束流在270°偏转磁铁系统输运过程中的损失计算

为计算医用加速器中束流经过270°偏转磁铁系统电子损失所造成的辐射剂量问题, 将束流传输相应的计算公式和蒙特卡罗抽样方法相结合, 在一阶近似条件下计算了电子在偏转系统中的输运过程, 分析了不同初始条件对电子输运和电子损失的影响；模拟结果表明能散是产生电子损失的主要因素之一. 计算得到了损失电子所处位置、能量和飞行方向等信息, 把计算得到的信息作为蒙特卡罗程序的输入源, 进一步计算出束流损失所产生的辐射剂量分布, 从而能更完善地设计医用加速器照射头的屏蔽. 文中给出在电子束初始半径为1mm、散角为5mrad、能散为10%条件下电子损失率为13.5%, 损失电子主要是向加速器照射头部上方辐射出去.     

束流在270°偏转磁铁系统输运过程中的损失计算

为计算医用加速器中束流经过270°偏转磁铁系统电子损失所造成的辐射剂量问题,将束流传输相应的计算公式和蒙特卡罗抽样方法相结合,在一阶近似条件下计算了电子在偏转系统中的输运过程,分析了不同初始条件对电子输运和电子损失的影响;模拟结果表明能散是产生电子损失的主要因素之一.计算得到了损失电子所处位置、能量和飞行方向等信息,把计算得到的信息作为蒙特卡罗程序的输入源,进一步计算出束流损失所产生的辐射剂量分布,从而能更完善地设计医用加速器照射头的屏蔽.文中给出在电子束初始半径为1mm、散角为5mrad、能散为10%条件下电子损失率为13.5%,损失电子主要是向加速器照射头部上方辐射出去.     

蒙特卡罗碰撞算法在CHIPIC软件中的数值实现

分析离子源中电子所参与的碰撞,利用电子与其它粒子间的空碰撞模型,研究电子之间的库仑碰撞,采用不同的存储和调用机制研制了两种碰撞模型的蒙特卡罗碰撞处理模块,将数值模块添加到粒子模拟软件CHIPIC中,对离子源JAERI 10A进行模拟验证,通过对模拟结果的分析,表明所设计的三维MCC算法正确.     

EACVD金刚石薄膜中氢分解过程的研究

采用蒙特卡罗方法模拟了电子辅助化学气相淀积（EACVD）金刚石薄膜中的氢分解过程,建立了电子碰撞使氢分解的模型,给出了电子能量分布及氢原子数的空间分布,讨论了电偏压和气压对氢分解的影响。这些结果对EACVD制造金刚石薄膜的研究有重要意义。     

X射线在介质中的剂量分布计算

研究了放射治疗中X射线在介质中的输运过程, 编程实现了基于蒙特卡罗方法的剂量计算. 并在便于图形处理的软件Matlab中对光子输运结果进行了可视化处理. 对X射线在均匀介质和非均匀介质中的蒙特卡罗模拟结果与实测结果、其他蒙特卡罗软件模拟结果进行了比较, 结果符合较好. 实验结果表明该方法既可以获得很快的仿真速度, 又能得到精确直观的剂量计算结果, 为提高放射治疗水平具有重要的指导意义和应用价值.     

各向异性生物组织中偏振光传输的模拟与实验

针对具有纤维状结构特征的生物组织(诸如肌肉、皮肤等),建立了包含球状散射体和具有取向分布的圆柱状散射体的仿体模型,并对偏振光在这类具有各向异性分布的复杂体系中的传输过程进行了蒙特卡罗模拟.给出了蒙特卡罗模拟程序的实现方法并验证了程序的可靠性,随后将程序用于模拟和分析一些肌肉组织的偏振成像实验.实验和模拟结果的一致性验证了用柱-球散射体混合的仿体模型来模拟各向异性生物组织的合理性.同时,通过模拟验证,得到了两个新的参量,分别可以用来表征组织样品中纤维的空间取向和组织样品的各向异性度.     

阳极杆箍缩二极管产生X射线能谱的模拟计算

采用粒子模拟,得到了阳极杆箍缩二极管阳极钨针上电子的空间分布和入射角分布,分析二极管工作状态得到了电子的能量分布.在此基础上建立阳极杆箍缩二极管的蒙特卡罗模型,模拟得到了阳极杆箍缩二极管的辐射能谱和X射线的平均能量,并与实验结果进行了比较.结果表明:09006炮光子平均能量为0.441 MeV,计算该能谱射线经过不同厚度铅衰减片后的剂量衰减情况,与叠片法PIN探测器所测的实验数据基本一致. 关键词： 阳极杆箍缩二极管 粒子模拟 蒙特卡罗方法 X射线能谱     

