Radiation Damage Model Research Articles

Real-time simulation of photovoltaic modules

A photovoltaic (PV) array simulator, consisting of a computer controlled d.c. power supply producing up to 100 W and associated control software, was designed and developed to generate real-time current-voltage ( I-V) output characteristic curves of photovoltaic cells under simulated conditions. The system is also capable of modelling radiation damage due to high energy particles. The system comprises a pre-regulator, a switch-mode regulator, a computer interface, and modelling and control software. The control software uses feedback of the output voltage and current to iteratively converge to the actual operating point for the connected load. Simulation results match the expected theoretical calculations well. The main advantage of the simulator is its ability to simulate different types and sizes of arrays under varying illumination and temperature using actual loads. The system can be used to study the short-term and long-term performances of PV modules and to predict end-of-life efficiency. The simulator is a far more cost effective and reliable replacement for actual field testing.

Problems and advances in the dosimetry of radionuclide targeted therapy.

One of the goals of conventional external beam radiotherapy is to construct treatment plans for which the dose distribution across the tumor is uniform. This can be achieved with tumor dose heterogeneities of less than 15%. Therefore the concepts of dose response and tumor control probability (TCP) in external beam therapy are clearly defined and unambiguous. However, the treatment of many disease sites in radiation therapy result in high doses to partial volumes of normal tissue structures. For example, in the treatment of pancreatic cancer, the location of the pancreas results in the unavoidable delivery of high doses to the kidneys and spinal cord. The radiation tolerance of the spinal cord is well known. It behaves according to a serial model of radiation damage, which means that a dose in excess of 50 Gy to any region of the spinal cord can produce transverse radiation myelitis. However, the response of kidney is according to a parallel model, i.e., the kidney consists of a large number of repeat units, nephrons, a certain fraction of which must be destroyed before loss of kidney function is observed. The objective of a treatment plan for pancreatic cancer is to manipulate the beam directions and weights, so as to minimize the volume of kidney receiving high dose irradiation in order to reduce the risk of kidney complication, consistent with the prescribed dose to the target volume, and a dose of 003C;45 Gy anywhere to the spinal cord.KeywordsSingle Photon Emission Compute TomographyLinear Energy TransferNormal Tissue Complication ProbabilityTumor Control ProbabilityPhosphor PlateThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Single activation energy model of radiation damage in solid state nuclear track detectors

Abstract Passage of heavy ions produces radiation damage trails known as latent tracks in a variety of solid state nuclear track detectors (SSNTDs). The empirical formulation of the Single Activation Energy Model is based on track annealing data collected in our laboratory from both isothermal and isochronal experiments performed on different types of SSNTDs, viz. glasses, plastics and minerals. Some equivalent versions of our model have been proposed but the concept of single activation energy is vindicated in all empirical formulations. It is interesting to remark that this model always yields a unique value of activation energy independent of the nature of ion beam used and its degree of annealing. The anisotropy of mineral SSNTDs is revealed by variation of activation energy along different crystal planes and even at different orientations of ion beam. Some recent experiments are a pointer to the successful exploitation of this model for future cosmic ray studies using SSNTDs.

Elucidation of primary radiation damage in DNA through application of ab initio molecular orbital theory.

This review summarizes the results of recent ab initio molecular orbital calculations performed on DNA constituents that attempt to further our understanding of the radiation-induced damage to DNA. The results reviewed include calculations performed on the four individual DNA bases, the base pairs in gas phase and modelled aqueous phase, the deoxyribose moiety, and a portion of the sugar-phosphate backbone. The emphasis is on the electron affinities and ionization potentials of the radical species calculated under various conditions (i.e. gas phase, aqueous phase, proton transfer, base stacking), as it has been shown that the initial ion radical distribution is largely a function of these two properties. Theoretical studies of the electronic excited states of the individual bases and radioprotection of the biomolecule by various thiol compounds are also reviewed. Finally, a summary is provided to allow for further elaboration of the current model for radiation damage to DNA and to show the present advantages and limitations of ab initio theory in the investigation of such processes.

The effects of acute irradiation on a forest biogeocenosis; experimental data, model and practical applications for accidental cases

The effects of acute irradiations of a mixed pine and birch forest in spring and autumn with a high power point-type gamma radiation source (1180 TBq 137Cs) have been described. Radiation dose relationships for numerous response reactions of woody and herbaceous plants (growth and development of organs of woody plants, cytogenetical, physiological and biochemical changes in trees, reproductive potential of plants, damage and dying off of the forest as a biogeocenosis on the whole) have been calculated. Post-radiation recovery of the forest was investigated. Changes involving the secondary reactions related to radiation damage and death of the trees are presented. A model for radiation damage of forests has been designed. Examples are given on the usage of this model in the description of radiation effects in forests in the event of accidental releases of radionuclides into environment.

The effects of acute irradiation on a forest biogeocenosis; experimental data, model and practical applications for accidental cases

The effects of acute irradiations of a mixed pine and birch forest in spring and autumn with a high power point-type gamma radiation source (1180 TBq 137Cs) have been described. Radiation dose relationships for numerous response reactions of woody and herbaceous plants (growth and development of organs of woody plants, cytogenetical, physiological and biochemical changes in trees, reproductive potential of plants, damage and dying off of the forest as a biogeocenosis on the whole) have been calculated. Post-radiation recovery of the forest was investigated. Changes involving the secondary reactions related to radiation damage and death of the trees are presented. A model for radiation damage of forests has been designed. Examples are given on the usage of this model in the description of radiation effects in forests in the event of accidental releases of radionuclides into environment.

Irradiation-induced defects in thin aluminium films studied by 1/f noise

The paper reports on the recovery of irradiation-induced defects in thin aluminium films as studied by measurements of the electrical 1/f noise. The defects are produced by irradiation with 1 MeV electrons at 10 K, which results in a strong increase of the noise. Subsequent isochronal annealing at progressively higher temperatures causes the 1/f noise measured at 10 K to recover in discrete steps which occur at the same temperatures as the well-known recovery stages of the irradiation-induced electrical resistivity increase. In the noise measurements at 40 K, however, an additional recovery step without analogue in the recovery spectrum of the electrical resistivity is observed at 70 K. The temperature dependence and annealing behaviour of the 1/f noise may be understood in terms of thermally activated motion of defects in a distorted lattice potential. A microscopic explanation of the present observation as well as of earlier measurements on Cu by Pelz and Clarke within the framework of the two-interstitial model of radiation damage of metals is presented.

Models of CNS radiation damage during space flight

The primary structural and functional arrangement of the different cell types within the CNS are reviewed. This was undertaken with a view to providing a better understanding of the complex interrelationships that may contribute to the pathogenesis of lesions in this tissue after exposure to ionizing radiation. The spectrum of possible CNS radiation-induced syndromes are discussed although not all have an immediate relevance to exposure during space flight. The specific characteristics of the lesions observed would appear to be dose related. Very high doses may produce an acute CNS syndrome that can cause death. Of the delayed lesions, selective coagulation necrosis of white matter and a later appearing vascular microangiopathy, have been reported in patients after cancer therapy doses. Lower doses, perhaps very low doses, may produce a delayed generalised CNS atrophy; this effect and the probability of the induction of CNS tumors could potentially have the greatest significance for space flight.

Radiation risk of the crew members of the expeditions on the “Mir” station during the 22nd solar activity cycle

The radiation risk at the end of the flight was calculated for the members of the main expeditions on the “Mir” station. It was based on the absorbed dose dynamics data measured by the board dosimeter. The radiation damage models created for standards of the radiation safety of the space flights were used in the calculations. The analysis of the obtaned values of the risk and its dynamics for some cosmonauts are presented in the topic. The risk values ΔP are close to the limited levels given by equation of ΔP = 0.6·10·T −4, where T - is flight duration in months.

On the steady state in radiation damage modelling

Steady state of the damage created by heavy ions or neutrons is characterized by the balance of production and annihilation processes of radiation-induced mobile defects and of the microstructure consisting of voids, stacking fault tetrahedra and dislocations. This dynamic equilibrium imposes constraints on the concentration of mobile defects and on the microstructure which make them interdependent. We discuss various contributions to the production rate of freely-migrating defects and recent observations which indicate that atomic mixing and the overlap of cascades with the microstructure may strongly influence at low temperatures and high fluences, both the defect production and the microstructural evolution. Implications of these effects are discussed with regard to modelling of radiation damage.

