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Biomedical subjects

W Düchting

Publications and source records attributed to W Düchting.

At least 19 recordsLinked to original sources
PubMed1995

Modeling of radiogenic responses induced by fractionated irradiation in malignant and normal tissue.

The aim of this contribution is to outline how methods of system analysis, control theory and computer science can be applied to simulate malignant and normal cell growth and to optimize cancer treatment. Based on biological observations and cell kinetic data, our group has constructed three types of computer models: 1) A cell cycle model describing the spatial (3D) and temporal growth of tumor spheroids; 2) A compartment model describing the growth of rapidly proliferating normal cells; 3) A compartment model simulating slowly proliferating normal tissues. These growth models have been extended by an irradiation model based on the linear-quadratic survival function. Different clinical fractionation schemes (standard-, super-, hyperfractionation and weekly high single dose) have been applied to the tissues mentioned above. The simulation results show that in the case of irradiating a rapidly growing tumor spheroid the hyperfractionation (3 x 1-1.5 Gy per day) leads to a particularly good anti-tumor effectiveness. On the other hand, the radiogenic response of rapidly growing normal tissue to a hyperfractionated treatment schedule is severe. The same result is observed when simulating the late reaction on slowly growing parenchymal tissue. Therefore, this therapeutic modality is ensured only if the overall dose is reduced from DTOTAL = 60 Gy to DTOTAL = 50 Gy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Radiogenic responses of normal cells induced by fractionated irradiation--a simulation study. Part II. Late responses.

AIM: 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. METHOD: 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. RESULTS: 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. CONCLUSIONS: 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.

Animals↗
PubMed1995

Radiogenic responses of normal tissue induced by fractionated irradiation--a simulation study. I. Acute effects.

AIM: Based on control theory, the attempt is made in this paper to construct a computer model which describes the time course of fast proliferating normal tissue after irradiation treatment. Subsequently, different clinical irradiation schemes are compared in regard to their radiogenic acute effects. MATERIAL AND METHODS: A cybernetic model of a cell renewal system consisting of stem-, transit- and 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. RESULTS: Three kinds of tissue (thick epidermis of man, thin epidermis of the mouse and jejunum of the mouse) have been irradiated in the model in accordance with different clinical irradiation schemes (standard-, super-, hyperfractionation and a single high dose per week). The simulation studies demonstrate that the acute reaction of normal tissue to hyperfractionation (3 times 1.5 Gy per day) is particularly severe. Furthermore, the radiation damage of the jejunum and of the thin epidermis of the mouse depends on the specific irradiation scheme and is only partially compensated. CONCLUSION: A comparison of the simulation results with clinical experience (and practice) demonstrates that the clinical reality can in quality be successfully represented by the model. This opens the door for connecting the side effects of irradiation to normal tissue with the corresponding tumor effectiveness (see our previous papers about irradiation of tumor spheroids.

Animals↗
PubMed1993

Computer simulation of fractionated radiotherapy: further results and their relevance to percutaneous irradiation and brachytherapy.

Based on previous papers, the present communication considers the simulation of the radiotherapeutic treatments of glioblastoma multiforme, rectum adenocarcinoma, and gynaecological tumors of cervix uteri (squamous and adenocarcinoma) in spheroid culture. Starting with a single tumor cell in a nutrient medium and after the corresponding growth of the tumor spheroids, varying irradiation schemes are applied to the carcinoma and are compared with regard to tumor kill effectiveness using the LQ-model. The two first-mentioned carcinoma are exposed to the dose fractionation schemes standard-, super-, hyperfractionation, and weekly high single dose. The result is that hyperfractionation (3 x 1.5 Gy/day) and weekly high single dose (1 x 6 Gy/week) yield the most effective tumor cell kill. The weekly high single dose may be realized by some different irradiation techniques, e. g. stereotactic irradiation or interstitial high dose rate brachytherapy. The treatment of the cervix uteri tumors is performed by a combined therapy form (high dose rate brachytherapy and percutaneous irradiation). A comparing simulation of two typical regimens yields a nearly equivalent tumor kill effectiveness. By the integration of in vitro tumor growth and clinical treatment schemes in a computer model, the possibility is made available to test the effectiveness of variable regimens with the help of computer experiments.

Administration, Cutaneous↗
PubMed1992

Computer simulation and modelling of tumor spheroid growth and their relevance for optimization of fractionated radiotherapy.

As previous papers show, our group developed computer models simulating spatial (3D) tumor growth of an in vitro tumor spheroid. These models were extended by implementing irradiation models based on the linear-quadratic survival function in order to simulate and optimize radiation therapy schemes. The key idea in this study is to simulate different fractionation schemes (standard-, super-, hyperfractionation, irradiation with a weekly high dose) and to compare the model results with regard to their tumor effectiveness. After introducing simplified model assumptions the following treatment plans, as a result, represent an optimal scheduling: 1. the hyperfractionation (3 x 1...1.5 Gy per day) in the case of rapidly growing tumors; 2. the hyperfractionation (3 x 1...1.5 Gy per day) for moderately fast growing tumors; and 3. the treatment with a weekly high single dose (1 x 6 Gy per week) in the case of slowly growing tumors. The transfer of the results gained by simulating in vitro-experiments to clinical tumors are discussed. Single observations in clinical practice concerning the therapeutical benefit indicate a rather good agreement with the simulation results. Thereby, the possibility is given to comprehend in vitro tumor growth and clinical therapy schemes in a model and to successfully simulate optimal treatment schedules by computer experiments. This method enables a reduction of time-consuming studies prior to clinical therapy.

