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The purpose of this study is to examine the total ionizing dose susceptibility for the UC1823A pulse width modulator manufactured by Texas Instruments, Inc. The part is suspected to be vulnerable to enhanced low dose rate sensitivity (ELDRS).
Recent enhanced low dose rate sensitivity (ELDRS) investigations carried out by RLP Research, Crane, Arizona State University (ASU), and Jet Propulsion Laboratory (JPL) have shown significant differences in the degradation of bipolar microcircuits with total dose in the presence of molecular hydrogen (H2) in packages. This has a significant impact on radiation hardness assurance and opens up opportunity to improve device performance. The objectives of this program are 1) to investigate and confirm the causal relationship between packaging recipes, hydrogen contamination, and total dose response of linear bipolar microcircuits; and 2) to develop a guideline that will take into account these effects at the radiation level for future NASA space missions. This program is geared to benefit all future NASA space missions using bipolar or BiCMOS linear devices.
Low dose rate (LDR) and high dose rate (HDR) experiments on field-oxide-field-effect-transistors (FOXFETs) and gated lateral pnp (GLPNP) bipolar transistors indicate that there is a dose rate enhancement factor (EF) associated with radiation-induced degradation. This EF is also affect by the presence of hydrogen in the oxide. In this work, we developed a one dimensional (1-D) numerical calculations code to investigate the key mechanisms that describe the dose rate sensitivity and the effect of hydrogen on dose rate effects. We used a finite-difference methodology for the numerical calculations that allow for computing solutions for the densities of the mobile species as well as for the electrostatic potential at nodes contained within a mesh superimposed on the solution domain. Results from calculations of damage EF indicate that oxide thickness, distribution of hole traps and hole capture cross-section affect dose rate sensitivity. In addition, calculations show that molecular hydrogen cracking at positively charged defects may be a key reaction relating hydrogen and dose rate response. Comparison to experimental data on bipolar and CMOS devices results in good agreement with the dose rate calculations of interface trap buildup
With exciting new Agency plans for a sustainable return to the moon, astronauts will once again leave earth’s protective magnetosphere only to endure higher levels of radiation from galactic cosmic rays (GCR) and the possibility of a large solar particle event (SPE). Gateway, lunar landers, and surface habitats will be designed to protect crew against SPE’s with vehicle optimization, storm shelter concepts, and/or active dosimetry; however, the ever-penetrating GCR will continue to pose the most significant health risks especially as lunar missions increase in duration and as NASA sets its aspirations on Mars. The primary risks of concern include epithelial carcinogenesis and leukemia, central nervous system effects resulting in potential in-mission cognitive or behavioral impairment and/or late neurological disorders, degenerative tissue effects including cataracts, circulatory and heart disease, as well as, potential immune system decrements impacting multiple aspects of crew health. Characterization and mitigation of these risks requires a significant reduction in the large biological uncertainties of chronic (low-dose rate) heavy ion exposures and the validation of countermeasures in a relevant space environment. NASA has developed the “GCR Simulator” at Brookhaven National Laboratory to generate a spectrum of ion beams that approximates the primary and secondary GCR field experienced at human organ locations within a deep-space vehicle. The majority of the dose is delivered from protons (~65-75%) and alpha particles (~10-20%) with heavier ions (Z≤3) contributing the remainder. The “GCR Simulator” exposes state-of-the art cellular and animal model systems to 33 sequential beams including 4 proton energies plus degrader, 4 helium energies plus degrader, and the five heavy ions of C, O, Si, Ti, and Fe. A polyethylene degrader is used with the 100 MeV/n H and He beams to provide a nearly continuous distribution of low energy particles. A 500 mGy exposure, delivering doses from each of the 33 beams, requires 75-90 minutes. To more closely simulate the low dose rates found in space, sequential field exposures can be divided into daily fractions over 2-4 weeks, with individual fractions as low as 0.1-0.2 mGy. In the large beam configuration (60 x 60 cm(exp 2)), 54 special housing cages can accommodate 2-3 mice each for a 70-75 min duration or ~15 individually housed rats. Emerging research results from our 2018 runs utilizing mixed heavy ion fields and protracted space exposures are forthcoming and deepen our understanding of the numerous health risks faced by our astronauts. This paper discusses NASA’s innovative technology solution for a ground-based GCR simulator at the NASA Space Radiation Laboratory to enable future exploration missions.
