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NASA NTRS2000

Power System Options Evaluated for the Radiation and Technology Demonstration Mission

The Radiation and Technology Demonstration (RTD) Mission is under joint study by three NASA Centers: the NASA Johnson Space Center, the NASA Goddard Space Flight Center, and the NASA Glenn Research Center at Lewis Field. This Earth-orbiting mission, which may launch on a space shuttle in the first half of the next decade, has the primary objective of demonstrating high-power electric thruster technologies. Secondary objectives include better characterization of Earth's Van Allen trapped-radiation belts, measurement of the effectiveness of the radiation shielding for human protection, measurement of radiation effects on advanced solar cells, and demonstration of radiation-tolerant microelectronics. During the mission, which may continue up to 1 year, the 2000-kg RTD spacecraft will first spiral outward from the shuttle-deployed, medium-inclination, low Earth orbit. By the phased operation of a 10-kW Hall thruster and a 10-kW Variable Specific Impulse Magneto-Plasma Rocket, the RTD spacecraft will reach a low-inclination Earth orbit with a radius greater than five Earth radii. This will be followed by an inward spiraling orbit phase when the spacecraft deploys 8 to 12 microsatellites to map the Van Allen belts. The mission will conclude in low Earth orbit with the possible retrieval of the spacecraft by the space shuttle. A conceptual RTD spacecraft design showing two photovoltaic (PV) array wings, the Hall thruster with propellant tanks, and stowed microsatellites is presented. Early power system studies assessed five different PV array design options coupled with a 120-Vdc power management and distribution system (PMAD) and secondary lithium battery energy storage. Array options include (1) state-of-the-art 10-percent efficient three-junction amorphous SiGe thin-film cells on thin polymer panels deployed with an inflatable (or articulated) truss, (2) SCARLET array panels, (3) commercial state-of-the-art, planar PV array rigid panels with 25-percent efficient, three-junction GaInP2/GaAs/Ge solar cells, (4) rigid panels with 25-percent efficient, three-junction GaInP2/GaAs/Ge solar cells, in a 2 -concentrator trough configuration, and (5) thin polymer panels with 25-percent efficient, three-junction GaInP2/GaAs/Ge solar cells deployed with an inflatable (or articulated) truss. To assess the relative merits of these PV array design options, the study group developed a dedicated Fortran code to predict power system performance and estimate system mass. This code also modeled Earth orbital environments important for accurately predicting PV array performance. The most important environmental effect, solar cell radiation degradation, was calculated from electron-proton fluence input from the industry standard AE8/AP8 trapped radiation models and the concept of damage equivalence. Power systems were sized to provide 10 kW of thruster power and approximately 1 kW of spacecraft power at end of life. Of the five PV array design options, the option 1 (thin-film cells) power system was the most massive 590 kg, whereas the option 4 (trough concentrator) power system was the lightest 260 kg. Arguably, the lowest cost would come from the option 3 (commercial array panels) power system with an acceptable, albeit greater, system mass of 320 kg. Predicted power system performance during the spiral-out mission phase is shown the preceding graph for the option 5 (flexible-panel) array. From the results, the radiation-induced power loss over time is evident as the spacecraft slowly spirals outward through the trapped proton belt. The importance of the spiral trip time is also evident in the two curves representing 74-day and 182-day spiral-out periods. The longer spiral time introduces a beginning-of-life power oversizing penalty greater than 1 kW. Future studies will analyze power system performance and mass with a 50-Vdc power management and distribution architecture favorable to the VASIMR thruster and longer missions.

Kerslake, Thomas W.↗

NASA NTRS1990

Thermal stability of electron-irradiated poly(tetrafluoroethylene) - X-ray photoelectron and mass spectroscopic study

Polytetrafluoroethylene (PTFE) was subjected to 3 keV electron bombardment and then heated in vacuum to 300 C. The behavior of the material as a function of radiation dose and temperature was studied by X-ray photoelectron spectroscopy (XPS) of the surface and mass spectroscopy of the species evolved. Lightly damaged material heated to 300 C evolved saturated fluorocarbon species, whereas unsaturated fluorocarbon species were evolved from heavily damaged material. After heating the heavily damaged material, those features in the XPS spectrum that were associated with damage diminished, giving the appearance that the radiation damage had annealed. The observations were interpreted by incorporating mass transport of severed chain fragments and thermal decomposition of severely damaged material into the branched and cross-linked network model of irradiated PTFE. The apparent annealing of the radiation damage was due to covering of the network by saturated fragments that easily diffused through the decomposed material to the surface region upon heating.

