Examining Failures and Repairs on Supercomputerswith Multi-GPU Compute Nodes
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Computer science↗
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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.
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A Brief Review of Fusion Enabling Laser-Induced Damage Reduction, Management, and Repair strategies on at the National Ignition Facility
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Lasers, Optics and optical instruments↗
Materials exhibiting biomimetic carbon fixation and self-repair
A composition can photocatalytically reduce carbon dioxide.
Strano, Michael S.↗
In Situ Structural Repair and Protection of LWR Components Using Cold Spray - Phase IIA
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Johnson, Kyle↗
C56-14B-Photocured Hydropower Repair Coatings- Phase I-Final Report
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36 MATERIALS SCIENCE↗
Mitigation and Repair Coatings for SNF Canisters: Thermal and Radiation Behaviors – 24425
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Knight, Andrew William↗
An experiment to assess the cost-benefits of code inspections in large scale software development
This experiment (currently in progress) is designed to measure costs and benefits of different code inspection methods. It is being performed with a real development team writing software for a commercial product. The dependent variables for each code unit's inspection are the elapsed time and the number of defects detected. We manipulate the method of inspection by randomly assigning reviewers, varying the number of reviewers and the number of teams, and, when using more than one team, randomly assigning author repair and non-repair of detected defects between code inspections. After collecting and analyzing the first 17 percent of the data, we have discovered several interesting facts about reviewers, about the defects recorded during reviewer preparation and during the inspection collection meeting, and about the repairs that are eventually made. (1) Only 17 percent of the defects that reviewers record in their preparations are true defects that are later repaired. (2) Defects recorded at the inspection meetings fall into three categories: 18 percent false positives requiring no author repair, 57 percent soft maintenance where the author makes changes only for readability or code standard enforcement, and 25 percent true defects requiring repair. (3) The median elapsed calendar time for code inspections is 10 working days - 8 working days before the collection meeting and 2 after. (4) In the collection meetings, 31 percent of the defects discovered by reviewers during preparation are suppressed. (5) Finally, 33 percent of the true defects recorded are discovered at the collection meetings and not during any reviewer's preparation. The results to date suggest that inspections with two sessions (two different teams) of two reviewers per session (2sX2p) are the most effective. These two-session inspections may be performed with author repair or with no author repair between the two sessions. We are finding that the two-session, two-person with repair (2sX2pR) inspections are the most expensive, taking 15 working days of calendar time from the time the code is ready for review until author repair is complete, whereas two-session, two-person with no repair (2sX2pN) inspections take only 10 working days, but find about 10 percent fewer defects.
Porter, A.↗
Variability in Galactic Cosmic Radiation- Induced DNA Damage Response in Inbred Mice Is Modulated by Genetics
In radiation biology, the ability to predict cancer risk associated with exposure to low doses of high-LET (Linear Energy Transfer) ionizing radiation remains a challenge. Epidemiological methods lack the sensitivity and power to provide detailed risk estimates for cancer and ignore individual sensitivity. We have hypothesized that DNA repair capacity is the primary factor differentiating peoples radiation sensitivity. We previously showed in immortalized human cell lines that characterizing the dose and time dependence of p53-binding protein 1 (53BP1) foci formation in the nucleus following X-rays exposure is sufficient to predict DNA repair response to any other LET in the same cell line. We now tested this hypothesis across a population of mice with different genetic background. Fibroblast cells were extracted and cultivated from 76 individual mice from 15 different strains and exposed to HZE (high (H) atomic number (Z) and energy (E) galactic cosmic ray particles) particles and X-rays. Individual radiation sensitivities were investigated by high throughput measurement of DNA repair kinetics that evaluated 53bp1 foci numbers as a surrogate for DNA double-strand breaks at various times post-irradiation. Instead of just counting foci which can be hard to distinguish for high-LET or high doses, we also took into account the track structure of high-LET particles to compute the remaining number of unrepaired tracks as a function of time post-irradiation. As expected, the percentage of unrepaired track over a 48 hours follow-up period increased with LET. In addition, repair rate was modulated by genetics, with animals from the same strain showing small variance while large rate differences were observed between strains. Radiation strain sensitivity ranking was estimated based on repair rates from exposure to each LET evaluated in this work, and ranking for high-LET correlated better with ranking from high dose of X-ray, not low dose. At the in-vivo level, drops in T-cells and B-cells number measured 24 hours after 0.1 Gy (Gray) X-ray exposure, correlated with slower DNA repair kinetic in fibroblast cells of the same strains of mice. At the genomic level, mouse genome wide association (GWA) analysis identified seven significant genetic loci on chromosomes 2, 3, 7, 10, 11, 13 and 19 with different significance depending on the LET. Interestingly, for the two highest LET, a common locus on Chromosome 10 was identified with high enrichment for DNA repair associated genes.Overall, this work suggests that repair kinetics of primary skin fibroblasts is a good surrogate marker for in-vivo radiation sensitivities in other tissues and that this response is modulated by genetics. Our study also confirms that DNA repair kinetics following high doses of X-ray can be used to predict radiation sensitivity to high-LET.