With exciting new Agency plans for a sustainable return to the moon, astronauts will once again leave earth’s protective magnetosphere only to endure higher levels of radiation from galactic cosmic rays (GCR) and the possibility of a large solar particle event (SPE). Gateway, lunar landers, and surface habitats will be designed to protect crew against SPEs with vehicle optimization, storm shelter concepts, and/or active dosimetry; however, the ever-penetrating GCR will continue to pose the most significant health risks especially as lunar missions increase in duration and as NASA sets its aspirations on Mars. The primary risks of concern include carcinogenesis, central nervous system effects resulting in potential in-mission cognitive or behavioral impairment and/or late neurological disorders, degenerative tissue effects including cataracts, circulatory and heart disease, as well as, potential immune system decrements impacting multiple aspects of crew health. Characterization and mitigation of these risks requires a significant reduction in the large biological uncertainties of chronic (low-dose rate) heavy ion exposures and the validation of countermeasures in a relevant space environment. NASA has developed the “GCR Simulator” at Brookhaven National Laboratory to generate a spectrum of ion beams that approximates the primary and secondary GCR field experienced at human organ locations within a deep-space vehicle. The majority of the dose is delivered from protons (~65-75%) and helium ions (~10-20%) with heavier ions (Z>3) contributing the remainder. The “GCR Simulator” exposes state-of-the art cellular and animal model systems to 33 sequential beams including 4 proton energies plus degrader, 4 helium energies plus degrader, and the five heavy ions of C, O, Si, Ti, and Fe. A polyethylene degrader is used with the 100 MeV/n H and He beams to provide a nearly continuous distribution of low energy particles. A 500 mGy exposure, delivering doses from each of the 33 beams, requires 75-90 minutes. To more closely simulate the low dose rates found in space, sequential field exposures can be divided into daily fractions over 2-6 weeks, with individual beam fractions as low as 0.1-0.2 mGy. In the large beam configuration (60 x 60 cm2), 54 special housing cages can accommodate 2-3 mice each for a 70-75 min duration or ~15 individually housed rats. Emerging research results from our 2018 runs utilizing mixed heavy ion fields and protracted space exposures are forthcoming and will deepen our understanding of the numerous health risks faced by astronauts. This talk discusses NASA’s innovative technology solution for a ground-based GCR simulator at the NASA Space Radiation Laboratory to enable future exploration missions.
With exciting new NASA plans for a sustainable return to the moon, astronauts will once again leave Earth’s protective magnetosphere only to endure higher levels of radiation from galactic cosmic radiation (GCR) and the possibility of a large solar particle event (SPE). Gateway, lunar landers, and surface habitats will be designed to protect crew against SPEs with vehicle optimization, storm shelter concepts, and/or active dosimetry; however, the ever penetrating GCR will continue to pose the most significant health risks especially as lunar missions increase in duration and as NASA sets its aspirations on Mars. The primary risks of concern include carcinogenesis, central nervous system (CNS) effects resulting in potential in-mission cognitive or behavioral impairment and/or late neurological disorders, degenerative tissue effects including circulatory and heart disease, as well as potential immune system decrements impacting multiple aspects of crew health. Characterization and mitigation of these risks requires a significant reduction in the large biological uncertainties of chronic (low-dose rate) heavy-ion exposures and the validation of countermeasures in a relevant space environment. Historically, most research on understanding space radiation-induced health risks has been performed using acute exposures of monoenergetic single-ion beams. However, the space radiation environment consists of a wide variety of ion species over a broad energy range. Using the fast beam switching and controls systems technology recently developed at the NASA Space Radiation Laboratory (NSRL) at Brookhaven National Laboratory, a new era in radiobiological research is possible. NASA has developed the “GCR Simulator” to generate a spectrum of ion beams that approximates the primary and secondary GCR field experienced at human organ locations within a deep-space vehicle. The majority of the dose is delivered from protons (approximately 65%–75%) and helium ions (approximately 10%–20%) with heavier ions (Z ≥ 3) contributing the remainder. The GCR simulator exposes state-of-the art cellular and animal model systems to 33 sequential beams including 4 proton energies plus degrader, 4 helium energies plus degrader, and the 5 heavy ions of C, O, Si, Ti, and Fe. A polyethylene degrader system is used with the 100 MeV/n H and He beams to provide a nearly continuous distribution of low-energy particles. A 500 mGy exposure, delivering doses from each of the 33 beams, requires approximately 75 minutes. To more closely simulate the low-dose rates found in space, sequential field exposures can be divided into daily fractions over 2 to 6 weeks, with individual beam fractions as low as 0.1 to 0.2 mGy. In the large beam configuration (60 × 60 cm 2 ), 54 special housing cages can accommodate 2 to 3 mice each for an approximately 75 min duration or 15 individually housed rats. On June 15, 2018, the NSRL made a significant achievement by completing the first operational run using the new GCR simulator. This paper discusses NASA’s innovative technology solution for a ground-based GCR simulator at the NSRL to accelerate our understanding and mitigation of health risks faced by astronauts. Ultimately, the GCR simulator will require validation across multiple radiogenic risks, endpoints, doses, and dose rates.