Investigation of Intrinsic Point Defects in Metals by Nuclear Quadrupole Double Resonance

Abstract The paper reviews the principal features of the Nuclear Quadrupole Double Resonance (NQDOR ) technique, with particular emphasis on its application to the investigation of imperfections in cubic metals. NQDOR permits measurements of the electric field gradients (EFG) at quadrupole-moment-carrying nuclei in the neighbourhood of point defects and thus to obtain “fingerprints” of these defects. An NQDOR facility set-up at the M ax-Planck-Institut für Metallforschung in Stuttgart is described. It has been used to study the intrinsic defects introduced into Cu and dilute Cu/Be alloys by low-temperature irradiation with electrons or protons or by cold-work. It is shown that all well-resolved irradiation-induced EFG observed in the present work are due to one kind of defect only, which is identified as the <100> dumbbell self-interstitial. When considered together with measurements of the electrical resistivity on the same specimens, the annealing behaviour of the NQDOR lines supports the so-called two-interstitial model of radiation damage in face-centred cubic metals rather than the one-interstitial model.

Reliability Degradation in NMOS Devices Subjected to High Energy Gamma-Ray Irradiation

Introduction The effects of radiation on memory devices is of great concern to manufacturers and users in high-tech industry. With the increase in space and nuclear applications of computer circuitry, such devices are likely to be exposed, circumstantially or accidentally, to high doses of radiation and may therefore exhibit failures or be electrically degraded. Radiation has been known to cause charge leakage leading to soft errors due to alpha-particle emissions in DRAMs. Since EPROMs utilize ultra-violet light for erasure, some effect on the volatility due to radiation was suspected. The test described in this article involved samples of 4116 DRAMs, 2114 SRAMs and 2716 EPROMs. Gamma rays were initially discovered by Becquerel and Curie around 1896. They are photons which were first defined as grains of light and later as quanta of electromagnetic radiation. In the electromagnetic spectrum, gamma-rays occupy the highest energy region. The energy of rays is measured in eV. Xrays are in the 100eV-100keV range, whereas gamma-rays lie in the 100keV-100MeV region. Gamma rays can be generated by means of radioactive isotopes, such as colbalt, or in this case by an electron accelerator. When the electrons are accelerated they absorb energy. Only high energy particles are able to penetrate nuclei and create reactions. These high energy electrons are channelled into an electron beam. When the electrons hit a target, they decelerate abruptly thus releasing all of their stored energy. An atom penetrated by such an electron is left in a more exited state. Gamma-rays are emitted when the nucleus reverts from its exited state to its ground state. Analysing the effects of radiation on semiconductor devices is of a complex nature. Since the experimental results are a function of various factors such as dose-rates, total doses, energy of rays, temperature, chip uniformity, etc. no concrete theoretical model for radiation damage has been arrived at to date.

Time and temperature dependence of cascade induced defect production in in situ experiments and computer simulation

Understanding of the defect production and annihilation processes in a cascade is important in modelling of radiation damage for establishing irradiation correlation. In situ observation of heavy ion radiation damage has a great prospect in this respect. Time and temperature dependence of formation and annihilation of vacancy clusters in a cascade with a time resolution of 30 ms has been studied with a facility which comprises a heavy ion accelerator and an electron microscope. Formation and annihilation rates of defect clusters have been separately measured by this technique. The observed processes have been analysed by simple kinetic equations, taking into account the sink effect of surface and the defect clusters themselves together with the annihilation process due to thermal emission of vacancies from the defect clusters. Another tool to study time and temperature dependence of defect production in a cascade is computer simulation. Recent results of molecular dynamics calculations on the temperature dependence of cascade evolution are presented, including directional and temperature dependence of the lengths of replacement collision sequences, temperature dependence of the process to reach thermal equilibrium and so on. These results are discussed under general time frame of radiation damage evolution covering from 10 −15 to 10 9 s, and several important issues for the general understanding have been identified.

DNA damage in non-proliferating cells subjected to ionizing irradiation at high or low dose rates.

Ionizing radiation damage to the genome of a non-cycling mammalian cell is analyzed using continuous time Markov chains. Immediate damage induced by the radiation is modeled as a batch Poisson arrival process of DNA double strand breaks (DSBs). Different kinds of radiation, for example gamma rays or alpha particles, have different batch probabilities. Enzymatic modulation of the immediate damage is modeled as a Markov process similar to the processes described by the master equation of stochastic chemical kinetics. An illustrative example is the restitution/complete exchange model, which postulates that radiation induced DSBs can subsequently either undergo enzymatically mediated repair (restitution) or can participate pairwise in chromosome exchanges, some of which make irremediable lesions such as dicentric chromosome aberrations. One may have rapid irradiation followed by enzymatic DSB processing or have prolonged irradiation with both DSB arrival and enzymatic DSB processing continuing throughout the irradiation period. A complete solution of the Markov chain is known for the case that the exchange rate constant is negligible so that no irremediable chromosome lesions are produced and DSBs are the only damage to the genome. Using PDEs for generating functions, a perturbation calculation is made assuming the exchange rate constant is small compared to the repair rate constant. Some non-perturbative results applicable to very prolonged irradiation are also obtained using matrix methods: Perron-Frobenius theory, variational methods and numerical approximations of eigenvalues. Applications to experimental results on expected values, variances and statistical distributions of DNA lesions are briefly outlined. Continuous time Markov chain models are the most systematic of those current radiation damage models which treat DSB-DSB interactions within the cell nucleus as homogeneous (e.g. ignore diffusion limitations). They contain most other homogeneous models as special cases, limiting cases or approximations. However, applying the continuous time Markov chain models to studying spatial dependence of DSB interactions, which is generally believed to be very important in some situations, presents difficulties.

Phonon scattering in lightly neutron-irradiated diamond.

We report measurements on the thermal conductivity of diamond irradiated with fast neutrons. Low levels of irradiation (${10}^{19}$ neutrons ${\mathrm{cm}}^{\mathrm{\ensuremath{-}}2}$) create vacancies and small regions of disordered carbon, whereas heavy doses (>${10}^{20}$ neutrons ${\mathrm{cm}}^{\mathrm{\ensuremath{-}}2}$) initiate vitrification. In this sense diamond is similar to the well-studied case of irradiated quartz. Our results in the low-dose regime are consistent with additional phonon scattering in the irradiated material by the extended regions of disordered carbon. The size and concentration of these regions as derived from the thermal-conductivity data correlate with those determined from the infrared spectra as well as with those estimated from a radiation-damage model. A comparison is made between the thermal conductivity of the irradiated material and that of synthetic vapor-deposited diamond films.

Bulk Defects and Radiation Damage in Detector Grade Silicon

ABSTRACTThe importance of bulk defects in Si to the performance of Si radiation detectors is discussed and the current state of knowledge about deep level defects, including those induced by radiation damage, is briefly reviewed. The importance and origins of the fluctuations in the spatial distribution of the shallow point defects which determine the uncompensated net impurity density are discussed and information on this problem in FZ silicon, multipass FZ silicon, neutron transmutation doped Si, and radiation damaged Si is presented and compared to what should be expected on the basis of simple modeling. A new model for radiation damage induced changes in the net uncompensated impurity density is reviewed and compared to experimental data on fast neutron damage in Si.

DNA damage caused by ionizing radiation

A survey is given of continuous-time Markov chain models for ionizing radiation damage to the genome of mammalian cells. In such models, immediate damage induced by the radiation is regarded as a batch-Poisson arrival process of DNA double-strand breaks (DSBs). Enzymatic modification of the immediate damage is modeled as a Markov process similar to those described by the master equation of stochastic chemical kinetics. An illustrative example is the restitution/complete-exchange model. The model postulates that, after being induced by radiation, DSBs subsequently either undergo enzymatically mediated restitution (repair) or participate pairwise in chromosome exchanges. Some of the exchanges make irremediable lesions such as dicentric chromosome aberrations. One may have rapid irradiation followed by enzymatic DSB processing or have prolonged irradiation with both DSB arrival and enzymatic DSB processing continuing throughout the irradiation period. Methods for analyzing the Markov chains include using an approximate model for expected values, the discrete-time Markov chain embedded at transitions, partial differential equations for generating functions, normal perturbation theory, singular perturbation theory with scaling, numerical computations, and certain matrix methods that combine Perron-Frobenius theory with variational estimates. Applications to experimental results on expected values, variances, and statistical distributions of DNA lesions are briefly outlined. Continuous-time Markov chains are the most systematic of those radiation damage models that treat DSB-DSB interactions within the cell nucleus as homogeneous (e.g., ignore diffusion limitations). They contain virtually all other relevant homogeneous models and semiempirical summaries as special cases, limiting cases, or approximations. However, the Markov models do not seem to be well suited for studying spatial dependence of DSB interactions, which is known to be important in some situations.

