Düchting W, Ulmer W, Ginsberg T, Kikhounga-N'Got O, Saile C
Department of Electrical Engineering and Computer Science, University of Siegen.
Strahlenther Onkol. 1995 Sep;171(9):525-33.
Based on controlled theory, a computed simulation model has been constructed which describes the time course of slowly responding normal cells after irradiation exposure. Subsequently, different clinical irradiation schemes are compared in regard to their delayed radiogenic responses referred to as late effects in radiological terminology.
A cybernetic model of a parenchymal tissue consisting of dominantly resting functional cells has been developed and transferred into a computer model. The radiation effects are considered by characteristic cell parameters as well as by the linear-quadratic model.
Three kinds of tissue (brain and lung parenchyma of the mouse, liver parenchyma of rat) have been irradiated in the model according to standard-, super-, hyperfractionation and a single high dose per week. The simulation studies indicate that the late reaction of brain parenchyma to hyperfractionation (3 x 1.5 Gy per day) and of lung parenchyma tissue with regard to all fractionation schemes applied is particularly severe. In contrast to these observations the behavior of liver parenchyma is not unique: If Dtotal amounts to 60 Gy there is no evidence for compensation of radiation damages, but if Dtotal is restricted to 30 Gy the corresponding evidence can be expected for all schemes. In the case of a high single dose of 6 Gy a reduction of the recovery time from 1 week to 2...2 days yields also an indication of a severe damage, even if Dtotal amounts only to 30 Gy.
A comparison of the simulation results basing to the survival of cell numbers with clinical experience and practice shows that the clinical reality can qualitatively be represented by the model. This opens the door for connecting side effects to normal tissue with the corresponding tumor efficacy (discussed in previous papers). The model is open to further refinement and to discussions referring to the phenomenon of late effects.
基于控制理论,构建了一个计算模拟模型,该模型描述了正常细胞在辐射暴露后的缓慢反应时间进程。随后,针对放射学术语中称为晚期效应的延迟放射反应,比较了不同的临床照射方案。
开发了一个由主要处于静止状态的功能细胞组成的实质组织的控制论模型,并将其转化为计算机模型。通过特征细胞参数以及线性二次模型来考虑辐射效应。
根据标准分割、超分割、超分割加速分割以及每周一次高剂量照射,对模型中的三种组织(小鼠的脑和肺实质、大鼠的肝实质)进行了照射。模拟研究表明,脑实质对超分割(每天3×1.5 Gy)的晚期反应以及肺实质组织对所有应用的分割方案的晚期反应尤为严重。与这些观察结果相反,肝实质的行为并不独特:如果总剂量达到60 Gy,则没有证据表明辐射损伤得到了补偿,但如果总剂量限制在30 Gy,则所有方案都可能有相应的证据。在单次高剂量6 Gy的情况下,恢复时间从1周缩短至2……2天也表明存在严重损伤,即使总剂量仅为30 Gy。
将基于细胞数量存活的模拟结果与临床经验和实践进行比较表明,该模型可以定性地反映临床实际情况。这为将正常组织的副作用与相应的肿瘤疗效联系起来(在先前的论文中讨论过)打开了大门。该模型有待进一步完善,并有待就晚期效应现象进行讨论。