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Register a new userTopological data analysis of contagion maps for examining spreading processes on networks
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Social and biological contagions are influenced by the spatial embeddedness of networks. Historically, many epidemics spread as a wave across part of the Earths surface; however, in modern contagions long-range edges -- for example, due to airline transportation or communication media -- allow clusters of a contagion to appear in distant locations. Here we study the spread of contagions on networks through a methodology grounded in topological data analysis and nonlinear dimension reduction. We construct contagion maps that use multiple contagions on a network to map the nodes as a point cloud. By analyzing the topology, geometry, and dimensionality of manifold structure in such point clouds, we reveal insights to aid in the modeling, forecast, and control of spreading processes. Our approach highlights contagion maps also as a viable tool for inferring low-dimensional structure in networks.
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The study of motifs in networks can help researchers uncover links between the structure and function of networks in biology, sociology, economics, and many other areas. Empirical studies of networks have identified feedback loops, feedforward loops, and several other small structures as motifs that occur frequently in real-world networks and may contribute by various mechanisms to important functions in these systems. However, these mechanisms are unknown for many of these motifs. We propose to distinguish between structure motifs (i.e., graphlets) in networks and process motifs (which we define as structured sets of walks) on networks and consider process motifs as building blocks of processes on networks. Using the steady-state covariances and steady-state correlations in a multivariate Ornstein--Uhlenbeck process on a network as examples, we demonstrate that the distinction between structure motifs and process motifs makes it possible to gain quantitative insights into mechanisms that contribute to important functions of dynamical systems on networks.
The vast majority of strategies aimed at controlling contagion processes on networks considers the connectivity pattern of the system as either quenched or annealed. However, in the real world many networks are highly dynamical and evolve in time concurrently to the contagion process. Here, we derive an analytical framework for the study of control strategies specifically devised for time-varying networks. We consider the removal/immunization of individual nodes according the their activity in the network and develop a block variable mean-field approach that allows the derivation of the equations describing the evolution of the contagion process concurrently to the network dynamic. We derive the critical immunization threshold and assess the effectiveness of the control strategies. Finally, we validate the theoretical picture by simulating numerically the information spreading process and control strategies in both synthetic networks and a large-scale, real-world mobile telephone call dataset
Dynamic-mode decomposition (DMD) is a versatile framework for model-free analysis of time series that are generated by dynamical systems. We develop a DMD-based algorithm to investigate the formation of functional communities in networks of coupled, heterogeneous Kuramoto oscillators. In these functional communities, the oscillators in the network have similar dynamics. We consider two common random-graph models (Watts--Strogatz networks and Barabasi--Albert networks) with different amounts of heterogeneities among the oscillators. In our computations, we find that membership in a community reflects the extent to which there is establishment and sustainment of locking between oscillators. We construct forest graphs that illustrate the complex ways in which the heterogeneous oscillators associate and disassociate with each other.
Many dynamical phenomena, e.g., pathogen transmission, disruptions in transport over networks, and (fake) news purveyance, concern spreading that plays out on top of networks with changing architectures over time - commonly known as temporal networks. Assessing a systems proneness to facilitate spreading phenomena, which we refer to as its spreading vulnerability, from its topological information alone remains a challenging task. We report a methodological advance in terms of a novel metric for topological complexity: entanglement entropy. Using publicly available datasets, we demonstrate that the metric naturally allows for topological comparisons across vastly different systems, and importantly, reveals that the spreading vulnerability of a system can be quantitatively related to its topological complexity. In doing so, the metric opens itself for applications in a wide variety of natural, social, biological and engineered systems.
In epidemic modeling, the term infection strength indicates the ratio of infection rate and cure rate. If the infection strength is higher than a certain threshold -- which we define as the epidemic threshold - then the epidemic spreads through the population and persists in the long run. For a single generic graph representing the contact network of the population under consideration, the epidemic threshold turns out to be equal to the inverse of the spectral radius of the contact graph. However, in a real world scenario it is not possible to isolate a population completely: there is always some interconnection with another network, which partially overlaps with the contact network. Results for epidemic threshold in interconnected networks are limited to homogeneous mixing populations and degree distribution arguments. In this paper, we adopt a spectral approach. We show how the epidemic threshold in a given network changes as a result of being coupled with another network with fixed infection strength. In our model, the contact network and the interconnections are generic. Using bifurcation theory and algebraic graph theory, we rigorously derive the epidemic threshold in interconnected networks. These results have implications for the broad field of epidemic modeling and control. Our analytical results are supported by numerical simulations.
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