STABILITY AND PERFORMANCE OF NETWORKED CONTROL SYSTEMS

Network control systems (NCSs), as one of the most active research areas, are arousing comprehensive concerns along with the rapid development of network. This dissertation mainly discusses the stability and performance of NCSs into the following two parts. In the first part, a new approach is proposed to reduce the data transmitted in networked control systems (NCSs) via model reduction method. Up to our best knowledge, we are the first to propose this new approach in the scientific and engineering society. The "unimportant" information of system states vector is truncated by balanced truncation method (BTM) before sending to the networked controller via network based on the balance property of the remote controlled plant controllability and observability. Then, the exponential stability condition of the truncated NCSs is derived via linear matrix inequality (LMI) forms. This method of data truncation can usually reduce the time delay and further improve the performance of the NCSs. In addition, all the above results are extended to the switched NCSs. The second part presents a new robust sliding mode control (SMC) method for general uncertain time-varying delay stochastic systems with structural uncertainties and the Brownian noise (Wiener process). The key features of the proposed method are to apply singular value decomposition (SVD) to all structural uncertainties, to introduce adjustable parameters for control design along with the SMC method, and new Lyapunov-type functional. Then, a less-conservative condition for robust stability and a new robust controller for the general uncertain stochastic systems are derived via linear matrix inequality (LMI) forms. The system states are able to reach the SMC switching surface as guaranteed in probability 1 by the proposed control rule. Furthermore, the novel Lyapunov-type functional for the uncertain stochastic systems is used to design a new robust control for the general case where the derivative of time-varying delay can be any bounded value (e.g., greater than one). It is theoretically proved that the conservatism of the proposed method is less than the previous methods. All theoretical proofs are presented in the dissertation. The simulations validate the correctness of the theoretical results and have better performance than the existing results

Collective stability of networks of winner-take-all circuits

The neocortex has a remarkably uniform neuronal organization, suggesting that common principles of processing are employed throughout its extent. In particular, the patterns of connectivity observed in the superficial layers of the visual cortex are consistent with the recurrent excitation and inhibitory feedback required for cooperative-competitive circuits such as the soft winner-take-all (WTA). WTA circuits offer interesting computational properties such as selective amplification, signal restoration, and decision making. But, these properties depend on the signal gain derived from positive feedback, and so there is a critical trade-off between providing feedback strong enough to support the sophisticated computations, while maintaining overall circuit stability. We consider the question of how to reason about stability in very large distributed networks of such circuits. We approach this problem by approximating the regular cortical architecture as many interconnected cooperative-competitive modules. We demonstrate that by properly understanding the behavior of this small computational module, one can reason over the stability and convergence of very large networks composed of these modules. We obtain parameter ranges in which the WTA circuit operates in a high-gain regime, is stable, and can be aggregated arbitrarily to form large stable networks. We use nonlinear Contraction Theory to establish conditions for stability in the fully nonlinear case, and verify these solutions using numerical simulations. The derived bounds allow modes of operation in which the WTA network is multi-stable and exhibits state-dependent persistent activities. Our approach is sufficiently general to reason systematically about the stability of any network, biological or technological, composed of networks of small modules that express competition through shared inhibition.Comment: 7 Figure

Synchronization and Redundancy: Implications for Robustness of Neural Learning and Decision Making

Learning and decision making in the brain are key processes critical to survival, and yet are processes implemented by non-ideal biological building blocks which can impose significant error. We explore quantitatively how the brain might cope with this inherent source of error by taking advantage of two ubiquitous mechanisms, redundancy and synchronization. In particular we consider a neural process whose goal is to learn a decision function by implementing a nonlinear gradient dynamics. The dynamics, however, are assumed to be corrupted by perturbations modeling the error which might be incurred due to limitations of the biology, intrinsic neuronal noise, and imperfect measurements. We show that error, and the associated uncertainty surrounding a learned solution, can be controlled in large part by trading off synchronization strength among multiple redundant neural systems against the noise amplitude. The impact of the coupling between such redundant systems is quantified by the spectrum of the network Laplacian, and we discuss the role of network topology in synchronization and in reducing the effect of noise. A range of situations in which the mechanisms we model arise in brain science are discussed, and we draw attention to experimental evidence suggesting that cortical circuits capable of implementing the computations of interest here can be found on several scales. Finally, simulations comparing theoretical bounds to the relevant empirical quantities show that the theoretical estimates we derive can be tight.Comment: Preprint, accepted for publication in Neural Computatio

Effect of Distributed Delays in Systems of Coupled Phase Oscillators

Communication delays are common in many complex systems. It has been shown that these delays cannot be neglected when they are long enough compared to other timescales in the system. In systems of coupled phase oscillators discrete delays in the coupling give rise to effects such as multistability of steady states. However, variability in the communication times inherent to many processes suggests that the description with discrete delays maybe insufficient to capture all effects of delays. An interesting example of the effects of communication delays is found during embryonic development of vertebrates. A clock based on biochemical reactions inside cells provides the periodicity for the successive and robust formation of somites, the embryonic precursors of vertebrae, ribs and some skeletal muscle. Experiments show that these cellular clocks communicate in order to synchronize their behavior. However, in cellular systems, fluctuations and stochastic processes introduce a variability in the communication times. Here we account for such variability by considering the effects of distributed delays. Our approach takes into account entire intervals of past states, and weights them according to a delay distribution. We find that the stability of the fully synchronized steady state with zero phase lag does not depend on the shape of the delay distribution, but the dynamics when responding to small perturbations about this steady state do. Depending on the mean of the delay distribution, a change in its shape can enhance or reduce the ability of these systems to respond to small perturbations about the phase-locked steady state, as compared to a discrete delay with a value equal to this mean. For synchronized steady states with non-zero phase lag we find that the stability of the steady state can be altered by changing the shape of the delay distribution. We conclude that the response to a perturbation in systems of phase oscillators coupled with discrete delays has a sharper functional dependence on the mean delay than in systems with distributed delays in the coupling. The strong dependence of the coupling on the mean delay time is partially averaged out by distributed delays that take into account intervals of the past.:Abstract i Acknowledgement iii I. INTRODUCTION 1. Coupled Phase Oscillators Enter the Stage 5 1.1. Adjusting rhythms – synchronization . . . . . . . . . . . . . . . . . . 5 1.2. Historical remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 1.3. Reducing variables – phase models . . . . . . . . . . . . . . . . . . . . 9 1.4. The Kuramoto order parameter . . . . . . . . . . . . . . . . . . . . . . 10 1.5. Who talks to whom – coupling topologies . . . . . . . . . . . . . . . . 12 2. Coupled Phase Oscillators with Delay in the Coupling 15 2.1. Communication needs time – coupling delays . . . . . . . . . . . . . . 15 2.1.1. Discrete delays consider one past time . . . . . . . . . . . . . . 16 2.1.2. Distributed delays consider multiple past times . . . . . . . . 17 2.2. Coupled phase oscillators with discrete delay . . . . . . . . . . . . . . 18 2.2.1. Phase locked steady states with no phase lags . . . . . . . . . 18 2.2.2. m-twist solutions: phase-locked steady states with phase lags 21 3. The Vertebrate Segmentation Clock – What Provides the Rhythm? 25 3.1. The clock and wavefront mechanism . . . . . . . . . . . . . . . . . . . 26 3.2. Cyclic gene expression on the cellular and the tissue level . . . . . . 27 3.3. Coupling by Delta-Notch signalling . . . . . . . . . . . . . . . . . . . . 29 3.4. The Delayed Coupling Theory . . . . . . . . . . . . . . . . . . . . . . . 30 3.5. Discrete delay is an approximation – is it sufficient? . . . . . . . . . 32 4. Outline of the Thesis 33 II. DISTRIBUTED DELAYS 5. Setting the Stage for Distributed Delays 37 5.1. Model equations with distributed delays . . . . . . . . . . . . . . . . . 37 5.2. How we include distributed delays . . . . . . . . . . . . . . . . . . . . 38 5.3. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 6. The Phase-Locked Steady State Solution 41 6.1. Global frequency of phase-locked steady states . . . . . . . . . . . . . 41 6.2. Linear stability of the steady state . . . . . . . . . . . . . . . . . . . . 42 6.3. Linear dynamics of the perturbation – the characteristic equation . 43 6.4. Summary and application to the Delayed Coupling Theory . . . . . . 50 7. Dynamics Close to the Phase-Locked Steady State 53 7.1. The response to small perturbations . . . . . . . . . . . . . . . . . . . 53 7.2. Relation between order parameter and perturbation modes . . . . . 54 7.3. Perturbation dynamics in mean-field coupled systems . . . . . . . . 56 7.4. Nearest neighbour coupling with periodic boundary conditions . . . 62 7.4.1. How variance and skewness influence synchrony dynamics . 73 7.4.2. The dependence of synchrony dynamics on the number of oscillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 7.5. Synchrony dynamics in systems with arbitrary coupling topologies . 88 7.6. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93 8. The m-twist Steady State Solution on a Ring 95 8.1. Global frequency of m-twist steady states . . . . . . . . . . . . . . . . 95 8.2. Linear stability of m-twist steady states . . . . . . . . . . . . . . . . . 97 8.3. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 9. Dynamics Approaching the m-twist Steady States 105 9.1. Relation between order parameter and perturbation modes . . . . . 105 9.2. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 10.Conclusions and Outlook 111 vi III. APPENDICES A. 119 A.1. Distribution composed of two adjacent boxcar functions . . . . . . . 119 A.2. The gamma distribution . . . . . . . . . . . . . . . . . . . . . . . . . . 124 A.3. Distribution composed of two Dirac delta peaks . . . . . . . . . . . . 125 A.4. Gerschgorin’s circle theorem . . . . . . . . . . . . . . . . . . . . . . . . 127 A.5. The Lambert W function . . . . . . . . . . . . . . . . . . . . . . . . . . 127 A.6. Roots of unity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 B. Simulation methods 12

Global μ

The impulsive complex-valued neural networks with three kinds of time delays including leakage delay, discrete delay, and distributed delay are considered. Based on the homeomorphism mapping principle of complex domain, a sufficient condition for the existence and uniqueness of the equilibrium point of the addressed complex-valued neural networks is proposed in terms of linear matrix inequality (LMI). By constructing appropriate Lyapunov-Krasovskii functionals, and employing the free weighting matrix method, several delay-dependent criteria for checking the global μ-stability of the complex-valued neural networks are established in LMIs. As direct applications of these results, several criteria on the exponential stability, power-stability, and log-stability are obtained. Two examples with simulations are provided to demonstrate the effectiveness of the proposed criteria

Low-dimensional spike rate models derived from networks of adaptive integrate-and-fire neurons : comparison and implementation

The spiking activity of single neurons can be well described by a nonlinear integrate-and-fire model that includes somatic adaptation. When exposed to fluctuating inputs sparsely coupled populations of these model neurons exhibit stochastic collective dynamics that can be effectively characterized using the Fokker-Planck equation. This approach, however, leads to a model with an infinite-dimensional state space and non-standard boundary conditions. Here we derive from that description four simple models for the spike rate dynamics in terms of low-dimensional ordinary differential equations using two different reduction techniques: one uses the spectral decomposition of the Fokker-Planck operator, the other is based on a cascade of two linear filters and a nonlinearity, which are determined from the Fokker-Planck equation and semi-analytically approximated. We evaluate the reduced models for a wide range of biologically plausible input statistics and find that both approximation approaches lead to spike rate models that accurately reproduce the spiking behavior of the underlying adaptive integrate-and-fire population. Particularly the cascade-based models are overall most accurate and robust, especially in the sensitive region of rapidly changing input. For the mean-driven regime, when input fluctuations are not too strong and fast, however, the best performing model is based on the spectral decomposition. The low-dimensional models also well reproduce stable oscillatory spike rate dynamics that are generated either by recurrent synaptic excitation and neuronal adaptation or through delayed inhibitory synaptic feedback. The computational demands of the reduced models are very low but the implementation complexity differs between the different model variants. Therefore we have made available implementations that allow to numerically integrate the low-dimensional spike rate models as well as the Fokker-Planck partial differential equation in efficient ways for arbitrary model parametrizations as open source software. The derived spike rate descriptions retain a direct link to the properties of single neurons, allow for convenient mathematical analyses of network states, and are well suited for application in neural mass/mean-field based brain network models.Characterizing the dynamics of biophysically modeled, large neuronal networks usually involves extensive numerical simulations. As an alternative to this expensive procedure we propose efficient models that describe the network activity in terms of a few ordinary differential equations. These systems are simple to solve and allow for convenient investigations of asynchronous, oscillatory or chaotic network states because linear stability analyses and powerful related methods are readily applicable. We build upon two research lines on which substantial efforts have been exerted in the last two decades: (i) the development of single neuron models of reduced complexity that can accurately reproduce a large repertoire of observed neuronal behavior, and (ii) different approaches to approximate the Fokker-Planck equation that represents the collective dynamics of large neuronal networks. We combine these advances and extend recent approximation methods of the latter kind to obtain spike rate models that surprisingly well reproduce the macroscopic dynamics of the underlying neuronal network. At the same time the microscopic properties are retained through the single neuron model parameters. To enable a fast adoption we have released an efficient Python implementation as open source software under a free license