1,242 research outputs found
A Neutron Star Binary Merger Model for GW170817/GRB170817a/SSS17a
The merging neutron star gravitational wave event GW170817 has been observed
throughout the entire electromagnetic spectrum from radio waves to
-rays. The resulting energetics, variability, and light curves are
shown to be consistent with GW170817 originating from the merger of two neutron
stars, in all likelihood followed by the prompt gravitational collapse of the
massive remnant. The available -ray, X-ray and radio data provide a
clear probe for the nature of the relativistic ejecta and the non-thermal
processes occurring within, while the ultraviolet, optical and infrared
emission are shown to probe material torn during the merger and subsequently
heated by the decay of freshly synthesized -process material. The simplest
hypothesis that the non-thermal emission is due to a low-luminosity short
-ray burst (sGRB) seems to agree with the present data. While low
luminosity sGRBs might be common, we show here that the collective prompt and
multi-wavelength observations are also consistent with a typical, powerful sGRB
seen off-axis. Detailed follow-up observations are thus essential before we can
place stringent constraints on the nature of the relativistic ejecta in
GW170817.Comment: 9 pages, 5 figures, accepted to ApJ Letter
Electromagnetic Evidence that SSS17a is the Result of a Binary Neutron Star Merger
11 hours after the detection of gravitational wave source GW170817 by the
Laser Interferometer Gravitational-Wave Observatory and Virgo Interferometers,
an associated optical transient SSS17a was discovered in the galaxy NGC 4993.
While the gravitational wave data indicate GW170817 is consistent with the
merger of two compact objects, the electromagnetic observations provide
independent constraints of the nature of that system. Here we synthesize all
optical and near-infrared photometry and spectroscopy of SSS17a collected by
the One-Meter Two-Hemisphere collaboration. We find that SSS17a is unlike other
known transients. The source is best described by theoretical models of a
kilonova consisting of radioactive elements produced by rapid neutron capture
(the r-process). We find that SSS17a was the result of a binary neutron star
merger, reinforcing the gravitational wave result.Comment: 21 pages, 4 figures, accepted to Scienc
The Dual Impact of HIV-1 Infection and Aging on Naïve CD4+ T-Cells: Additive and Distinct Patterns of Impairment
HIV-1-infected adults over the age of 50 years progress to AIDS more rapidly than adults in their twenties or thirties. In addition, HIV-1-infected individuals receiving antiretroviral therapy (ART) present with clinical diseases, such as various cancers and liver disease, more commonly seen in older uninfected adults. These observations suggest that HIV-1 infection in older persons can have detrimental immunological effects that are not completely reversed by ART. As naïve T-cells are critically important in responses to neoantigens, we first analyzed two subsets (CD45RA+CD31+ and CD45RA+CD31-) within the naïve CD4+ T-cell compartment in young (20–32 years old) and older (39–58 years old), ART-naïve, HIV-1 seropositive individuals within 1–3 years of infection and in age-matched seronegative controls. HIV-1 infection in the young cohort was associated with lower absolute numbers of, and shorter telomere lengths within, both CD45RA+CD31+CD4+ and CD45RA+CD31-CD4+ T-cell subsets in comparison to age-matched seronegative controls, changes that resembled seronegative individuals who were decades older. Longitudinal analysis provided evidence of thymic emigration and reconstitution of CD45RA+CD31+CD4+ T-cells two years post-ART, but minimal reconstitution of the CD45RA+CD31-CD4+ subset, which could impair de novo immune responses. For both ART-naïve and ART-treated HIV-1-infected adults, a renewable pool of thymic emigrants is necessary to maintain CD4+ T-cell homeostasis. Overall, these results offer a partial explanation both for the faster disease progression of older adults and the observation that viral responders to ART present with clinical diseases associated with older adults
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