The purpose of this test was to validate the Intersil HSYE-117RH-Q flight lot for use in the fabrication of Europa Clipper Propulsion subsystem flight hardware. This test shall serve as the radiation lot acceptance test (RLAT) for the flight lot date with wafer lot number G3X3CQC and lot date code (LDC) 1830. Low dose rate (LDR) irradiations have been performed by the manufacturer, but only to 100 krad(Si). This test was a follow-on to the original Radiation Lot-Specific Acceptance Testing (RLAT) performed on this LDC. Application-specific load currents were used for the line regulation and load regulation measurements. All other parameters were measured with standard bias conditions as specified in the datasheet.
ABSTRACT Aims Humans and animals acutely intoxicated with the organophosphate soman can develop sustained status epilepticus (SE) that rapidly becomes refractory to benzodiazepines. We compared the antiseizure efficacy of midazolam, a current standard of care treatment for OP‐induced SE, versus combined therapy with midazolam and allopregnanolone (ALLO) in a rat model of soman‐induced SE. Methods Soman‐intoxicated male rats with robust seizure behavior and high‐amplitude electroencephalographic (EEG) activity were administered midazolam (0.65 mg, i.m.) 20 min after seizure initiation and 10 min later either a second dose of midazolam or ALLO (12 or 24 mg/kg, i.m.). Seizure behavior and EEG were monitored for 4 h after treatment. Brains were collected at the end of the monitoring period for histological analyses. Results Animals receiving 2 doses of midazolam exhibited persistent SE. Sequential dosing with midazolam followed by ALLO suppressed electrographic seizure activity. The combination therapy also significantly reduced soman‐induced neurodegeneration and neuroinflammation compared to 2 doses of midazolam. High but not low dose ALLO was associated with transitory and reversible respiratory compromise during the 1 h period after dosing. Conclusions Treatment with midazolam followed by ALLO was more effective than 2 doses of midazolam in suppressing benzodiazepine‐refractory, soman‐induced SE, and in mitigating its acute neuropathological consequences.
To investigate the critical target, dose response and dose-rate response for the induction of chromosomal instability by ionizing radiation, bromodeoxyuridine (BrdU)-substituted and unsubstituted GM10115 cells were exposed to a range of doses (0.1-10 Gy) and different dose rates (0.092-17.45 Gy min(-1)). The status of chromosomal stability was determined by fluorescence in situ hybridization approximately 20 generations after irradiation in clonal populations derived from single progenitor cells surviving acute exposure. Overall, nearly 700 individual clones representing over 140,000 metaphases were analyzed. In cells unsubstituted with BrdU, a dose response was found, where the probability of observing delayed chromosomal instability in any given clone was 3% per gray of X rays. For cells substituted with 25-66% BrdU, however, a dose response was observed only at low doses (<1.0 Gy); at higher doses (>1.0 Gy), the incidence of chromosomal instability leveled off. There was an increase in the frequency and complexity of chromosomal instability per unit dose compared to cells unsubstituted with BrdU. The frequency of chromosomal instability appeared to saturate around approximately 30%, an effect which occurred at much lower doses in the presence of BrdU. Changing the gamma-ray dose rate by a factor of 190 (0.092 to 17.45 Gy min(-1)) produced no significant differences in the frequency of chromosomal instability. The enhancement of chromosomal instability promoted by the presence of the BrdU argues that DNA comprises at least one of the critical targets important for the induction of this end point of genomic instability.
The formation of double‐strand breaks (DSBs) and chromosomal aberrations (CAs) is of great importance in radiation research and, specifically, in space applications. We are presenting a new particle track and DNA damage model, in which the particle stochastic track structure is combined with the random walk (RW) structure of chromosomes in a cell nucleus. The motivation for this effort stems from the fact that the model with the RW chromosomes, NASARTI (NASA radiation track image) previously relied on amorphous track structure, while the stochastic track structure model RITRACKS (Relativistic Ion Tracks) was focused on more microscopic targets than the entire genome. We have combined chromosomes simulated by RWs with stochastic track structure, which uses nanoscopic dose calculations performed with the Monte‐Carlo simulation by RITRACKS in a voxelized space. The new simulations produce the number of DSBs as function of dose and particle fluence for high‐energy particles, including iron, carbon and protons, using voxels of 20 nm dimension. The combined model also calculates yields of radiation‐induced CAs and unrejoined chromosome breaks in normal and repair deficient cells. The joined computational model is calibrated using the relative frequencies and distributions of chromosomal aberrations reported in the literature. The model considers fractionated deposition of energy to approximate dose rates of the space flight environment. The joined model also predicts of the yields and sizes of translocations, dicentrics, rings, and more complex‐type aberrations formed in the G0/G1 cell cycle phase during the first cell division after irradiation. We found that the main advantage of the joined model is our ability to simulate small doses: 0.05‐0.5 Gy. At such low doses, the stochastic track structure proved to be indispensable, as the action of individual delta‐rays becomes more important.
The formation of double‐strand breaks (DSBs) and chromosomal aberrations (CAs) is of great importance in radiation research and, specifically, in space applications. We are presenting a new particle track and DNA damage model, in which the particle stochastic track structure is combined with the random walk (RW) structure of chromosomes in a cell nucleus. The motivation for this effort stems from the fact that the model with the RW chromosomes, NASARTI (NASA radiation track image) previously relied on amorphous track structure, while the stochastic track structure model RITRACKS (Relativistic Ion Tracks) was focused on more microscopic targets than the entire genome. We have combined chromosomes simulated by RWs with stochastic track structure, which uses nanoscopic dose calculations performed with the Monte‐Carlo simulation by RITRACKS in a voxelized space. The new simulations produce the number of DSBs as function of dose and particle fluence for high‐energy particles, including iron, carbon and protons, using voxels of 20 nm dimension. The combined model also calculates yields of radiation‐induced CAs and unrejoined chromosome breaks in normal and repair deficient cells. The joined computational model is calibrated using the relative frequencies and distributions of chromosomal aberrations reported in the literature. The model considers fractionated deposition of energy to approximate dose rates of the space flight environment. The joined model also predicts of the yields and sizes of translocations, dicentrics, rings, and more complex‐type aberrations formed in the G0/G1 cell cycle phase during the first cell division after irradiation. We found that the main advantage of the joined model is our ability to simulate small doses: 0.05‐0.5 Gy. At such low doses, the stochastic track structure proved to be indispensable, as the action of individual delta‐rays becomes more important.
Determining the biological effects of low doses of radiation with high linear energy transfer (LET) is complicated by the stochastic nature of charged-particle interactions. Populations of cells exposed to very low radiation doses contain a few cells which have been hit by a charged particle, while the majority of the cells receive no radiation damage. At somewhat higher doses, a few cells receive two or more events. Because the effects of damage produced by separate events can interact in the cell, we have had to make assumptions about the nature of these interactions in order to interpret the results of the experiments. Many of those assumptions can be tested if we can be sure of the number of charged-particle events which occur in individual cells, and correlate this number with the biological effect. We have developed a special irradiation facility at Pacific Northwest Laboratory (PNL) to control the actual number of charged particle tracks that pass through cell nuclei. The beam from a 2 MeV tandem accelerator is collimated to approximately 5 microns. Cells, grown in special dishes with 1.5 microns thick plastic bottoms, are positioned so that the desired portion of the cell aligns with the collimator. A shutter in the beam line is opened and closed after the desired number of particle tracks has been counted. This approach can be used to investigate the effects of the interaction between irradiated and unirradiated cells in an organized system, as well as to study the effects of spatial and temporal distribution of radiation damage within single cells.(ABSTRACT TRUNCATED AT 250 WORDS).
