Wyniki wyszukiwania - BazTech

1

Angiogeneza nowotworów jako obiekt sterowania

Świerniak A., Gala G., Onofrio A., Gandolfi A.

Przegląd Elektrotechniczny

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2008

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R. 84, nr 4

124-127

PL

W pracy przedstawiony i przeanalizowany został model terapii skierowanej przeciwko powstającej w procesie angiogenezy nowotworów sieci naczyniowej i tym samym pośrednio umożliwiającej wyleczenie choroby. Dyskutowany jest model zaproponowany przez Hahnfeldta a także pewna jego modyfikacja. Przedstawiona analiza dotyczy warunków stabilności przekładających się na możliwość asymptotycznej anihilacji guza oraz warunków koniecznych optymalizacji protokołów terapii.

EN

A model of tumor growth taking into account its vascularization due to angiogenesis and antiangiogenic cancer chemotherapy is proposed and analised. The model is a modified Hahnfeldt model and the analysis has two goals: first of all we check stability of the equilibrium point of the model using Lyapunov first and second methods to find conditions leading to tumour eradication, and then we propose an optimization problem and give necessary conditions of its solution basing on the Pontryagin maximum principle.

2

Mathematical modelling of tumour cords

Bertuzzi A., Fasano A., Gandolfi A.

Journal of Medical Informatics & Technologies

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2001

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Vol. 2, Part. 1

IP23--IP31

EN

In some tumours, cylindrical arrangements of tumour cells growing around blood vessels (tumour cords) have been observed. In this paper we review some mathematical models aimed to describe the cell kinetics of the tumour cell population within a cord assumed to be at the steady state, and the dynamics of these structures, in particular after cytotoxic treatments. The models here considered view the cell population as a continuum and take into account cell motion.

3

A Model for estimating cell kinetic parameters of experimental tumours studied by BrdUrd labelling and flow cytometry

Bertuzzi A., Gandolfi A.

Archives of Control Sciences

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1999

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Vol. 9, no. 1/2

41-56

EN

A mathematical model that describes the time evolution of the DNA-BrdUrd distribution, as measured in experimental tumours after labelling with BrdUrd, is proposed in this paper. Cell-to-cell heterogeneity within the tumour of the rate of progression across cell cycle phases is taken into account, and a strict correlation between the durations of S and G2M phases is assumed. The model relates observable quantities to the parameters that characterize the cell population kinetics (such as the potential doubling time, T pot), and appears thus to be suitable for parameter estimation. Simulations that illustrate the dependence of model response on the kinetic parameters are presented.