Wheeler, Donald R.↗

NASA NTRS1979

Long-term temperature effects on GaAs solar cells

The thermal degradation of AlGaAs solar cells resulting from a long-term operation in a space environment is investigated. The solar cell degradation effects caused by zinc and aluminum diffusion as well as deterioration by arsenic evaporation are presented. Also, the results are presented of experimental testing and measurements of various GaAs solar cell properties while the solar cell was operating in the temperature range of 27 C to 350 C. In particular, the properties of light current voltage curves, dark current voltage curves, and spectral response characteristics are given. Finally, some theoretical models for the annealing of radiation damage over various times and temperatures are included.

Heinbockel, J. H.↗

NASA NTRS1989

Indium phosphide solar cell research in the US: Comparison with nonphotovoltaic sources

Highlights of the InP solar cell research program are presented. Homojunction cells with AMO efficiences approaching 19 percent were demonstrated while 17 percent was achieved for indium tin oxide (ITO)/InP cells. The superior radiation resistance of these latter two cell configurations over both Si and GaAs were demonstrated. InP cells on board the LIPS III satellite show no degradation after more than a year in orbit. Computer modeling calculations were directed toward radiation damage predictions and the specification of concentrator cell parameters. Computed array specific powers, for a specific orbit, are used to compare the performance of an InP solar cell array to solar dynamic and nuclear systems.

Weinberg, I.↗

NASA NTRS1977

Effects of defect recombination centers on radiation damage in solar cells

Defect production in silicon is modeled on a computer by solving a large system of rate equations. The model includes the main, known defects that are stable at operating temperatures of solar cells in outer space; most of these defects are secondary and tertiary defects. The preliminary result shows that the presence of defect recombination centers for primary defects (i.e., vacancy and interstitial) can effectively reduce the production rates of those stable defects and, consequentially, improve the lifetime of solar cells operating in radiation environment. The characteristics of the defect recombination center required for better solar cell performance along with prospective candidates are discussed.

Cheng, L. J.↗

NASA NTRS2008

Predicting Chandra CCD Degradation with the Chandra Radiation Model

Not long after launch of the Chandra X-Ray Observatory, it was discovered that the Advanced CCD Imaging Spectrometer (ACIS) detector was rapidly degrading due to radiation. Analysis by Chandra personnel showed that this degradation was due to 10w energy protons (100 - 200 keV) that scattered down the optical path onto the focal plane. In response to this unexpected problem, the Chandra Team developed a radiation-protection program that has been used to manage the radiation damage to the CCDs. This program consists of multiple approaches - scheduled sating of the ACIS detector from the radiation environment during passage through radiation belts, real-time monitoring of space weather conditions, on-board monitoring of radiation environment levels, and the creation of a radiation environment model for use in computing proton flux and fluence at energies that damage the ACIS detector. This radiation mitigation program has been very successful. The initial precipitous increase in the CCDs' charge transfer inefficiency (CTI) resulting from proton damage has been slowed dramatically, with the front-illuminated CCDS having an increase in CTI of only 2.3% per year, allowing the ASIS detector's expected lifetime to exceed requirements. This paper concentrates on one aspect of the Chandra radiation mitigation program, the creation of the Chandra Radiation Model (CRM). Because of Chandra's highly elliptical orbit, the spacecraft spends most of its time outside of the trapped radiation belts that present the severest risks to the ACIS detector. However, there is still a proton flux environment that must be accounted for in all parts of Chandra's orbit. At the time of Chandra's launch there was no engineering model of the radiation environment that could be used in the outer regions of the spacecraft's orbit, so the CRM was developed to provide the flux environment of 100 - 200 keV protons in the outer magnetosphere, magnetosheath, and solar wind regions of geospace. This presentation describes CRM, its role in Chandra operations, and its prediction of the ACIS CTI increase.

