17 research outputs found
Puzzled by GRB 060218
We study the optical-UV/X-ray spectral energy distribution of GRB 060218
during the prompt phase and during what seems to be the afterglow phase. The
results are puzzling, since if the opt-UV and the X-ray emission belong to a
single backbody (BB), then its luminosity is too large, and this BB cannot be
interpreted as the signature of the shock breakout of the supernova. There are
also serious problems in associating the emission expected by the supernova
shock breakout with either the opt-UV or the X-ray emission. In the former case
we derive too small ejecta velocities; in the latter case, on the contrary, the
required velocity is too large, corresponding to the large radius of a BB
required to peak close to the UV band. We then present what we think is the
most conservative alternative explanation, namely a synchrotron spectrum,
self-absorbed in the opt-UV and extending up to the X-ray band, where we
observe the emission of the most energetic electrons, which are responsible for
the exponential roll-over of the spectrum. The obtained fit can explain the
entire spectrum except the BB observed in the X-rays, which must be a separate
component. The puzzling feature of this interpretation is that the same model
is required to explain the spectrum also at later times, up to 1e5 s, because
the opt-UV emission remains constant in shape and also (approximately) in
normalisation. In this case the observed X-ray flux is produced by self-Compton
emission. Thus the prompt emission phase should last for ~1e5 s or more.
Finally, we show that the BB observed in X-rays, up to 7000 seconds, can be
photospheric emission from the cocoon or stellar material, energized by the GRB
jet at radii comparable to the stellar radius (i.e. 1e10-1e11 cm), not very far
from where this material becomes transparent (e.g. 1e12 cm).Comment: revised version accepted for publication in MNRAS (Letters
Autoantibodies against type I IFNs in patients with life-threatening COVID-19
Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men
Vascular Remodeling in Health and Disease
The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall