The rarity of terrestrial gamma-ray flashes

We report on the first search for Terrestrial Gamma-ray Flashes (TGFs) from altitudes where they are thought to be produced. The Airborne Detector for Energetic Lightning Emissions (ADELE), an array of gamma-ray detectors, was flown near the tops of Florida thunderstorms in August/September 2009. The plane passed within 10 km horizontal distance of 1213 lightning discharges and only once detected a TGF. If these discharges had produced TGFs of the same intensity as those seen from space, every one should have been seen by ADELE. Separate and significant nondetections are established for intracloud lightning, negative cloud-to-ground lightning, and narrow bipolar events. We conclude that TGFs are not a primary triggering mechanism for lightning. We estimate the TGF-to-flash ratio to be on the order of 10^(−2) to 10^(−3) and show that TGF intensities cannot follow the well-known power-law distribution seen in earthquakes and solar flares, due to our limits on the presence of faint events

A terrestrial gamma ray flash observed from an aircraft

On 21 August 2009, the Airborne Detector for Energetic Lightning Emissions (ADELE), an array of six gamma-ray detectors, detected a brief burst of gamma rays while flying aboard a Gulfstream V jet near two active thunderstorm cells. The duration and spectral characteristics of the event are consistent with the terrestrial gamma ray flashes (TGFs) seen by instruments in low Earth orbit. A long-duration, complex +IC flash was taking place in the nearer cell at the same time, at a distance of ~10 km from the plane. The sferics that are probably associated with this flash extended over 54 ms and included several ULF pulses corresponding to charge moment changes of up to 30 C km, this value being in the lower half of the range of sferics associated with TGFs seen from space. Monte Carlo simulations of gamma ray propagation in the Earth's atmosphere show that a TGF of normal intensity would, at this distance, have produced a gamma ray signal in ADELE of approximately the size and spectrum that was actually observed. We conclude that this was the first detection of a TGF from an aircraft. We show that because of the distance, ADELE's directional and spectral capabilities could not strongly constrain the source altitude of the TGF but that such constraints would be possible for TGFs detected at closer range

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease