Dynamical systems on networks typically involve several dynamical processes evolving at different timescales. For instance, in Alzheimer\'s disease, the spread of toxic protein throughout the brain not only disrupts neuronal activity but is also influenced by neuronal activity itself, establishing a feedback loop between the fast neuronal activity and the slow protein spreading. Motivated by the case of Alzheimer\'s disease, we study the multiple-timescale dynamics of a heterodimer spreading process on an adaptive network of Kuramoto oscillators. Using a minimal two-node model, we establish that heterogeneous oscillatory activity facilitates toxic outbreaks and induces symmetry breaking in the spreading patterns. We then extend the model formulation to larger networks and perform numerical simulations of the slow-fast dynamics on common network motifs and on the brain connectome. The simulations corroborate the findings from the minimal model, underscoring the significance of multiple-timescale dynamics in the modeling of neurodegenerative diseases.

Here, we present an effective application of adaptive cooperative networks, namely assisting disables in navigating in a crowd in a pandemic or emergency situation. To achieve this, we model crowd movement and introduce a cooperative learning approach to enable cooperation and self-organization of the crowd members with impaired health or on wheelchairs to ensure their safe movement in the crowd. Here, it is assumed that the movement path and the varying locations of the other crowd members can be estimated by each agent. Therefore, the network nodes (agents) should continuously reorganize themselves by varying their speeds and distances from each other, from the surrounding walls, and from obstacles within a predefined limit. It is also demonstrated how the available wireless trackers such as AirTags can be used for this purpose. The model effectiveness is examined with respect to the real-time changes in environmental parameters and its efficacy is verified.

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Adaptive interactions are an important property of many real-word network systems. A feature of such networks is the change in their connectivity depending on the current states of the interacting elements. In this work, we study the question of how the heterogeneous character of adaptive couplings influences the emergence of new scenarios in the collective behavior of networks. Within the framework of a two-population network of coupled phase oscillators, we analyze the role of various factors of heterogeneous interaction, such as the rules of coupling adaptation and the rate of their change in the formation of various types of coherent behavior of the network. We show that various schemes of heterogeneous adaptation lead to the formation of transient phase clusters of various types.

The interplay between disease spreading and personal risk perception is of key importance for modelling the spread of infectious diseases. We propose a planar system of ordinary differential equations (ODEs) to describe the co-evolution of a spreading phenomenon and the average link density in the personal contact network. Contrary to standard epidemic models, we assume that the contact network changes based on the current prevalence of the disease in the population, i.e. the network adapts to the current state of the epidemic. We assume that personal risk perception is described using two functional responses: one for link-breaking and one for link-creation. The focus is on applying the model to epidemics, but we also highlight other possible fields of application. We derive an explicit form for the basic reproduction number and guarantee the existence of at least one endemic equilibrium, for all possible functional responses. Moreover, we show that for all functional responses, limit cycles do not exist. This means that our minimal model is not able to reproduce consequent waves of an epidemic, and more complex disease or behavioural dynamics are required to reproduce epidemic waves.

In this work, we propose a dynamical systems perspective on the modeling of sepsis and its organ-damaging consequences. We develop a functional two-layer network model for sepsis based upon the interaction of parenchymal cells and immune cells via cytokines, and the coevolutionary dynamics of parenchymal, immune cells, and cytokines. By means of the simple paradigmatic model of phase oscillators in a two-layer system, we analyze the emergence of organ threatening interactions between the dysregulated immune system and the parenchyma. We demonstrate that the complex cellular cooperation between parenchyma and stroma (immune layer) either in the physiological or in the pathological case can be related to dynamical patterns of the network. In this way we explain sepsis by the dysregulation of the healthy homeostatic state (frequency synchronized) leading to a pathological state (desynchronized or multifrequency cluster) in the parenchyma. We provide insight into the complex stabilizing and destabilizing interplay of parenchyma and stroma by determining critical interaction parameters. The coupled dynamics of parenchymal cells (metabolism) and nonspecific immune cells (response of the innate immune system) is represented by nodes of a duplex layer. Cytokine interaction is modeled by adaptive coupling weights between nodes representing immune cells (with fast adaptation timescale) and parenchymal cells (slow adaptation timescale), and between pairs of parenchymal and immune cells in the duplex network (fixed bidirectional coupling). The proposed model allows for a functional description of organ dysfunction in sepsis and the recurrence risk in a plausible pathophysiological context.

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In this study, we provide a dynamical systems perspective to the modelling of pathological states induced by tumors or infection. A unified disease model is established using the innate immune system as the reference point. We propose a two-layer network model for carcinogenesis and sepsis based upon the interaction of parenchymal cells and immune cells via cytokines, and the co-evolutionary dynamics of parenchymal, immune cells, and cytokines. Our aim is to show that the complex cellular cooperation between parenchyma and stroma (immune layer) in the physiological and pathological case can be qualitatively and functionally described by a simple paradigmatic model of phase oscillators. By this, we explain carcinogenesis, tumor progression, and sepsis by destabilization of the healthy homeostatic state (frequency synchronized), and emergence of a pathological state (desynchronized or multifrequency cluster). The coupled dynamics of parenchymal cells (metabolism) and nonspecific immune cells (reaction of innate immune system) are represented by nodes of a duplex layer. The cytokine interaction is modeled by adaptive coupling weights between the nodes representing the immune cells (with fast adaptation time scale) and the parenchymal cells (slow adaptation time scale) and between the pairs of parenchymal and immune cells in the duplex network (fixed bidirectional coupling). Thereby, carcinogenesis, organ dysfunction in sepsis, and recurrence risk can be described in a correct functional context.

We investigate the effects of external and autonomous global interaction fields on an adaptive network of social agents with an opinion formation dynamics based on a simple imitation rule. We study the competition between global fields and adaptive rewiring on the space of parameters of the system. The model represents an adaptive society subject to global mass media such as a directed opinion influence or feedback of endogenous cultural trends. We show that, in both situations, global mass media contribute to consensus and to prevent the fragmentation of the social network induced by the coevolutionary dynamics. We present a discussion of these results in the context of dynamical systems and opinion formation dynamics.

The COVID-19 pandemic has proved to be one of the most disruptive public health emergencies in recent memory. Among non-pharmaceutical interventions, social distancing and lockdown measures are some of the most common tools employed by governments around the world to combat the disease. While mathematical models of COVID-19 are ubiquitous, few have leveraged network theory in a general way to explain the mechanics of social distancing. In this paper, we build on existing network models for heterogeneous, clustered networks with random link activation/deletion dynamics to put forth realistic mechanisms of social distancing using piecewise constant activation/deletion rates. We find our models are capable of rich qualitative behavior, and offer meaningful insight with relatively few intervention parameters. In particular, we find that the severity of social distancing interventions and when they begin have more impact than how long it takes for the interventions to take full effect.