NASA's CubeQuest Challenge - From Ground Tournaments to Lunar and Deep Space Derby

The First Flight of NASA's Space Launch System will feature 13 CubeSats that will launch into cis-lunar space. Three of these CubeSats are winners of the CubeQuest Challenge, part of NASA's Space Technology Mission Directorate (STMD) Centennial Challenge Program. In order to qualify for launch on EM-1, the winning teams needed to win a series of Ground Tournaments, periodically held since 2015. The final Ground Tournament, GT-4, was held in May 2017, and resulted in the Top 3 selection for the EM-1 launch opportunity. The Challenge now proceeds to the in-space Derbies, where teams must build and test their spacecraft before launch on EM-1. Once in space, they will compete for a variety of Communications and Propulsion-based challenges. This is the first Centennial Challenge to compete in space and is a springboard for future in-space Challenges. In addition, the technologies gained from this challenge will also propel development of deep space CubeSats

CubeQuest Challenge: Advanced CubeSat Technologies for Affordable Deep Space Science and Exploration Missions

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Affordable Vehicle Avionics

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NASA Cube Quest Challenge: Citizen Inventors Advance CubeSats into Deep Space on 2018 EM-1 Mission

Cube Quest Challenge, sponsored by Space Technology Mission Directorate\u27s Centennial Challenges program, is NASA\u27s first in-space prize competition. Cube Quest is open to any U.S.-based, nongovernment CubeSat developer. Entrants will compete for one of three available 6U CubeSat dispenser slots on the EM-1 mission - the first un-crewed lunar flyby of the Orion spacecraft launched by the Space Launch System in early 2018. The Cube Quest Challenge will award up to $5M in prizes. The advanced CubeSat technologies demonstrated by Cube Quest winners will enable NASA, universities, and industry to more quickly and affordably accomplish science and exploration objectives. This paper describes the teams, their novel CubeSat designs, and the emerging technologies for CubeSat operations in deep space environment. Over a 2-year development period, teams demonstrate progress and vie for one of three available dispenser slots on NASA\u27s SLS vehicle through a series of ground-based competitions called Ground Tournaments . The first Ground Tournament (GT-1) was conducted in August of 2015. The remaining three events are at roughly 6-month intervals. Judges assess the team\u27s designs and mission plans for technical excellence and compliance with rules and safety requirements. The top three winners of the fourth Ground Tournament, scheduled for March 2017, will be selected for integration with the SLS vehicle. After being dispensed in a trans-lunar injection trajectory, the three competing CubeSats will boldly go where no CubeSat has operated before, to compete at the moon and well beyond. The in-space competition is also open to qualified teams that can procure their own launch. There are two competition tracks: Lunar Derby requires teams to successfully achieve and maintain a lunar orbit, while the Deep Space Derby will be conducted only after CubeSats have achieved a range of over 4M km from Earth. Once in either lunar orbit or beyond 4M km, teams will attempt to achieve or exceed communications data goals (rates and data volume over time), to survive the longest (up to a year), and to successfully communicate from the farthest distance (for the Deep Space Derby). To survive in deep space and demonstrate the rigor needed to operate at the moon or beyond and attempt prizes, teams will have to push the envelope of CubeSat capabilities. Teams will have to demonstrate advancements in propulsion in order to get into lunar orbit, in navigation without GPS or Earth\u27s magnetic field, in reliability, in fault tolerance and radiation hardening to survive and operate in deep space beyond the Van Allen belts, and in long distance communications capabilities that no CubeSat has previously demonstrated. Twelve teams of citizen inventors registered for GT-1 and ten for GT-2. About two thirds of the competitors are from academia, while the remaining teams are small companies. At GT-1 there was one high school team and a team comprised of one individual engineer. Cube Quest is open to any team at no charge. Teams develop CubeSats on their own time without government support

CubeSat Lunar and Deep Space Challenges

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CubeSat Lunar and Deep Space Challenges

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‘It's all the way you look at it, you know’: reading Bill ‘Bojangles’ Robinson's film career

This paper engages with a major paradox in African American tap dancer Bill ‘Bojangles’ Robinson's film image – namely, its concurrent adherences to and contestations of dehumanising racial iconography – to reveal the complex and often ambivalent ways in which identity is staged and enacted. Although Robinson is often understood as an embodiment of popular cultural imagery historically designed to dehumanise African Americans, this paper shows that Robinson's artistry displaces these readings by providing viewing pleasure for black, as much as white, audiences. Robinson's racially segregated scenes in Dixiana (1930) and Hooray for Love (1935) illuminate classical Hollywood's racial codes, whilst also showing how his inclusion within these otherwise all-white films provides grounding for creative and self-reflexive artistry. The films' references to Robinson's stage image and artistry overlap with minstrelsy-derived constructions of ‘blackness’, with the effect that they heighten possible interpretations of his cinematic persona by evading representational conclusion. Ultimately, Robinson's films should be read as sites of representational struggle that help to uncover the slipperiness of performances of African American identities in 1930s Hollywood

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

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 hospitalization2–4 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

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