Nonlinear Models of Neural and Genetic Network Dynamics:\ud \ud Natural Transformations of Łukasiewicz Logic LM-Algebras in a Łukasiewicz-Topos as Representations of Neural Network Development and Neoplastic Transformations \ud

A categorical and Łukasiewicz-Topos framework for Algebraic Logic models of nonlinear dynamics in complex functional systems such as Neural Networks, Cell Genome and Interactome Networks is introduced. Łukasiewicz Algebraic Logic models of both neural and genetic networks and signaling pathways in cells are formulated in terms of nonlinear dynamic systems with n-state components that allow for the generalization of previous logical models of both genetic activities and neural networks. An algebraic formulation of variable next-state/transfer functions is extended to a Łukasiewicz Topos with an N-valued Łukasiewicz Algebraic Logic subobject classifier description that represents non-random and nonlinear network activities as well as their transformations in developmental processes and carcinogenesis.\u

Łukasiewicz-Topos Models of Neural Networks, Cell Genome and Interactome Nonlinear Dynamic Models

A categorical and Łukasiewicz-Topos framework for Algebraic Logic models of nonlinear dynamics in complex functional systems such as Neural Networks, Cell Genome and Interactome Networks is introduced. Łukasiewicz Algebraic Logic models of both neural and genetic networks and signaling pathways in cells are formulated in terms of nonlinear dynamic systems with n-state components that allow for the generalization of previous logical models of both genetic activities and neural networks. An algebraic formulation of variable 'next-state functions' is extended to a Łukasiewicz Topos with an n-valued Łukasiewicz Algebraic Logic subobject classifier description that represents non-random and nonlinear network activities as well as their transformations in developmental processes and carcinogenesis

Neural Networks, Cell Genome and Interactome Nonlinear Dynamic Models

Operational logic and bioinformatics models of nonlinear dynamics in complex functional systems such as neural networks, genomes and cell interactomes are proposed. Łukasiewicz Algebraic Logic models of genetic networks and signaling pathways in cells are formulated in terms of nonlinear dynamic systems with n-state components that allow for the generalization of previous logical models of both genetic activities and neural networks. An algebraic formulation of variable 'next-state functions' is extended to a Łukasiewicz Topos with an n-valued Łukasiewicz Algebraic Logic subobject classifier description that represents non-random and nonlinear network activities as well as their transformations in developmental processes and carcinogenesis

System Identification for Nonlinear Control Using Neural Networks

An approach to incorporating artificial neural networks in nonlinear, adaptive control systems is described. The controller contains three principal elements: a nonlinear inverse dynamic control law whose coefficients depend on a comprehensive model of the plant, a neural network that models system dynamics, and a state estimator whose outputs drive the control law and train the neural network. Attention is focused on the system identification task, which combines an extended Kalman filter with generalized spline function approximation. Continual learning is possible during normal operation, without taking the system off line for specialized training. Nonlinear inverse dynamic control requires smooth derivatives as well as function estimates, imposing stringent goals on the approximating technique

On the Inability of Markov Models to Capture Criticality in Human Mobility

We examine the non-Markovian nature of human mobility by exposing the inability of Markov models to capture criticality in human mobility. In particular, the assumed Markovian nature of mobility was used to establish a theoretical upper bound on the predictability of human mobility (expressed as a minimum error probability limit), based on temporally correlated entropy. Since its inception, this bound has been widely used and empirically validated using Markov chains. We show that recurrent-neural architectures can achieve significantly higher predictability, surpassing this widely used upper bound. In order to explain this anomaly, we shed light on several underlying assumptions in previous research works that has resulted in this bias. By evaluating the mobility predictability on real-world datasets, we show that human mobility exhibits scale-invariant long-range correlations, bearing similarity to a power-law decay. This is in contrast to the initial assumption that human mobility follows an exponential decay. This assumption of exponential decay coupled with Lempel-Ziv compression in computing Fano's inequality has led to an inaccurate estimation of the predictability upper bound. We show that this approach inflates the entropy, consequently lowering the upper bound on human mobility predictability. We finally highlight that this approach tends to overlook long-range correlations in human mobility. This explains why recurrent-neural architectures that are designed to handle long-range structural correlations surpass the previously computed upper bound on mobility predictability