High-LET Radiation↗
BLOOD-BASED MULTI-SCALE MODEL FOR CANCER RISK FROM GCR IN GENETICALLY DIVERSE POPULATIONS
OBJECTIVES AND METHODS This project addresses the challenge of understanding and predicting individual radiation sensitivity by integrating genetics, demographics and biomarker characteristics across species (mice and humans). We hypothesize that ex vivo DNA repair response to GCR components is a central determinant of cancer risk from space radiation and can serve as a biomarker of radiation risk in combination with genetics. Automated image quantification of 53BP1+ radiation-induced foci (RIF) during the first 4-48 h post-irradiation was performed as a function of dose and LET in non-immortalized primary skin fibroblasts derived from 76 mice across 15 strains (5 inbred reference strains and 10 collaborative-cross strains) exposed to X rays (0.1, 1 and 4 Gy), 350 MeV/n 40Ar and 600 MeV/n 56Fe (1.1 and 3 particles/100μm2), as well as in peripheral blood mononuclear cells (PBMCs) from 768 healthy donors (matched ethnicity, 50/50 male/female, 18-70 years old) exposed to gamma rays (0.1 and 1 Gy), 350 MeV/n 28Si, 350 MeV/n 40Ar and 600 MeV/n 56Fe (1.1 and 3 particles/100μm2). QUANTIFICATION OF 53BP1+ FOCI IN VITRO AND ASSOCIATIONS TO IN VIVO RADIATION SUSCEPTIBILITY IN 15 MOUSE STRAINS We reported in vitro repair kinetic and repairable fractions of RIF for the 15 mouse strains and introduced a mathematical model for RIF as a function of time, dose and LET. We noted that the metabolic activity of cells modulates the RIF response, and we introduced the open access tool terRIFic (Tool for Enhanced Results of RIF In Cells, https://radbiolab.shinyapps.io/terrific/) to correct for such bias using confluence level. Notably, at 4h post-irradiation, RIF/Gy decreased with dose or LET: as the dose or LET increases, so does the proximity of DNA double-strand-breaks (DSB) and our data suggest that proximal DSBs are brought together inside isolated RIF for repair. The RIF/Gy trend was inverted at 24h, suggesting RIF with high DSB content are more difficult to repair. We showed that in vitro metrics correlate with in vivo measurements in the same 15 mouse strains, such as survival levels of immune cells or spontaneous cancer incidence, suggesting a relationship between the efficiency of DSB repair and cancer risk or radiation toxicity. In addition to the efficiency of repair and persistent RIF, the amount of spontaneous foci before irradiation was also found to be strain dependent. Finally, we performed genome-wide association study in the same 15 mouse strains using all RIF phenotypes measured in vitro, identifying genes of interest and validating RIF as an ideal biomarker for individual radiation sensitivity. BASELINE 53BP1+ FOCI PREDICTS INDIVIDUAL HUMAN RESPONSE TO GCR COMPONENTS Based on the analysis of radiation responses of 576 donor PBMCs (using quantification of 53BP1+ foci, oxidative stress and cell death), we observed a wide variability of subject- and LET-dependent radiation responses, with radiation-induced DNA repair foci increasing with LET, though oxidative stress being notably reduced by high-LET irradiation, potentially due to a switch between hydrogen peroxide and oxygen radical-based mechanisms. We identified a relationship between few spontaneous DNA foci at baseline and increased DNA repair after irradiation, accompanied by an alteration in immunoregulatory cytokine secretion, which might be adapted as biomarkers to predict ionizing radiation sensitivity. Among demographic variables, only latent cytomegalovirus infection and age were predictive of high baseline foci formation. Finally, we have performed low-throughput whole genome sequencing of all samples and are currently in the process of identifying the genes and pathways associated with low and high-LET ionizing radiation sensitivity in humans.
53BP1↗
BRCA1 Mutation: A Predictive Marker for Radiation Therapy?
DNA repair, in particular, DNA double-strand break (DSB) repair, is essential for the survival of both normal and cancer cells. An elaborate repair mechanism has been developed in cells to efficiently repair the damaged DNA. The pathways predominately involved in DSB repair are homologous recombination and classic nonhomologous end-joining, although the alternative NHEJ pathway, a third DSB repair pathway, could also be important in certain contexts. The protein of BRCA1 encoded by the tumor suppressor gene BRCA1 regulates all DSB repair pathways. Given that DSBs represent the most biologically significant lesions induced by ionizing radiation and that impaired DSB repair leads to radiation sensitivity, it has been expected that cancer patients with BRCA1 mutations should benefit from radiation therapy. However, the clinical data have been conflicting and inconclusive. We provide an overview about the current status of the data regarding BRCA1 deficiency and radiation therapy sensitivity in both experimental models and clinical investigations. In addition, we discuss a strategy to potentiate the effects of radiation therapy by poly(ADP-ribose) polymerase inhibitors, the pharmacologic drugs being investigated as monotherapy for the treatment of patients with BRCA1/2 mutations.
62 RADIOLOGY AND NUCLEAR MEDICINE↗
Differential sensitivities of cellular XPA and PARP-1 to arsenite inhibition and zinc rescue
Arsenite directly binds to the zinc finger domains of the DNA repair protein poly (ADP ribose) polymerase (PARP)-1, and inhibits PARP-1 activity in the base excision repair (BER) pathway. PARP inhibition by arsenite enhances ultraviolet radiation (UVR)-induced DNA damage in keratinocytes, and the increase in DNA damage is reduced by zinc supplementation. However, little is known about the effects of arsenite and zinc on the zinc finger nucleotide excision repair (NER) protein xeroderma pigmentosum group A (XPA). In this study, we investigated the difference in response to arsenite exposure between XPA and PARP-1, and the differential effectiveness of zinc supplementation in restoring protein DNA binding and DNA damage repair. Arsenite targeted both XPA and PARP-1 in human keratinocytes, resulting in zinc loss from each protein and a pronounced decrease in XPA and PARP-1 binding to chromatin as demonstrated by Chip-on-Western assays. Zinc effectively restored DNA binding of PARP-1 and XPA to chromatin when zinc concentrations were equal to those of arsenite. In contrast, zinc was more effective in rescuing arsenite-augmented direct UVR-induced DNA damage than oxidative DNA damage. Taken together, our findings indicate that arsenite interferes with PARP-1 and XPA binding to chromatin, and that zinc supplementation fully restores DNA binding activity to both proteins in the cellular context. Interestingly, rescue of arsenite-inhibited DNA damage repair by supplemental zinc was more sensitive for DNA damage repaired by the XPA-associated NER pathway than for the PARP-1-dependent BER pathway. This study expands our understanding of arsenite's role in DNA repair inhibition and co-carcinogenesis. - Highlights: • Arsenite suppresses the chromatin binding activity of XPA and PARP-1. • Arsenite has greater effect on retention of direct DNA damage such as CPDs and 6.4-PPs. • Arsenite inhibits DNA repair through both BER and NER pathways.
60 APPLIED LIFE SCIENCES↗
Post-Closure Inspection Report for the Tonopah Test Range, Nevada: For Calendar Year 2017, Revision 0
This report provides the results of the annual post-closure inspections conducted at the closed corrective action units (CAUs) located on the Tonopah Test Range (TTR) and the Nevada Test and Training Range (NTTR). This report covers calendar year 2017 and includes visual inspection and repair activities completed at the following CAUs: CAU 400: Bomblet Pit and Five Points Landfill (TTR) CAU 407: Roller Coaster RadSafe Area (TTR) CAU 424: Area 3 Landfill Complexes (TTR) CAU 453: Area 9 UXO Landfill (TTR) CAU 487: Thunderwell Site (TTR) Visual inspections were conducted according to the post-closure plans in the approved closure reports and subsequent correspondence with the Nevada Division of Environmental Protection. The annual post-closure inspections were conducted on May 23, 2017. No maintenance or repair issues were noted at CAU 400 and CAU 487. Maintenance items and subsequent repairs include the following: CAU 407: A large animal burrow was observed in the southeast corner of the cover during the inspection. Two additional animal burrows were discovered during repair actions. All cover defects were repaired on January 9, 2018. CAU 424: CAS 03-08-002-A304 (Landfill Cell A3-4): A new monument was installed and the subsidence area was repaired on January 9, 2018. CAU 424: CAS 03-08-002-A308 (Landfill Cell A3-8): Lava rock, used to mark the two eastern monument locations, was noted as missing during the inspection. The lava rock was replaced on January 9, 2018. CAU 453: Five large animal burrows, located near the east–central portion of cover, was noted during the inspection. Eight additional animal burrows were discovered during repair actions. All cover defects were repaired on January 9, 2018.