Minow, Joseph I.↗

NASA NTRSDate not supplied

Neurovascular Responses to Simulated Deep Space Radiation in a Human Organ-on-a-Chip Model

A major health risk for human deep space exploration is central nervous system (CNS) damage by galactic cosmic ray radiation. Simulated galactic cosmic rays or their components, especially the high-linear energy transfer (LET) particles such as 56Fe ions, have been shown to cause CNS damage, neuroinflammation and cognitive dysfunction in rodent models, but their effects on human CNS remain to be investigated. CNS damage from any insult, including ionizing radiation, is partially mediated by the blood-brain barrier (BBB), which regulates interactions between CNS and the rest of the body. The main cellular regulators of BBB permeability are astrocytes, which also modulate neuroinflammation. However, there have been few studies on BBB and astrocyte functions in regulating CNS responses, especially in human tissue analogs. Therefore, we utilized a high-throughput 3D organ-on-a-chip system, seeded with human induced pluripotent stem cell-derived astrocytes and brain endothelial cells, or brain endothelial cells alone, to study human neurovascular responses to simulated deep space radiation. We investigated the permeability and morphology of vascular structures formed by endothelial cells, as well as oxidative stress and secreted cytokines and chemokine levels over 1-7 days after irradiation with 0.25 – 0.5 Gy 5-ion simplified simulated galactic cosmic rays or 0.3 – 0.8 Gy high-LET 600 MeV/n 56Fe particles, and compared the outcomes to low-LET X-ray irradiation. We observed that simulated deep space radiation caused delayed astrocyte activation in a pattern resembling CNS responses to brain injury, caused oxidative stress and the production of inflammatory cytokines, and compromised BBB integrity by damaging tight junctions, thus increasing vascular permeability. Furthermore, our results indicate that astrocytes have a dual role in regulating radiation responses: they exacerbate blood-brain barrier permeability early after irradiation, followed by switching to a more protective scar-like phenotype by reducing oxidative stress and pro-inflammatory cytokine and chemokine secretion. In a follow-up study using the same platform, we investigated the dose-rate effects of ionizing radiation, by exposing our model to chronic, low dose-rate, gamma radiation. Our model was significantly improved by adding additional cell types composing the BBB, modelling immune cell infiltration into the brain, and studying the effect of an antioxidant, to measure more complex outcomes and model more closely the effect of deep space radiation on the human BBB. In summary, our results present a human neurovascular model for space radiation studies and potential future automated payload adaptation, and suggest astrocyte regulatory mechanisms as targets for countermeasures to mitigate human neurovascular impairments during deep space exploration.

Ionizing radiation↗

NASA NTRSDate not supplied

AMMPER: a user-friendly agent-based model that recapitulates simple metabolic responses of yeast to deep-space radiation

For humans venturing to deep space, radiation exposure poses a major health risk. Fundamental research into the biological effects of space radiation are essential for enabling exploration, and the first experimental organisms we send to deep space will be microbial. Yet there are many ways in which microorganisms are likely to experience the effects of high-energy particle radiation (such as Galactic Cosmic Rays) differently from multicellular animals, partly due to the simple fact that microbes are small and unicellular-- less likely to get hit in the first place, and less likely to communicate damage between cells. Computational modeling can aid in designing experiments and predicting the biological effects of radiation, but thus far particle radiation models have not focused on microbes. Here we present the latest developments in AMMPER, the Agent-based Model for Microbial Populations Exposed to Radiation. Originally written in 2021, AMMPER is a Python-based model that incorporates radiation track data from NASA's RITRACKS software and simulates the growth, damage, and death of yeast cells in 3D. It is now freely available as an open-source package on NASA's GitHub repository. Recent improvements include the ability to simulate the dynamics of alamarBlue, a color-changing redox dye commonly used to track metabolic activity in microbial spaceflight experiments. We demonstrate that a simple blue-pink-clear transition model is able to recapitulate key features observed in empirical data from ground studies. AMMPER also includes a new graphical user interface and introductory tutorial to facilitate ease of use by a wider audience. AMMPER can help us to understand how spatially heterogeneous particle radiation damage at the single-cell level can translate to growth differences at the population level, ultimately allowing us to better interpret experiments using microbes as model organisms and how well their results apply to humans.

yeast↗

NASA NTRS2012

New Modeling Approaches to Study DNA Damage by the Direct and Indirect Effects of Ionizing Radiation

