89 research outputs found

    Unmarried Fathers’ Earnings Trajectories: Does Partnership Status Matter?

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    Married men earn more than unmarried men. Previous research suggests that marriage itself causes some of the difference, but includes few men who fathered children out of wedlock. This paper asks whether increasing marriage (and possibly cohabitation) following a non-marital birth is likely to increase fathers’ earnings and labor supply. The analyses are based on a new birth cohort study the Fragile Families and Child Wellbeing Study which follows unmarried parents for the first five years after their child’s birth. Results provide some support for the idea that increasing marriage will lead to increased fathers’ earnings.Cohabitation, marriage, income, men, males, earnings, income, children

    HAZMAT VI: The Evolution of Extreme Ultraviolet Radiation Emitted from Early M Star

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    Quantifying the evolution of stellar extreme ultraviolet (EUV, 100 -- 1000 A\overset{\circ}{A}) emission is critical for assessing the evolution of planetary atmospheres and the habitability of M dwarf systems. Previous studies from the HAbitable Zones and M dwarf Activity across Time (HAZMAT) program showed the far- and near-UV (FUV, NUV) emission from M stars at various stages of a stellar lifetime through photometric measurements from the Galaxy Evolution Explorer (GALEX). The results revealed increased levels of short-wavelength emission that remain elevated for hundreds of millions of years. The trend for EUV flux as a function of age could not be determined empirically because absorption by the interstellar medium prevents access to the EUV wavelengths for the vast majority of stars. In this paper, we model the evolution of EUV flux from early M stars to address this observational gap. We present synthetic spectra spanning EUV to infrared wavelengths of 0.4 ±\pm 0.05 M_{\odot} stars at five distinct ages between 10 and 5000 Myr, computed with the PHOENIX atmosphere code and guided by the GALEX photometry. We model a range of EUV fluxes spanning two orders of magnitude, consistent with the observed spread in X-ray, FUV, and NUV flux at each epoch. Our results show that the stellar EUV emission from young M stars is 100 times stronger than field age M stars, and decreases as t1^{-1} after remaining constant for a few hundred million years. This decline stems from changes in the chromospheric temperature structure, which steadily shifts outward with time. Our models reconstruct the full spectrally and temporally resolved history of an M star's UV radiation, including the unobservable EUV radiation, which drives planetary atmospheric escape, directly impacting a planet's potential for habitability.Comment: 23 pages, 15 figures, accepted to Ap

    HAZMAT. IV. Flares and Superflares on Young M Stars in the Far Ultraviolet

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    M stars are powerful emitters of far-ultraviolet light. Over long timescales, a significant, possibly dominant, fraction of this emission is produced by stellar flares. Characterizing this emission is critical to understanding the atmospheres of the stars producing it and the atmospheric evolution of the orbiting planets subjected to it. Ultraviolet emission is known to be elevated for several hundred million years after M stars form. Whether or not the same is true of ultraviolet flare activity is a key concern for the evolution of exoplanet atmospheres. Hubble Space Telescope (HST) observations by the HAZMAT program (HAbitable Zones and M dwarf Activity across Time) detected 18 flares on young (40 Myr) early M stars in the Tucana-Horologium association over 10 hr of observations, 10 having energy >1030 erg. These imply that flares on young M stars are 100-1000× more energetic than those occurring at the same rate on “inactive,” field age M dwarfs. However, when energies are normalized by quiescent emission, there is no statistical difference between the young and field age samples. The most energetic flare observed, dubbed the “Hazflare,” emitted an energy of 1032.1 erg in the FUV, 30× more energetic than any stellar flare previously observed in the FUV with HST’s COS or STIS spectrographs. It was accompanied by 15,500 ± 400 K blackbody emission bright enough to designate it as a superflare (E > 1033 erg), with an estimated bolometric energy of {10}{33.6-0.2+0.1} erg. This blackbody emitted {18}-1+2% of its flux in the FUV (912-1700 Å), where molecules are generally most sensitive to photolysis. Such hot superflares in young, early M stars could play an important role in the evolution of nascent planetary atmospheres. Based on observations made with the NASA/ESA Hubble Space Telescope, obtained from the data archive at the Space Telescope Science Institute. STScI is operated by the Association of Universities for Research in Astronomy, Inc., under NASA contract NAS 5-26555

    Diagnosis of Partial Body Radiation Exposure in Mice Using Peripheral Blood Gene Expression Profiles

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    In the event of a terrorist-mediated attack in the United States using radiological or improvised nuclear weapons, it is expected that hundreds of thousands of people could be exposed to life-threatening levels of ionizing radiation. We have recently shown that genome-wide expression analysis of the peripheral blood (PB) can generate gene expression profiles that can predict radiation exposure and distinguish the dose level of exposure following total body irradiation (TBI). However, in the event a radiation-mass casualty scenario, many victims will have heterogeneous exposure due to partial shielding and it is unknown whether PB gene expression profiles would be useful in predicting the status of partially irradiated individuals. Here, we identified gene expression profiles in the PB that were characteristic of anterior hemibody-, posterior hemibody- and single limb-irradiation at 0.5 Gy, 2 Gy and 10 Gy in C57Bl6 mice. These PB signatures predicted the radiation status of partially irradiated mice with a high level of accuracy (range 79–100%) compared to non-irradiated mice. Interestingly, PB signatures of partial body irradiation were poorly predictive of radiation status by site of injury (range 16–43%), suggesting that the PB molecular response to partial body irradiation was anatomic site specific. Importantly, PB gene signatures generated from TBI-treated mice failed completely to predict the radiation status of partially irradiated animals or non-irradiated controls. These data demonstrate that partial body irradiation, even to a single limb, generates a characteristic PB signature of radiation injury and thus may necessitate the use of multiple signatures, both partial body and total body, to accurately assess the status of an individual exposed to radiation

    Gene Expression Signatures of Radiation Response Are Specific, Durable and Accurate in Mice and Humans

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    Background: Previous work has demonstrated the potential for peripheral blood (PB) gene expression profiling for the detection of disease or environmental exposures. Methods and Findings: We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses. Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy). A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100 % specific at distinguishing irradiated from septic animals. We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90 % and 81%, respectively. Conclusions: We conclude that PB gene expression profiles can be identified in mice and humans that are accurate i

    Evaluating the Effects of SARS-CoV-2 Spike Mutation D614G on Transmissibility and Pathogenicity.

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    Global dispersal and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of a selective advantage but may also be due to a random founder effect. We investigate the hypothesis for positive selection of spike D614G in the United Kingdom using more than 25,000 whole genome SARS-CoV-2 sequences. Despite the availability of a large dataset, well represented by both spike 614 variants, not all approaches showed a conclusive signal of positive selection. Population genetic analysis indicates that 614G increases in frequency relative to 614D in a manner consistent with a selective advantage. We do not find any indication that patients infected with the spike 614G variant have higher COVID-19 mortality or clinical severity, but 614G is associated with higher viral load and younger age of patients. Significant differences in growth and size of 614G phylogenetic clusters indicate a need for continued study of this variant

    Genetic mechanisms of critical illness in COVID-19.

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    Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
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