54 ENVIRONMENTAL SCIENCES↗
Analysis of ionizing radiation induced DNA damage response in human adult stem cells and differentiated neurons
Findings of neurodegenerative features associated with human radiosensitive syndromes such as Ataxia telangiectasia suggest that DNA repair efficiency is crucial for maintaining the functional integrity of central nervous system. To gain a better understanding of ionizing radiation (IR) induced DNA damage response in undifferentiated and differentiated neural cell types and to evaluate the role of ATM in DNA double strand break (DSB) repair, an in vitro human neural cell differentiation model system was utilized in this study. As compared to adult stem cells, differentiated neurons displayed an attenuated DSB repair response (as judged by the persistence of 53BP1 foci) after IR exposure and the attenuation was even more pronounced in stem cells and neurons after suppression of ATM (Ataxia Telangiectasia Mutated) gene product suggesting the importance of ATM for an optimal DSB repair efficiency in human neural cell types. In corroboration with an attenuated DNA damage response, a sharp decline in the expression levels of several DSB repair genes was observed in neurons. Furthermore, our results suggest that cellular differentiation modulates the expression of several genes thereby compromising the DSB repair fidelity in post mitotic neurons. Further studies are required to verify whether or not ATM mediated exacerbation of DNA repair deficiency in differentiated neurons leads to neurodegeneration.
53 binding protein 1↗
Update on Investigations of Viability of Cold Spray and FSW as a Spent Nuclear Fuel Dry Storage Canister Mitigation Tool
The purpose of this work is to investigate the use of cold spray and friction stir welding or processing (FSW/P) for repair and mitigation of chloride-induced stress corrosion cracking (CISCC) in dry cask storage system (DCSS) canisters to ensure integrity far beyond their original license period. This report provides a viability analysis of cold spray and friction stir welding for repair and fabrication of DCSS canisters. This report presents experimental work and a research strategy to optimize and evaluate cold spray and FSW/P for CISCC resistance. The literature reports that the following three conditions must exist for CISCC to occur: tensile stress, corrosive environment, and susceptible material. These conditions must be understood and accounted for while evaluating CISCC susceptibility. Furthermore, non-obvious factors, such as surface conditions and geometric confinement, can dramatically increase the intensity of one or more of the three listed conditions for CISCC. Arc welding should be considered for either temporary or permanent repair when combined with a mitigation technology. It is known that alloys used in the existing inventory of spent nuclear fuel storage canisters become sensitized in areas around fusion welds. Technologies, such as cold spray or FSW, can mitigate the sensitization caused by fusion welds. FSW/P and cold spray, potential alternatives for fabrication and repair, are solid-phase processes. No melting occurs and the energy input can be controlled such that no harm is done to the base metal during these processes. FSW/P should be considered for use in new fabrication of canisters and repair of existing canisters. Low heat input and grain refinement result in material with improved mechanical properties and comparable generalized corrosion performance relative to base metal. FSW/P offers the potential of through-thickness CISCC resistance. Cold spray should be considered for production, mitigation, and repair of canisters. Cold spray has demonstrated the ability to deposit stainless steel, Inconel alloys, and other alloys on stainless steel 304L such that galvanic potential is matched and resistance to pitting is improved. The technical basis for cold spray mitigation and repair within the overpack using remote robotic equipment is established. A non-obvious application to the research community is the sealing of crevices. All reported instances of CISCC in the fielded nuclear applications were associated with crevice corrosion. This can be avoided by cold spraying to seal crevices. The bulk of the work planned for FY 2020 will be generating coupons for CISCC testing by collaborative projects at Pacific Northwest National Laboratory and Sandia National Laboratories. First an exploratory study will be executed that will include screening studies and process optimization. This task will identify the effect of process parameters on microstructure and CISCC resistance. Optimized parameters will be used to produce a smaller number of coupons for full testing and evaluation. Test methods for evaluating CISCC resistance must meet the following criteria: (1) normalized surface geometry and exposed process microstructure, (2) account for residual stresses, (3) be in a controlled and appropriate test environment, and (4) be numerically quantifiable and repeatable. Failure to meet these criteria could lead to results that cannot be used for comparative analysis of processes and materials.
12 MANAGEMENT OF RADIOACTIVE AND NON-RADIOACTIVE W↗
Acoustic Emission Weld Monitoring in the 2195 Aluminum-Lithium Alloy
Due to its low density, the 2195 aluminum-lithium alloy was developed as a replacement for alloy 2219 in the Space Shuttle External Tank (ET). The external tank is the single largest component of the space shuttle system. It is 154 feet long and 27.6 feet in diameter, and serves as the structural backbone for the shuttle during launch, absorbing most of the 7 million plus pounds of thrust produced. The almost 4% decrease in density between the two materials provides an extra 7500 pounds of payload capacity necessary to put the International Space Station components into orbit. The ET is an all-welded structure; hence, the requirement is for up to five rewelds without hot cracking. Unfortunately, hot cracking during re-welding or repair operations was occurring and had to be dealt with before the new super lightweight tank could be used. Weld metal porosity formation was also of concern because it leads to hot cracking during weld repairs. Accordingly, acoustic emission (AE) nondestructive testing was employed to monitor the formation of porosity and hot cracks in order to select the best filler metal and optimize the weld schedule. The purpose of this work is to determine the feasibility of detecting hot cracking in welded aluminum-lithium (Al-Li) structures through the analysis of acoustic emission data. By acoustically characterizing the effects of reheating during a repair operation, the potential for hidden flaws coalescing and becoming "unstable" as the panel is repaired could be reduced. Identification of regions where microcrack growth is likely to occur and the location of active flaw growth in the repair weld will provide the welder with direct feedback as to the current weld quality enabling adjustments to the repair process be made in the field. An acoustic emission analysis of the source mechanisms present during welding has been conducted with the goals of locating regions in the weld line that are susceptible to damage from a repair operation, identifying the formation of critically sized flaws and providing accept/reject criteria for the quality of a weld as it is performed.
Walker, James L.↗
Genomic and Phenotypic Associations to Predict Human Sensitivity to SpaceRadiation
High-linear energy transfer (LET) ionizing radiation is a major health hazard for astronauts who will be exposed to galactic cosmic rays during upcoming lunar and Mars missions. Predicting and mitigating this risk requires understanding the factors underlying individual radiation sensitivity. We started to address this challenge by identifying the genomic and phenotypic associations with sensitivity to low and high-LET ionizing radiation ex vivo in over 750 healthy human donors. We exposed primary human blood mononuclear cells to simulated galactic cosmic ray components: 350MeV/n 28Si, 350MeV/n 40Ar and 600MeV/n 56Fe particles, at 1.1 and 3 particles/100 sq.m fluences, as well as 0.1 Gy and 1 Gy doses of gamma rays, and analyzed the outcomes at 4 and 24 hours post-irradiation. We quantified DNA damage and repair responses based on 53BP1+ radiation-induced foci formation, together with oxidative stress and changes in secreted factors including immune cytokines and exosomes. We also analyzed phenotypic associations with spontaneous DNA repair foci at baseline prior to irradiation. We identified an increase in spontaneous DNA repair associated with age and latent viral infection, and observed that human spontaneous DNA repair foci at baseline can serve as a negative predictor of DNA repair and immunoregulatory cytokine production after irradiation. Furthermore, we observed a wide variability of subject- and LET-dependent radiation responses, with radiation-induced DNA repair foci increasing by dose and LET, and high-LET particle radiation resulting in more residual DNA damage compared to low-LET particles and gamma rays. We have developed multiple metrics to quantify human radio sensitivity across the spectrum of conditions. Here we present their dependence on radiation quality and phenotypic variables, including an age-dependent decrease in DNA repair after irradiation, and genomic associations with radio sensitivity based on low-coverage whole genome sequencing. We anticipate that our work will pave the way for understanding the spectrum of human radio sensitivity and identifying targets for countermeasure development to reduce DNA and cellular damage and radiation carcinogenesis during deep space exploration.