This study compares two statistical models to construct summary dose-response curves for low boom community noise surveys. Data from two NASA field surveys are used that consist of multiple responses per survey participant. These data require an approach that accounts for the correlation among repeated annoyance observations from the same participant. A multilevel model accounts for the correlation by allowing estimated parameters to vary with each survey participant. On the other hand, a population average model utilizes generalized estimating equations and accounts for the correlation via a userspecified within-subject correlation structure. A visual comparison of the dose-response curves for these two methods reveals similar results. When comparing specific points along the summary curves, the multilevel model yields more precise confidence bounds than the population average model. The similarity between the summary curves derived from each model lends validity to both approaches for approximating a population representative summary curve, though modeling assumptions may lend favor to the multilevel logistic modeling approach over the population average model.
Our objective is to demonstrate an innovative method combining machine learning with comparative effectiveness research techniques and to investigate a hitherto unstudied question about the effectiveness of common prescribing patterns. For Operation Enduring Freedom/Operation Iraqi Freedom veterans with major depressive disorder, we generate pharmacotherapy pathways (of antidepressants) using process mining and machine learning. We select the medication episodes that were started at subtherapeutic doses by the first assigned primary care physician and observe the paths that those medication episodes follow. Using 2-stage least squares, we test the effectiveness of starting at a low dose and staying low for longer versus ramping up fast while balancing observable and unobservable characteristics of patients and providers through instrumental variables. We leverage predetermined provider practice patterns as instruments. We collected outpatient pharmacy data for selective serotonin reuptake inhibitors and selective norepinephrine reuptake inhibitors, patient and provider characteristics (as control variables), and the instruments for our cohort. All data were extracted for the period between 2006 and 2020. There is a statistically significant positive effect (0.68, 95% CI 0.11–1.25) of “ramping up fast” on engagement in care. When we examine the effect of “ramping up slow”, we see an insignificant negative impact on engagement in care (−0.82, 95% CI −1.89 to 0.25). As expected, the probability of drop-out also seems to have a negative effect on engagement in care (−0.39, 95% CI −0.94 to 0.17). We further validate these results by testing with medication possession ratios calculated periodically as an alternative engagement in care metric. Our findings contradict the “Start low, go slow” adage, indicating that ramping up the dose of an antidepressant faster has a significantly positive effect on engagement in care for our population.
In logistic dose-response modeling, failing to account for uncertainty in estimated doses can cause an artificial flattening or attenuation of the slope of the summary curve. In Lee et al. [J. Acoust. Soc. Am. 147(4), pp. 2222-2234 (2020)], data from two NASA low-amplitude sonic boom community noise survey tests were modeled using a Bayesian multilevel logistic regression (MLR) statistical model that assumed there was no uncertainty in the noise dose estimates. However, in these community tests, the noise dose uncertainty was estimated by Page et al. [NASA/CR-2014-218180 and NASA/CR-2020-220589/Volume I] using a leave-one-out method. In the current work, a term was added to extend the Bayesian MLR model to account for the estimated noise dose uncertainty quantified in the Page et al. analyses. This uncertainty term was included in two ways, either as classical or as Berkson uncertainty, and yield similar results. When the uncertainty is accounted for in the Bayesian MLR model, the dose-response curves become 5-10% steeper, but the difference in the noise dose that elicits a 5% highly annoyed response is small (less than 1 dB). This result is encouraging for future X-59 community tests whose survey area will be sparsely populated with noise monitors.