Brain Neoplasms↗
PubMed1989

Computer simulation of clinical irradiation schemes applied to in vitro tumor spheroids.

In this contribution the attempt is made to study the effect of irradiation on in vitro tumor spheroids by computer simulation applying clinical treatment schedules. The starting point is a computer model stimulating the spatial (three-dimensional) growth of a tumor spheroid, developed by our group previously. In the present paper, this model is extended by creating a comfortable data input with a graphical interface. This expansion includes characteristic features of radiotherapy (sensitivity, repair capacity, reoxygenation, repopulation) and therapy schedules. In this way, it is possible to test different clinical irradiation schemes on in vitro tumor spheroids by computer experiments (standard and non-standard fractionations). In the long run the aim of our work is to optimize irradiation schedules by computer simulation prior to clinical therapy.

Adenocarcinoma↗
PubMed1985

Recent progress in modelling and simulation of three-dimensional tumor growth and treatment.

This paper illustrates how to apply methods of systems analysis, control theory and simulation to the field of biology and medicine. For this purpose normal and abnormal cell growth has been modelled at different levels. It was possible to simulate three-dimensional tumor growth and different kinds of treatment. The paper shows how tumor treatment may be optimized in the long run using computer simulation experiments as a powerful new tool prior to clinical therapy.

Cell Communication↗
PubMed1984

Analysis, forecasting, and control of three-dimensional tumor growth and treatment.

The main point of this contribution is to show how ideas of control theory, automata theory and computer science can be applied to the field of cancer research. We are stressing the modelling of three-dimensional tumor growth and the simulation of different kinds of tumor therapy (surgery, radiation therapy, chemotherapy). In the future it will be possible to schedule the optimized methods and time of tumor treatment by computer simulation prior to clinical therapy.

Cell Communication↗
PubMed1983

Aspects of modelling and simulating tumor growth and treatment.

The proliferation of malignant cells and tumor growth can be studied at various levels and from different viewpoints in the field of tumor biology and oncology. The aim of this paper is to outline how control theory and computer science can pave the way to new approaches to interpreting tumor growth and treatment. The present development is based on the hypothesis that the proliferation of malignant cells may be simulated by an unstable closed-loop control circuit. This type of model only describes the number of cells as a function of time. Therefore, an extended model permitting the study of the spatial structure of tumor growth is chosen. This approach leads to three-dimensional models simulating tumor growth in a vascularized tissue segment and opens the possibility of determining optimized chemotherapeutic tumor-treatment schedules. In the future it may become possible to perform computer simulations of different kinds of tumor treatment prior to clinical therapy.

Animals↗
PubMed1981

Three-dimensional pattern generation applied to spheroidal tumor growth in a nutrient medium.

This paper is concerned with the three-dimensional simulation of tumor growth. For this purpose a cell cycle model of a tumor cell and rules for its multiplication have been developed. Then algorithms and program packages have been constructed describing the spatial and temporal tumor growth. There is a description of several case studies simulating the growth of a single tumor cell in a nutrient medium and a treatment by surgery, radiotherapy and chemotherapy. The simulation results correspond fairly well with the experimentally observed data. As a result it becomes possible to schedule an optimal treatment of tumor diseases by means of computer simulation.

Animals↗
PubMed1980

Spread of cancer cells in tissues: modelling and simulation.

Continuing previous studies in which tumor diseases were interpreted as unstable control loops, the present paper tries to determine the spatial structure and the time behaviour of cell renewal systems. For this purpose a computer model for the two-dimensional cell space was developed, which is described by a set of specifications and growth statements. Selected case studies are then simulated by means of a digital computer (CYBER 76). The development of this model enables a deeper insight into the structure and function of disturbed cell renewal processes. Furthermore, it is possible with this computer model to simulate simple basic cases which, in reality, could hardly or not at all be tested.

Animals↗
PubMed1980

Computer studies of the spatial structure and temporal growth of tumor cells.

In the present paper we attempt to determine the spatial structure and the time behaviour of cell renewal systems, continuing previous studies in which tumor diseases were interpreted as unstable control loops. A computer model wa developed for the two-dimensional cell space, which is described by a set of specifications and growth statements. Selected case studies are then simulated by means of a digital computer (CYBER 76). In the development of this model special emphasis was given to (i) the existence of several cell systems with different mean life spans, growing in competition; (ii) the variability of the mean life spans of a cell and of the initial configuration of cell patterns; (iii) the description of the cell-to-cell interactions; (iv) the perturbation of normal cell growth by tumor cells and their elimination in medicine comparable with a direct irradiation or removal by surgery; (v) the consideration of the loss of tumor cells. The development of this model enables a deeper insight into the structure and function of disturbed cell renewal processes. Systematic studies were made on the influence of the size of a tumor nucleus and the mean life span of a tumor cell on the tumor growth assuming constant cell loss. Furthermore it is possible with this computer model to simulate simple basic cases which are difficult to test in real life.

Cell Division↗
PubMed1979

Simulation of disturbed cell renewal systems by means of a microprocessor system.

In this contribution a computer model is presented which enables a simulation of disturbed cell growth and cell renewal systems by means of a microprocessor system. The results consist of a time course study of the number of cells and of the local configuration of cells in a cell matrix at any arbitrary discrete moment. A similarity to morphological cuts and cell kinetic curves obtained by experiments is obvious.

Cell Division↗