Acceleration of late radiation damage of the kidney by unilateral nephrectomy

Both increased proliferation as measured by labeling index and the appearance of abnormally large nuclei in renal proximal tubule cells, which have been observed in mouse kidneys after irradiation, were enhanced by subsequent unilateral nephrectomy. Nephrectomy alone induced only a transient increase in labeling index, lasting less than 1 month, whereas nephrectomy after irradiation induced an increase above that of the irradiated kidneys without nephrectomy lasting as long as 9 months. The incidence of large nuclei in kidneys from mice unilaterally nephrectomized 1 week after irradiation showed a rapid increase with time, peaking at 4.6% at 6 months, compared to more gradual increases with peaks at about 4.0% at 9 or 12 months in irradiated kidneys without nephrectomy or those in which nephrectomy was done prior to irradiation. This result demonstrates that nephrectomy after irradiation accelerates the appearance of this indicator of radiation damage, rather than enhancing the maximum amount of damage. Unilateral nephrectomy after irradiation also increased kidney damage 9 months later, as indicated by kidney weight loss and increased blood urea nitrogen. These results are consistent with our model for radiation damage of the kidney in which radiation induces cell proliferation and the appearance of reproductively dead, large nuclear cells that are lost at subsequent attempts to divide; the acceleration of radiation damage by unilateral nephrectomy performed after radiation could very well be a result of nephrectomy-induced enhancement in the proliferation of proximal tubule cells.

The role of non-protein sulphydryls in determining the chemical repair rates of free radical precursors of DNA damage and cell killing in Chinese hamster V79 cells.

Chinese hamster V79 fibroblasts were irradiated in the gas explosion apparatus and the chemical repair rates of the oxygen-dependent free radical precursors of DNA double-strand breaks (dsb) and lethal lesions measured using filter elution (pH 9.6) and a clonogenic assay. Depletion of cellular GSH levels, from 4.16 fmol/cell to 0.05 fmol/cell, by treatment with buthionine sulphoximine (50 mumol dm-3; 18 h), led to sensitization as regards DNA dsb induction and cell killing. This was evident at all time settings but was particularly pronounced when the oxygen shot was given 1 ms after the irradiation pulse. A detailed analysis of the chemical repair kinetics showed that depletion of GSH led to a reduction in the first-order rate constant for dsb precursors from 385 s-1 to 144 s-1, and for lethal lesion precursors from 533 s-1 to 165 s-1. This is generally consistent with the role of GSH in the repair-fixation model of radiation damage at the critical DNA lesions. However, the reduction in chemical repair rate was not proportional to the severe thiol depletion (down to approximately 1% for GSH) and a residual repair capacity remained (approximately 30%). This was found not to be due to compartmentalization of residual GSH in the nucleus, as the repair rate for dsb precursors in isolated nuclei, washed virtually free of GSH, was identical to that found in GSH-depleted cells (144 s-1), also the OER remained substantially above unity. This suggests that other reducing agents may have a role to play in the chemical repair of oxygen-dependent damage. One possible candidate is the significant level of protein sulphydryls present in isolated nuclei.

Repair Capacity and Kinetics in Spheroids from a Lung Metastasis of a Human Soft Tissue Sarcoma: A Growth Delay Study

Spheroids grown from the human cell line EF8 of a lung metastasis of a human malignant fibrous histiocytoma were given fractionated irradiation with 60Co gamma rays at passages 31 and 32. The mean diameter of the spheroids at the time of treatment was 250 microns. Growth delay was used as the end point in these studies. Two experiments were carried out to determine the capacity and kinetics of repair of sublethal damage. In the first experiment, one, two, and five fractions were given at three or four dose levels with fixed intervals of 360 min. In the second experiment, schedules with two and four dose fractions and intervals of 0, 20, 60, 120, and 360 min were used, each at two dose levels. Data analysis was performed by a direct method based on the alpha/beta model and first-order repair kinetics of radiation damage. In both experiments, the alpha/beta value of EF8 spheroids was estimated to be about 8 (6-10) Gy. The rate constant of repair, mu, and its 95% confidence interval were estimated to be 0.62 (0.40-0.84) 10(-2) min-1, equivalent to a half-time of repair (T1/2) of 112 (83-172) min. A more detailed analysis of the data of the second experiment revealed a significant dependence of the rate constant of repair, mu, on the total radiation effect induced by the fractionated radiation treatments with short overall times. With increasing level of effect, mu decreased. These data indicate that the half-time of recovery of a human tumor can be longer than that of the surrounding normal tissue, in this case lung, at least for a limited range of doses and for some fractionation schedules.