Chromosome aberration yields were assessed in DNA double-strand break repair (DSB) deficient cells after acute doses of gamma-rays or high-LET iron nuclei, or low dose-rate (0.018 Gy/hr) gamma-rays. We studied several cell lines including fibroblasts deficient in ATM (product of the gene that is mutated in ataxia telangiectasia patients) or NBS (product of the gene mutated in the Nijmegen breakage syndrome), and gliomablastoma cells that are proficient or lacking in DNA-dependent protein kinase, DNA-PK activity. Chromosomes were analyzed using the fluorescence in-situ hybridization (FISH) chromosome painting method in cells at the first division post-irradiation and chromosome aberrations were identified as either simple exchanges (translocations and dicentrics) or complex exchanges (involving >2 breaks in 2 or more chromosomes). Gamma radiation induced higher yields of both simple and complex exchanges in the DSB repair defective cells than in the normal cells. The quadratic dose-response terms for both chromosome exchange types were significantly higher for the ATM and NBS defective lines than for normal fibroblasts. However, the linear dose-response term was significantly higher only for simple exchanges in the NBS cells. Large increases in the quadratic dose response terms indicate the important roles of ATM and NBS in chromatin modifications that facilitate correct DSB repair and minimize aberration formation. Differences in the response of AT and NBS deficient cells at lower doses suggests important questions about the applicability of observations of radiation sensitivity at high dose to low dose exposures. For all iron nuclei irradiated cells, regression models preferred purely linear and quadratic dose responses for simple and complex exchanges, respectively. All the DNA repair defective cell lines had lower Relative biological effectiveness (RBE) values than normal cells, the lowest being for the DNA-PK-deficient cells, which was near unity. To further investigate the sensitivity differences for low and low high doses, we performed chronic low dose-rate irradiation, and have begun studies with ATM and Nibrin inhibitors and siRNA knockout of these proteins. Results support the conclusion that for the endpoint of simple chromosomal aberrations (translocation or dicentrics), the increased radiation sensitivity of AT cells found at high doses (>1 Gy) does not carry over to low doses or doserates, while NBS cells show increased sensitivity for both high and low dose exposures.
The intent was to review the research pertaining to human exposure to carbon dioxide (CO2) and to recommend allowable exposure limits for extravehicular activity (EVA). Respiratory, renal, and gastrointestinal systems may be adversely affected by chronic low dose CO2 exposure. Ventilation was increased 15 percent with 1 percent CO2 and 50 percent with 2 percent CO2. Chronic exposure to less than 2 percent CO2 led to 20 day cycles of uncompensated and compensated respiratory acidosis. Acid-base changes were small. Histopathologic changes in guinea pig lungs have been noted with long term exposure to 1 percent CO2. No changes were seen with exposure to 0.5 percent CO2. Cycling of bone calcium stores with associated changes in blood and urinary calcium levels occurs with long term CO2 exposure. Histologic changes in bone have been noted in guinea pigs exposed to 1 percent CO2. Renal calcification has been noted in guinea pigs with exposure to as low as 0.5 percent CO2. An increase in gastric acidity was noted in subjects with long term exposure to 1 percent CO2. Cardiovascular and neurologic function were largely unaffected. A decrease in the incidence of respiratory, renal, and gastrointestinal disease was noted in submariners coincident with a decrease in ambient CO2 from 1.2 percent to 0.8-0.9 percent. Oxygen (O2) and CO2 stimulate respiration independently and cumulatively. The addition of CO2 to high dose O2 led to the faster onset of seizure activity in mice. Experiments evaluating the physiologic responses to intermittent, repetitive exposures to low dose CO2 and 100 percent O2 mixtures should be performed. A reduction in the current NASA standard for CO2 exposure during EVA of 1 percent (7.6 mmHg) for nominal and 2 percent (15.2 mmHg) for heavy exertion to 0.5 percent (3.8 mmHg) for nominal and 1 percent (7.6 mmHg) for heavy exertion may be prudent. At a minimum, the current NASA standard should not be liberalized.
Volumetric arc therapy (VMAT) is a radiation therapy (RT) technique that spares normal tissues from high and intermediate RT doses but increases the volume of tissues receiving low doses of RT compared with 3-dimensional conformal RT (3DCRT). We hypothesized that palliative VMAT would reduce the detriment to patient quality of life (QOL) compared with palliative 3DCRT.