DNA is damaged both by the direct and indirect effects of radiation. In the direct effect, the DNA itself is ionized, whereas the indirect effect involves the radiolysis of the water molecules surrounding the DNA and the subsequent reaction of the DNA with radical products. While this problem has been studied for many years, many unknowns still exist. To study this problem, we have developed the computer code RITRACKS [1], which simulates the radiation track structure for heavy ions and electrons, calculating all energy deposition events and the coordinates of all species produced by the water radiolysis. In this work, we plan to simulate DNA damage by using the crystal structure of a nucleosome and calculations performed by RITRACKS. The energy deposition events are used to calculate the dose deposited in nanovolumes [2] and therefore can be used to simulate the direct effect of the radiation. Using the positions of the radiolytic species with a radiation chemistry code [3] it will be possible to simulate DNA damage by indirect effect. The simulation results can be compared with results from previous calculations such as the frequencies of simple and complex strand breaks [4] and with newer experimental data using surrogate markers of DNA double ]strand breaks such as . ]H2AX foci [5].

Plante, Ianik↗

NASA NTRSDate not supplied

Neurovascular effects of simulated space radiation

A major health risk for human deep space exploration is central nervous system (CNS) damage by ionizing radiation. Simulated galactic cosmic rays or their components, especially high-linear energy transfer particles such as 56Fe ions, have been shown to cause CNS damage, neuroinflammation and cognitive dysfunction in rodent models, but their effects on human CNS remain to be investigated. CNS damage from any insult, including ionizing radiation, is partially mediated by the blood-brain barrier (BBB), which regulates interactions between CNS and the rest of the body. Astrocytes are major cellular regulators of BBB permeability and also modulate neuroinflammation and neurodegeneration. However, BBB and astrocyte functions in regulating CNS responses to space radiation remain little investigated, especially in human organ analogs. Therefore, we developed and utilized a high-throughput 3D human neurovascular organ-on-a-chip model, seeded with induced pluripotent stem cell-derived cells. The effects of time course, ionizing radiation dose and dose rate were mapped by exposing the model to either acute, high dose rate radiation with simulated galactic cosmic rays or 600 MeV/n 56Fe particles, or protracted, low dose rate gamma radiation using a 57Co sealed source setup. We investigated BBB permeability, oxidative stress, cellular damage and secreted factors over the time period between 24 hours – 2 weeks after 0.1 – 0.8 Gy irradiation. We observed that ionizing radiation exposure increased BBB permeability, caused oxidative stress, damaged endothelial cells and altered expression of inflammatory cytokines with a subset of outcomes dependent on ionizing radiation dose rate. Furthermore, our results indicated that astrocyte functions were primarily deleterious at early time points and protective later after irradiation, resembling CNS responses to injury in vivo. Our findings in organ models were complemented by studies on true spaceflight using mouse spatial and single cell multi-omics, which similarly indicated spaceflight-mediated changes in astrocyte functions. In summary, our study evaluates the regulation of neurovascular responses to simulated space radiation, suggesting astrocytes as targets for countermeasures to mitigate CNS damage in deep space exploration.

Radiation↗

NASA NTRSDate not supplied

Low Energy Ionizing Radiation and Plasma Contributions to Radiation Dose in Materials at Sun-Earth Lagrange Points

- High energy radiation environments responsible for radiation damage to thick materials are well characterized and modeled: - Galactic cosmic rays — Badhwar-O’Neil 2020, CREME96, Nymmik - Solar particle events — Emission of Solar Protons, SAPPHIRE, JPL, King 1972 - Trapped radiation belts — AE8/AP8, AE9/AP9/IRENE - Low energy radiation environments responsible for radiation damage to thin materials relevant to Lagrange points and interplanetary missions have not been treated as comprehensively to date: - Solar wind - Magnetosheath - Magnetotail - Concern to spacecraft design and operations is radiation damage to surfaces and thin materials with mission critical applications on exterior of spacecraft - Applications: thermal control coatings, sunshields, multilayer insulation, optical thin film coatings, solar sails, thermo-optical properties of space exposed materials - Damage processes: radiation degradation (total dose), light ion sputtering, proton blistering of soft metals, modification of optical properties (α/ε), modification of charging properties (SEY, surface conductivity)

Joseph I. Minow↗

NASA NTRS2011

New Modeling Approaches to Investigate Cell Signaling in Radiation Response

Ionizing radiation damages individual cells and tissues leading to harmful biological effects. Among many radiation-induced lesions, DNA double-strand breaks (DSB) are considered the key precursors of most early and late effects [1] leading to direct mutation or aberrant signal transduction processes. In response to damage, a flow of information is communicated to cells not directly hit by the radiation through signal transduction pathways [2]. Non-targeted effects (NTE), which includes bystander effects and genomic instability in the progeny of irradiated cells and tissues, may be particularly important for space radiation risk assessment [1], because astronauts are exposed to a low fluence of heavy ions and only a small fraction of cells are traversed by an ion. NTE may also have important consequences clinical radiotherapy [3]. In the recent years, new simulation tools and modeling approaches have become available to study the tissue response to radiation. The simulation of signal transduction pathways require many elements such as detailed track structure calculations, a tissue or cell culture model, knowledge of biochemical pathways and Brownian Dynamics (BD) propagators of the signaling molecules in their micro-environment. Recently, the Monte-Carlo simulation code of radiation track structure RITRACKS was used for micro and nano-dosimetry calculations [4]. RITRACKS will be used to calculate the fraction of cells traversed by an ion and delta-rays and the energy deposited in cells in a tissue model. RITRACKS also simulates the formation of chemical species by the radiolysis of water [5], notably the .OH radical. This molecule is implicated in DNA damage and in the activation of the transforming growth factor beta (TGF), a signaling molecule involved in NTE. BD algorithms for a particle near a membrane comprising receptors were also developed and will be used to simulate trajectories of signaling molecules in the micro-environment and characterize autocrine and paracrine cell communication and signal transduction.

Plante, Ianik↗

NASA NTRS1965

Theoretical and experimental studies of radiation-induced damage to semiconductor surfaces and the effects of this damage on semiconductor device performance Semiannual progress report no. 3, 1 Mar. - 31 Aug. 1965

Effects of radiation-induced damage on performance of semiconductor devices - surface recombination velocity model

RADIATION EFFECT↗

NASA NTRSDate not supplied

Deep Space Radiation Affects Neurovascular Functions in Human Organ-on-a-Chip Models

A major health risk for human deep space exploration is central nervous system (CNS) damage by galactic cosmic ray radiation. Simulated galactic cosmic rays or their components, especially the high- linear energy transfer (LET) particles such as 56 Fe ions, cause CNS damage, neuroinflammation and cognitive dysfunction in rodent models, but their effects on human CNS remain to be investigated. CNS damage from any insult, including ionizing radiation, is partially mediated by the blood-brain barrier (BBB), which regulates the interactions between CNS and the rest of the body. The main cellular regulators of BBB permeability are astrocytes, which also modulate neuronal health and neuroinflammation. However, there have been few studies on BBB and astrocyte functions in regulating CNS responses, especially in human tissue/organ analogs. Therefore, we utilized a high-throughput human 3D organ-on-a-chip system, seeded with induced pluripotent stem cell-derived endothelial cells, astrocytes and neurons, to study human neurovascular responses to simulated deep space radiation. We investigated BBB permeability, oxidative stress, cellular and tissue damage, and secreted factors over the time period of 24 hours-1 week after irradiation with 0.25-0.5 Gy 5-ion simplified simulated galactic cosmic rays and 0.3-0.8 Gy high-LET 600MeV/n 56 Fe particles, and compared the outcomes to low-LET irradiation with 0.1-1 Gy doses of X-rays and gamma rays. Both high and low-LET radiation increased neurovascular permeability, caused oxidative stress, damaged endothelial cells and tight junctions, and altered expression of inflammatory cytokines. Ionizing radiation- induced neurovascular permeability and oxidative stress peaked at 3 days after irradiation and were further exacerbated by the presence of astrocytes. Furthermore, in response to particle irradiation, astrocytes stimulated interleukin-1 signaling by inhibiting the expression of interleukin-1 receptor antagonist. Thus, we also evaluated interleukin-1 receptor antagonist as a potential countermeasure against particle radiation. Ultimately, our results may help develop countermeasures to mitigate human CNS damage in deep space exploration.

