Filamentary structures of ionized gas in Cygnus X

Interstellar matter and star formatio

Associations of autozygosity with a broad range of human phenotypes

In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding coefficients (FROH) for >1.4 million individuals, we show that FROH is significantly associated (p < 0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: FROH equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44–66%] in the odds of having children. Finally, the effects of FROH are confirmed within full-sibling pairs, where the variation in FROH is independent of all environmental confounding

Polarized point sources in the LOFAR Two-meter Sky Survey: A preliminary catalog

The polarization properties of radio sources at very low frequencies (<200 MHz) have not been widely measured, but the new generation of low-frequency radio telescopes, including the Low Frequency Array (LOFAR: a Square Kilometre Array Low pathfinder), now gives us the opportunity to investigate these properties. In this paper, we report on the preliminary development of a data reduction pipeline to carry out polarization processing and Faraday tomography for data from the LOFAR Two-meter Sky Survey (LOTSS) and present the results of this pipeline from the LOTSS preliminary data release region (10h45m–15h30m right ascension, 45°–57° declination, 570 square degrees). We have produced a catalog of 92 polarized radio sources at 150 MHz at 4.′3 resolution and 1 mJy rms sensitivity, which is the largest catalog of polarized sources at such low frequencies. We estimate a lower limit to the polarized source surface density at 150 MHz, with our resolution and sensitivity, of 1 source per 6.2 square degrees. We find that our Faraday depth measurements are in agreement with previous measurements and have significantly smaller errors. Most of our sources show significant depolarization compared to 1.4 GHz, but there is a small population of sources with low depolarization indicating that their polarized emission is highly localized in Faraday depth. We predict that an extension of this work to the full LOTSS data would detect at least 3400 polarized sources using the same methods, and probably considerably more with improved data processing

Polarized point sources in LOTSS-HETDEX

Item does not contain fulltextVisibility data taken from LOTSS, imaged in polarization, and had RM synthesis applied. Resulting RM spectra were searched for polarization peaks. Detected peaks that were determined to not be foreground or instrumental effects were collected in this catalog. Source locations (for peak searches) were selected from TGSS-ADR1 (J/A+A/598/A78). Due to overlap between fields, some sources were detected multiple times, as recorded in the Ndet column. Polarized sources were cross-matched with the high-resolution LOTSS images (Shimwell+, in prep), and WISE and PanSTARRS images, which were used to determine the source classification and morphology. (1 data file)

Polarized point sources in LOTSS-HETDEX

Visibility data taken from LOTSS, imaged in polarization, and had RM synthesis applied. Resulting RM spectra were searched for polarization peaks. Detected peaks that were determined to not be foreground or instrumental effects were collected in this catalog. Source locations (for peak searches) were selected from TGSS-ADR1 (J/A+A/598/A78). Due to overlap between fields, some sources were detected multiple times, as recorded in the Ndet column. Polarized sources were cross-matched with the high-resolution LOTSS images (Shimwell+, in prep), and WISE and PanSTARRS images, which were used to determine the source classification and morphology. (1 data file)

Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis.

Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10 &lt;sup&gt;-10&lt;/sup&gt; ). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression r &lt;sub&gt;g&lt;/sub&gt; = 0.63, insomnia r &lt;sub&gt;g&lt;/sub&gt; = 0.47), physical health (overweight r &lt;sub&gt;g&lt;/sub&gt; = 0.19, waist-to-hip ratio r &lt;sub&gt;g&lt;/sub&gt; = 0.32), smoking (r &lt;sub&gt;g&lt;/sub&gt; = 0.54), cognitive ability (intelligence r &lt;sub&gt;g&lt;/sub&gt; = -0.40), educational attainment (years of schooling r &lt;sub&gt;g&lt;/sub&gt; = -0.46) and reproductive traits (age at first birth r &lt;sub&gt;g&lt;/sub&gt; = -0.58, father's age at death r &lt;sub&gt;g&lt;/sub&gt; = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB