering the opportunity to identify brain systems involved in clinical syndromes across diverse samples and associated genetic, environmental, demographic, cognitive, and psychosocial factors

    Novel genetic loci associated with hippocampal volume

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    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
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