论文标题
闪光的差异组织对闪光超高剂量率的差异:{\ it silico}研究
Differential tissue sparing of FLASH ultra high dose rates: an {\it in-silico} study
论文作者
论文摘要
目的:提出一种通过轨道间反应扩散机制对闪光超高剂量率(UHDR)进行差异组织的理论。方法:我们使用用于多孔和无序介质分子传输的随机网络上的耦合反应扩散方程系统来计算粒子轨迹结构的时间进化。该网络代表组织中细胞内和细胞间扩散通道。通过将随机波动纳入网络站点之间的连通性,已经构建了轨道间距规模的空间细胞异质性。结果:我们证明了轨道之间的相位分离的发生,这是细胞内和细胞间结构增加的复杂性。在疾病的弱极限(例如在水和正常组织中),相邻的轨道相互融化并形成了非反应性物种的渗透网络。相比之下,在障碍的强限制下,轨道像具有可忽略的轨道重叠的孤立岛一样分别演变。因此,化学结构域之间的时空相关性随着组织的细胞间复杂性的增加而降低(例如,从正常组织到分形型恶性组织)。结论:正常组织和肿瘤组织中Flash UHDR的差异差异可以通过组织类型之间的细胞间结构复杂性和细胞内结构复杂性的差异来解释。癌细胞的结构复杂性阻止了轨道的聚类和化学相互作用,而这种相互作用则占上风,因此导致在正常组织中的差异。
Purpose: To propose a theory for the differential tissue sparing of FLASH ultra high dose rates (UHDR) through inter-track reaction-diffusion mechanism. Methods: We calculate the time-evolution of particle track-structures using a system of coupled reaction-diffusion equations on a random network designed for molecular transport in porous and disordered media. The network is representative of the intra- and inter-cellular diffusion channels in tissues. Spatial cellular heterogeneities over the scale of track spacing have been constructed by incorporating random fluctuations in the connectivity among network sites. Results: We demonstrate the occurrence of phase separation among the tracks as the complexity in intra- and inter-cellular structural increases. At the weak limit of disorder, such as in water and normal tissue, neighboring tracks melt into each other and form a percolated network of nonreactive species. In contrast, at the strong limit of disorder, tracks evolve individually like isolated islands with negligible inter-track overlap. Thus, the spatio-temporal correlation among the chemical domains decreases as the inter-cellular complexity of the tissue increases (e.g. from normal tissue to fractal-type malignant tissue). Conclusions: The differential sparing of FLASH UHDR in normal and tumor tissue may be explained by differences in inter- and intra-cellular structural complexities between the tissue types. The structural complexities of cancerous cells prevent clustering and chemical interaction of tracks, whereas this interaction prevails and thus leads to sparing in normal tissue.