GWAS radiation human↗
Genomic and Phenotypic Predictors of Human Ex Vivo Sensitivity to Simulated Deep Space Radiation
High-linear energy transfer (LET) ionizing radiation is a major health hazard for astronauts who will be exposed to galactic cosmic rays during upcoming lunar and Mars missions. Predicting and mitigating this risk requires understanding the factors underlying individual radiation sensitivity. We started to address this challenge by identifying the genomic and phenotypic associations with sensitivity to low and high-LET ionizing radiation ex vivo in over 750 healthy human donors. We exposed primary human blood mononuclear cells to simulated galactic cosmic ray components: 350 MeV/n 28Si, 350 MeV/n 40Ar and 600 MeV/n 56Fe particles, at 1.1 and 3 particles/100 sq.m fluences, as well as 0.1 Gy and 1 Gy doses of gamma rays, and analyzed the outcomes at 4 and 24 hours post-irradiation. We quantified DNA damage and repair responses based on 53BP1+ radiation-induced foci formation, together with oxidative stress and changes in secreted factors including immune cytokines and exosomes. We also analyzed phenotypic associations with spontaneous DNA repair foci at baseline prior to irradiation. We identified an increase in spontaneous DNA repair associated with age and latent viral infection, and observed that human spontaneous DNA repair foci at baseline can serve as a negative predictor of DNA repair and immunoregulatory cytokine production after irradiation. Furthermore, we observed a wide variability of subject- and LET-dependent radiation responses, with radiation-induced DNA repair foci increasing by dose and LET, and high-LET particle radiation resulting in more residual DNA damage compared to low-LET particles and gamma rays. We have developed multiple metrics to quantify human radiosensitivity across the spectrum of conditions. Here we present their dependence on radiation quality and phenotypic variables, including an age-dependent decrease in DNA repair after irradiation, and genomic associations with radiosensitivity based on low-coverage whole genome sequencing. We anticipate that our work will pave the way for understanding the spectrum of human radiosensitivity and identifying targets for countermeasure development to reduce DNA and cellular damage and radiation carcinogenesis during deep space exploration.
GWAS↗
Genomic and phenotypic predictors of human ex vivo sensitivity to simulated deep space radiation
High-linear energy transfer (LET) ionizing radiation is a major health hazard for astronauts who will be exposed to galactic cosmic rays during upcoming lunar and Mars missions. Predicting and mitigating this risk requires understanding the factors underlying individual radiation sensitivity. We started to address this challenge by identifying the genomic and phenotypic associations with sensitivity to low and high-LET ionizing radiation ex vivo in over 750 healthy human donors. We exposed primary human blood mononuclear cells to simulated galactic cosmic ray components: 350MeV/n (28)Si, 350MeV/n (40)Ar and 600MeV/n (56)Fe particles, at 1.1 and 3 particles/100µm^(2) fluences, as well as 0.1 Gy and 1 Gy doses of gamma rays, and analyzed the outcomes at 4 and 24 hours post-irradiation. We quantified DNA damage and repair responses based on 53BP1^(+) radiation-induced foci formation, together with oxidative stress and changes in secreted factors including immune cytokines and exosomes. We also analyzed phenotypic associations with spontaneous DNA repair foci at baseline prior to irradiation. We identified an increase in spontaneous DNA repair associated with age and latent viral infection, and observed that human spontaneous DNA repair foci at baseline can serve as a negative predictor of DNA repair and immunoregulatory cytokine production after irradiation. Furthermore, we observed a wide variability of subject- and LET-dependent radiation responses, with radiation-induced DNA repair foci increasing by dose and LET, and high-LET particle radiation resulting in more residual DNA damage compared to low-LET particles and gamma rays. We have developed multiple metrics to quantify human radiosensitivity across the spectrum of conditions. Here we present their dependence on radiation quality and phenotypic variables, including an age-dependent decrease in DNA repair after irradiation, and genomic associations with radiosensitivity based on low-coverage whole genome sequencing. We anticipate that our work will pave the way for understanding the spectrum of human radiosensitivity and identifying targets for countermeasure development to reduce DNA and cellular damage and radiation carcinogenesis during deep space exploration.
GWAS↗