Sonali D Verma↗

NASA NTRS2022

Evolution of Biological Satellites: From Low Earth Orbit to NASA’s BioSentinel Deep Space Mission

NASA has set its sights on human exploration in deep space with the Artemis missions, with an ambitious plan to put astronauts back on the Moon and to eventually land human missions on Mars. Such missions will require significant countermeasures, likely both technological and biomedical, to protect biology from chronic radiation exposure. Small satellites like CubeSats can inform these countermeasures by querying relevant space environments with model organisms over relevant durations. NASA has launched five biological CubeSats into low Earth orbit (LEO) from GeneSat in 2006 to EcAMSat in 2017. Each one of these missions increased our understanding of the effects of spaceflight, while refining technologies and imparting valuable lessons to the next generation of CubeSats. The Artemis I rocket will carry ten CubeSats, each of them with its own objective. One in particular, BioSentinel, will conduct the first study of the biological response to interplanetary space radiation beyond LEO since Apollo 17. Once it reaches its heliocentric orbit – after a short lunar fly-by – BioSentinel will measure the DNA damage response to ambient radiation in a model organism, the budding yeast Saccharomyces cerevisiae, which will be compared to information provided by an onboard radiation sensor and to data obtained in LEO (on ISS) and on Earth. Once in interplanetary space, fluidic cards containing desiccated yeast cells will be activated by growth medium addition at different time points throughout the mission. Growth and metabolic activity will be tracked continuously via optical density. BioSentinel is a complete, autonomous spacecraft capable of conducting experiments in deep space. Its 4U BioSensor payload is a fully automated and adaptable platform that can perform biological measurements with a range of microorganisms in multiple space environments, including the ISS, free flyers, and other platforms like the Lunar Gateway and lander vehicles.

Sergio R Santa Maria↗

NASA NTRSDate not supplied

BioSentinel: NASA’s First Deep Space Biological Mission

Since Apollo 17 in 1972, NASA has sent no humans or other biological organisms outside of Earth’s protective magnetosphere. NASA’s current Artemis program plans to put astronauts back on the Moon and eventually land human missions on Mars. One of the major challenges to long-duration crewed travel and habitation in deep space is an in-depth understanding of the biological effects of space radiation, often convoluted by the impact of reduced gravity. Such missions will require significant countermeasures, likely both technological and biomedical, to protect organisms from chronic radiation exposure. Small satellite missions like CubeSats can inform these countermeasures by investigating model organisms in relevant space environments. The BioSentinel mission is comprised of four segments developed at NASA Ames Research Center: a 6U CubeSat (1U = 10-cm cube), an ISS payload launched in December 2021 and two ground units, one for the mission’s CubeSat and one for the ISS payload. The last three segments have been operational since January 2022 and serve as experimental controls. BioSentinel’s 6U CubeSat is planned to launch as a secondary payload on the Artemis-1 rocket. It will be deployed on a lunar fly-by trajectory and into a heliocentric orbit. BioSentinel will be the first interplanetary satellite to study the biological response to space radiation outside Low Earth Orbit (LEO) in almost 50 years. BioSentinel is a complete, autonomous spacecraft capable of conducting experiments in deep space. Its 4U BioSensor payload is a fully automated and adaptable platform that can perform biological measurements with a range of microorganisms in multiple space environments, including the ISS, free flyers, and other platforms like the Lunar Gateway and lander vehicles. Once it reaches its orbit, BioSentinel’s CubeSat will measure the DNA damage response to ambient radiation in a model organism, the budding yeast Saccharomyces cerevisiae, which will be compared to information provided by an onboard radiation sensor and to data obtained in LEO (on ISS) and on Earth. Once in interplanetary space, fluidic cards containing desiccated yeast will be activated by growth medium addition at different time points throughout the mission. Growth and metabolic activity will be tracked continuously via optical measurements. This paper describes BioSentinel’s objectives, science, data management, and preliminary results from the ISS and ISS ground control segments.

BioSentinel↗

NASA NTRSDate not supplied

BioSentinel: NASA’s First Deep Space Biological Mission

BioSentinel↗

NASA NTRS1999

On The Development of Biophysical Models for Space Radiation Risk Assessment

Experimental techniques in molecular biology are being applied to study biological risks from space radiation. The use of molecular assays presents a challenge to biophysical models which in the past have relied on descriptions of energy deposition and phenomenological treatments of repair. We describe a biochemical kinetics model of cell cycle control and DNA damage response proteins in order to model cellular responses to radiation exposures. Using models of cyclin-cdk, pRB, E2F's, p53, and GI inhibitors we show that simulations of cell cycle populations and GI arrest can be described by our biochemical approach. We consider radiation damaged DNA as a substrate for signal transduction processes and consider a dose and dose-rate reduction effectiveness factor (DDREF) for protein expression.

Cucinotta, F. A.↗