JMCT与子通道程序耦合方法研究及验证

蒙特卡罗与热工水力的耦合计算是目前反应堆数值模拟的重要研究方向,在蒙特卡罗方法连续能量点截面的基础上结合热工程序的温度反馈,反应堆中子计算的准确性得到大幅提高。为了提高计算精度,堆芯模型分辨率也需进一步提高,相比于组件均匀化模型,pin-by-pin的建模方式能够获得更好的结果。利用蒙特卡罗程序JMCT与子通道程序COBRA-EN实现了蒙特卡罗-热工的内耦合,内耦合方式通过内存进行数据传递,其计算效率及安全性均优于外耦合方法。随后利用NURISP项目迷你堆的pin-by-pin模型对耦合程序进行验证。计算结果与同类耦合程序相似,验证了程序的准确性。同时,对耦合过程的收敛性问题进行了初步分析。     

基于蒙特卡罗方法的XHA600D医用电子直线加速器的入射电子束参数研究

使用蒙特卡罗方法研究入射电子束参数对XHA600D医用电子直线加速器产生的剂量分布的影响,并确定优化的入射电子束参数。根据厂商提供的XHA600D加速器治疗头的几何、材料参数,使用蒙特卡罗程序EGSnrc对不同的入射电子束参数进行模拟并记录其在水模体中产生的剂量分布,将模拟结果与测量结果进行比较。模拟的入射电子束参数包括平均能量、径向强度分布、角度展宽和能量展宽;实验测量数据包括4 cm×4 cm、10 cm×10 cm、30 cm×30 cm射野条件下的百分深度剂量与离轴剂量。结果表明当入射电子束的平均能量为6 MeV、径向强度的半高宽(Full Width at Half Maximum, FWHM)为0.25 cm、角度展宽为0.15°时,模拟结果和测量结果吻合非常好。这些参数可以作为建立适用于XHA600D加速器的TPS(Treatment Planning System)剂量计算模型的基础参数。     

蒙特卡罗方法模拟薄膜电致发光器件中碰撞离化的作用

基于经验赝势法得到的能带结构数据，采用分段多项式拟合获得ZnS能带结构的解析表达式 ，建立解析能带模型.使用建立的模型计算得到各能谷的态密度和总的散射速率,并与文献 的计算结果进行了对比，验证该解析能带模型既具有非抛物型多能谷能带模型运算速度快、 使用方便的优势,又具有与采用全导带模型相近的计算精度.进一步利用该模型进行蒙特卡罗 模拟，得到第一导带和第二导带中电子数随电场强度的变化、不同电场中能量分布函数以及 包含与不包含碰撞离化情况下电子能量随时间变化的曲线.讨论在外加电场下，电子在导带 内各个能谷间和 关键词： 蒙特卡罗模拟 解析能带模型 多项式拟合 碰撞离化     

Effect of a magnetic field on the track structure of low-energy electrons: a Monte Carlo study

The increasing use of MRI-guided radiation therapy evokes the necessity to investigate the potential impact of a magnetic field on the biological effectiveness of therapeutic radiation beams. While it is known that a magnetic field, applied during irradiation, can improve the macroscopic absorbed dose distribution of electrons in the tumor region, effects on the microscopic distribution of energy depositions and ionizations have not yet been investigated. An effect on the number of ionizations in a DNA segment, which is related to initial DNA damage in form of complex strand breaks, could be beneficial in radiation therapy. In this work we studied the effects of a magnetic field on the pattern of ionizations at nanometric level by means of Monte Carlo simulations using the Geant4-DNA toolkit. The track structure of low-energy electrons in the presence of a uniform static magnetic field of strength up to 14 T was calculated for a simplified DNA segment model in form of a water cylinder. In the case that no magnetic field is applied, nanodosimetric results obtained with Geant4-DNA were compared with those from the PTB track structure code. The obtained results suggest that any potential enhancement of complexity of DNA strand breaks induced by irradiation in a magnetic field is not related to modifications of the low-energy secondary electrons track structure.     

DNA damage induced by low-energy electrons: electron transfer and diffraction

Thin films of the short single strand of DNA, GCAT, in which guanine (G) or adenine (A) have been removed, were bombarded under vacuum by 4 to 15 eV electrons. The fragments corresponding to base release and strand breaks (SB) were analyzed by high performance liquid chromatography and their yields compared with those obtained from unmodified GCAT. From such a comparison, it is shown that, using GCAT as a model system, (1) most SB result from electron capture by DNA bases followed by electron transfer to the phosphate group and (2) the initial capture probability depends on the coherence of the electron wave within the tetramer.     

DNA strand breaks induced by 0-4 eV electrons: the role of shape resonances

Collisions of 0-4 eV electrons with thin DNA films are shown to produce single strand breaks. The yield is sharply structured as a function of electron energy and indicates the involvement of pi* shape resonances in the bond breaking process. The cross sections are comparable in magnitude to those observed in other compounds in the gas phase in which pi* electrons are transferred through the molecule to break a remote bond. The results therefore support aspects of a theoretical study by Barrios et al. [J. Phys. B 106, 7991 (2002)]] indicating that such a mechanism could produce strand breaks in DNA.     

