Performance Test Results of the NASA-457M v2 Hall Thruster

Performance testing of a second generation, 50 kW-class Hall thruster labeled NASA-457M v2 was conducted at the NASA Glenn Research Center. This NASA-designed thruster is an excellent candidate for a solar electric propulsion system that supports human exploration missions. Thruster discharge power was varied from 5 to 50 kW over discharge voltage and current ranges of 200 to 500 V and 15 to 100 A, respectively. Anode efficiencies varied from 0.56 to 0.71. The peak efficiency was similar to that of other state-of-the-art high power Hall thrusters, but outperformed these thrusters at lower discharge voltages. The 0.05 to 0.18 higher anode efficiencies of this thruster compared to its predecessor were primarily due to which of two stable discharge modes the thruster was operated. One stable mode was at low magnetic field strengths, which produced high anode efficiencies, and the other at high magnetic fields where its predecessor was operated. Cathode keeper voltages were always within 2.1 to 6.2 V and cathode voltages were within 13 V of tank ground during high anode efficiency operation. However, during operation at high magnetic fields, cathode-to-ground voltage magnitudes increased dramatically, exceeding 30 V, due to the high axial magnetic field strengths in the immediate vicinity of the centrally-mounted cathode. The peak thrust was 2.3 N and this occurred at a total thruster input power of 50.0 kW at a 500 V discharge voltage. The thruster demonstrated a thrust-to-power range of 76.4 mN/kW at low power to 46.1 mN/kW at full power, and a specific impulse range of 1420 to 2740 s. For a discharge voltage of 300 V, where specific impulses would be about 2000 s, thrust efficiencies varied from 0.57 to 0.63

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

Morphometry for alpha particle hits of critical targets in the lungs. Final technical report

The objective of this study is to provide detailed data on the number, location and type of critical target cells in the airspaces and to use these data in order to make risk assessments of the health effects of radon and radon progeny in the lungs. This will be done by quantitative morphometric study of the distribution of the various cell types and mucous lining layers in the lungs. The results provide anatomically correct models for dosimetry in the rate and human airways which significantly improve the ability to do risk assessment for radon exposures by providing quantitative data for specific cell types and provide a basis for mechanism based comparison between data available in animal exposures and human epidemiology