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Modelling tumour-immunity interactions with different stimulation functions

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EN
Tumour immunotherapy is aimed at the stimulation of the otherwise inactive immune system to remove, or at least to restrict, the growth of the original tumour and its metastases. The tumour-immune system interactions involve the stimulation of the immune response by tumour antigens, but also the tumour induced death of lymphocytes. A system of two non-linear ordinary differential equations was used to describe the dynamic process of interaction between the immune system and the tumour. Three different types of stimulation functions were considered: (a) Lotka-Volterra interactions, (b) switching functions dependent on the tumour size in the Michaelis-Menten form, and (c) Michaelis-Menten switching functions dependent on the ratio of the tumour size to the immune capacity. The linear analysis of equilibrium points yielded several different types of asymptotic behaviour of the system: unrestricted tumour growth, elimination of tumour or stabilization of the tumour size if the initial tumour size is relatively small, otherwise unrestricted tumour growth, global stabilization of the tumour size, and global elimination of the tumour. Models with switching functions dependent on the tumour size and the tumour to the immune capacity ratio exhibited qualitatively similar asymptotic behaviour.
EN
This paper addresses the problem of model-based global stability analysis of discrete-time Takagi-Sugeno multiregional dynamic output controllers with static antiwindup filters. The presented analyses are reduced to the problem of a feasibility study of the Linear Matrix Inequalities (LMIs), derived based on Lyapunov stability theory. Two sets of LMIs are considered candidate derived from the classical common quadratic Lyapunov function, which may in some cases be too conservative, and a fuzzy Lyapunov function candidate, which has been proven to significantly reduce the conservatism level, although at the cost of increasing the number of LMIs. Two numerical examples illustrate the main result.
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Normalized finite fractional differences: Computational and accuracy breakthroughs

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EN
This paper presents a series of new results in finite and infinite-memory modeling of discrete-time fractional differences. The introduced normalized finite fractional difference is shown to properly approximate its fractional difference original, in particular in terms of the steady-state properties. A stability analysis is also presented and a recursive computation algorithm is offered for finite fractional differences. A thorough analysis of computational and accuracy aspects is culminated with the introduction of a perfect finite fractional difference and, in particular, a powerful adaptive finite fractional difference, whose excellent performance is illustrated in simulation examples.
4
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Nonlinear control for a diesel engine: a CLF-based approach

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EN
In this paper, we propose a control Lyapunov function based on a nonlinear controller for a turbocharged diesel engine. A model-based approach is used which predicts the experimentally observed engine performance for a biodiesel. The basic idea is to develop an inverse optimal control and to employ a Lyapunov function in order to achieve good performances. The obtained controller gain guarantees the global convergence of the system and regulates the flows for the variable geometry turbocharger as well as exhaust gas recirculation systems in order to minimize the N Ox emission and the smoke of a biodiesel engine. Simulation of the control performances based on professional software and experimental results show the effectiveness of this approach.
EN
This paper addresses the problems of robust fault estimation and fault-tolerant control for Takagi-Sugeno (T-S) fuzzy systems with time delays and unknown sensor faults. A fuzzy augmented state and fault observer is designed to achieve the system state and sensor fault estimates simultaneously. Furthermore, based on the information of on-line fault estimates, an observer-based dynamic output feedback fault-tolerant controller is developed to compensate for the effect of faults by stabilizing the resulting closed-loop system. Sufficient conditions for the existence of both a state observer and a fault-tolerant controller are given in terms of linear matrix inequalities. A simulation example is given to illustrate the effectiveness of the proposed approach.
PL
Rodzina czynników transkrypcyjnych NF-κ B pełni ważną rolę w regulacji odpowiedzi immunologicznej oraz profliferacji i przeżyciu komórek, w związku z czym niepoprawna aktywacja NF-κ prowadzi do poważnych problemów zdrowotnych. Jednak skomplikowany sposób aktywacji i regulacji NF-κ nie jest jeszcze w pełni zbadany. W tej pracy proponujemy i analizujemy dwie wersje modelu matematycznego uwzględniającego dodatnie sprzężenie zwrotne między NF-κB i cytokinami oraz ujemne sprzężenie zwrotne między NF-κB i jego inhibitorami. Ten model matematyczny obrazuje przejściową aktywację NF-κB, i jest jednocześnie na tyle prosty, aby pozwolić na otrzymanie analitycznych warunków na stabilność stanów stacjonarnych. Oczekujemy, że lepsze zrozumienie systemu regulacji NF-κB zwiększy efektywność terapii opartych na inhibicji tego czynnika transkrypcyjnego. Ponadto, zmodyfikowany model jest na tyle ogólny, że jego analiza może się okazać przydatna w modelowaniu innych procesów biologicznych.
EN
The family of transcription factors NF-κB plays a crucial role in immune response regulation, cell proliferation and cell survival; therefore, deregulated NF-κB activation results in severe health problems. However, its elaborate regulatory network is not yet fully understood. In this paper, we propose and analyze modifications of a mathematical model of the regulatory network that considers the positive feedback between NF-κB and cytokines and the negative feedback between NF-κBand its inhibitors. This mathematical framework captures the transient dynamics of NF-κB while remaining simple enough to obtain a stability condition of the equilibria. We anticipate that a deeper understanding of the NF-κB framework will increase the effectiveness of therapeutic strategies based on NF-κB inhibition.
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