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The paper addresses the problem of calculating the noise-induced switching rates in systems with delay-distributed kernels and Gaussian noise. A general variational formulation for the switching rate is derived for any distribution kernel, and the obtained equations of motion and boundary conditions represent the most probable, or optimal, path, which maximizes the probability of escape. Explicit analytical results for the switching rates for small mean time delays are obtained for the uniform and bi-modal (or two-peak) distributions. They suggest that increasing the width of the distribution leads to an increase in the switching times even for longer values of mean time delays for both examples of the distribution kernel, and the increase is higher in the case of the two-peak distribution. Analytical predictions are compared to the direct numerical simulations and show excellent agreement between theory and numerical experiment. [ABSTRACT FROM AUTHOR]

In real-world systems, interactions between elements do not happen instantaneously, due to the time required for a signal to propagate, reaction times of individual elements, and so forth. Moreover, time delays are normally nonconstant and may vary with time. This means that it is vital to introduce time delays in any realistic model of neural networks. In order to analyze the fundamental properties of neural networks with time-delayed connections, we consider a system of two coupled two-dimensional nonlinear delay differential equations. This model represents a neural network, where one subsystem receives a delayed input from another subsystem. An exciting feature of the model under consideration is the combination of both discrete and distributed delays, where distributed time delays represent the neural feedback between the two subsystems, and the discrete delays describe the neural interaction within each of the two subsystems. Stability properties are investigated for different commonly used distribution kernels, and the results are compared to the corresponding results on stability for networks with no distributed delays. It is shown how approximations of the boundary of the stability region of a trivial equilibrium can be obtained analytically for the cases of delta, uniform, and weak gamma delay distributions. Numerical techniques are used to investigate stability properties of the fully nonlinear system, and they fully confirm all analytical findings. [ABSTRACT FROM AUTHOR]

This paper studies the stability of synchronized states in networks, where couplings between nodes are characterized by some distributed time delay, and develops a generalized master stability function approach. Using a generic example of Stuart-Landau oscillators, it is shown how the stability of synchronized solutions in networks with distributed delay coupling can be determined through a semi-analytic computation of Floquet exponents. The analysis of stability of fully synchronized and of cluster or splay states is illustrated for several practically important choices of delay distributions and network topologies. [ABSTRACT FROM AUTHOR]

This paper studies the effects of distributed-delay coupling on the dynamics in a system of non-identical coupled Stuart-Landau oscillators. For uniform and gamma delay distribution kernels, the conditions for amplitude death are obtained in terms of average frequency, frequency detuning and the parameters of the coupling, including coupling strength and phase, as well as the mean time delay and the width of the delay distribution. To gain further insights into the dynamics inside amplitude death regions, the eigenvalues of the corresponding characteristic equations are computed numerically. Oscillatory dynamics of the system is also investigated, using amplitude and phase representation. Various branches of phase-locked solutions are identified, and their stability is analysed for different types of delay distributions. [ABSTRACT FROM AUTHOR]

We discuss different mathematical models of gene regulatory networks as relevant to the onset and development of cancer. After discussion of alternativemodelling approaches, we use a paradigmatic two-gene network to focus on the role played by time delays in the dynamics of gene regulatory networks. We contrast the dynamics of the reduced model arising in the limit of fast mRNA dynamics with that of the full model. The review concludes with the discussion of some open problems. [ABSTRACT FROM AUTHOR]