Low-energy electron diffraction and resonances in DNA and other helical macromolecules

We propose a framework to calculate the intermolecular multiple elastic scattering of low-energy electrons from helical macromolecules and indicate how it affects the resonant capture cross section. Using a model of DNA, an appreciable enhancement of the elastic and resonant capture cross sections is predicted at incident energies below 15 eV. These results may qualitatively explain the observed prominence of low-energy resonances in strand breaking of plasmid DNA.     

DNA strand breaks induced by concerted interaction of H radicals and low-energy electrons

We propose a mechanism of DNA single strand breaks induced by low-energy electrons. Density functional theory calculations have been performed on a neutral, hydrogenated, and/or negatively charged nucleotide of cytosine in the gas phase to identify barriers for the phosphate-sugar O–C bond cleavage. Attachment of the first excess electron induces intermolecular proton transfer to cytosine. The resulting neutral radical of hydrogenated cytosine binds another excess electron, and the excess charge is localized primarily on the C6 atom. A barrier encountered for proton transfer from the C2’ atom of the adjacent sugar unit to the C6 atom of cytosine is 3.6 and 5.0 kcal/mol, based on the MPW1K and B3LYP electronic energies corrected for zero-point vibrations, respectively. The proton transfer is followed by a barrier-free sugar-phosphate C–O bond cleavage. The proton transfer is impossible for the neutral nucleotide, as there is no local minimum for the product. In the case of anionic and hydrogenated nucleotides the same barrier determined at the B3LYP level is as large as 29.3 and 22.4 kcal/mol respectively. This illustrates that the consecutive hydrogenation and electron attachment make the nucleotide of cytosine susceptible to a strand break. The rate of the C–O bond cleavage in the anion of hydrogenated nucleotide of cytosine is estimated to be ca. 10¹⁰  s^-1. The proposed mechanism proceeds through bound anionic states, not through metastable states with finite lifetimes and discrete energy positions with respect to the neutral target. The results suggest that at least for DNA without hydration even very low-energy electrons may cleave the DNA backbone.     

Dissociative electron attachment to phosphoric acid esters: the direct mechanism for single strand breaks in DNA

We use dibutyl phosphate to simulate the behavior of the phosphate group in DNA towards the attack of low energy electrons. We find that the compound undergoes effective dissociative electron attachment within a low energy resonant feature at 1 eV and a further resonance peaking at 8 eV. The dissociative electron attachment (DEA) reactions are associated with the direct cleavage of the C-O and the P-O bond but also the excision of the PO-, PO3-, H2PO3- units. For the phosphate group coupled in the DNA network these reactions represent single strand breaks. We hence propose that the most direct mechanism of single strand breaks occurring in DNA at subexcitation energies (< 4 eV) is due to DEA directly to the phosphate group.     

Ion-induced electron production in tissue-like media and DNA damage mechanisms

This work is the first stage in the development of an inclusive approach to calculation of the DNA damage caused by irradiation of biological tissue by ion/proton beams. The project starts with an analysis of ionization caused by the projectiles and the characteristics of secondary electrons produced in tissue-like media. We consider interactions with the medium on a microscopic level and this allows us to obtain the energy spectrum and abundance of secondary electrons as functions of the projectile’s kinetic energy. The physical information obtained in this analysis is related to biological processes responsible for the DNA damage induced by the projectile. In particular, we consider double strand breaks of DNA caused by secondary electrons and free radicals, and local heating in the ion’s track. The heating may enhance the biological effectiveness of electron/free radical nteractions with the DNA and may even be considered as an independent mechanism of DNA damage. Numerical estimates are performed for the case of carbon-ion beams. The obtained dose-depth curves are compared with results of the MCHIT model based on the GEANT4 toolkit.     

Role of secondary low-energy electrons in the concomitant chemoradiation therapy of cancer

Solid films of DNA with and without the chemotherapeutic agent cisplatin bonded to guanine were bombarded with electrons of 1, 10, 100, and 60,000 eV causing single and double strand breaks. In the presence of cisplatin this damage was increased by factors varying from 1.3 to 4.4 owing to an increase in bond dissociation triggered by the formation of transient anions. This mechanism may lie at the basis of the efficiency of concomitant cisplatin-radiation therapy.     

Effect of intense, ultrashort laser pulses on DNA plasmids in their native state: strand breakages induced by in situ electrons and radicals

Single strand breaks are induced in DNA plasmids, pBR322 and pUC19, in aqueous media exposed to strong fields generated using ultrashort laser pulses (820 nm wavelength, 45 fs pulse duration, 1 kHz repetition rate) at intensities of 1-12 TW?cm(-2). The strong fields generate, in situ, electrons and radicals that induce transformation of supercoiled DNA into relaxed DNA, the extent of which is quantified. Introduction of electron and radical scavengers inhibits DNA damage; results indicate that OH radicals are the primary (but not sole) cause of DNA damage.