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.

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.

The concept of memory is traditionally associated with organisms possessing a nervous system. However, even very simple organisms store information about past experiences to thrive in a complex environment-successfully exploiting nutrient sources, avoiding danger, and warding off predators. How can simple organisms encode information about their environment? We here follow how the giant unicellular slime mold Physarum polycephalum responds to a nutrient source. We find that the network-like body plan of the organism itself serves to encode the location of a nutrient source. The organism entirely consists of interlaced tubes of varying diameters. Now, we observe that these tubes grow and shrink in diameter in response to a nutrient source, thereby imprinting the nutrient\'s location in the tube diameter hierarchy. Combining theoretical model and experimental data, we reveal how memory is encoded: a nutrient source locally releases a softening agent that gets transported by the cytoplasmic flows within the tubular network. Tubes receiving a lot of softening agent grow in diameter at the expense of other tubes shrinking. Thereby, the tubes\' capacities for flow-based transport get permanently upgraded toward the nutrient location, redirecting future decisions and migration. This demonstrates that nutrient location is stored in and retrieved from the networks\' tube diameter hierarchy. Our findings explain how network-forming organisms like slime molds and fungi thrive in complex environments. We here identify a flow networks\' version of associative memory-very likely of relevance for the plethora of living flow networks as well as for bioinspired design.

Cyclic oligochalcogenides (COCs) are emerging as promising systems to penetrate cells. Clearly better than and different to the reported diselenolanes and epidithiodiketopiperazines, we introduce the benzopolysulfanes (BPS), which show efficient delivery, insensitivity to inhibitors of endocytosis, and compatibility with substrates as large as proteins. This high activity coincides with high reactivity, selectively toward thiols, exceeding exchange rates of disulfides under tension. The result is a dynamic-covalent network of extreme sulfur species, including cyclic oligomers, from dimers to heptamers, with up to nineteen sulfurs in the ring. Selection from this unfolding adaptive network then yields the reactivities and selectivities needed to access new uptake pathways. Contrary to other COCs, BPS show high retention on thiol affinity columns. The identification of new modes of cell penetration is important because they promise new solutions to challenges in delivery and beyond.

We study a model for switching strategies in the Prisoner\'s Dilemma game on adaptive networks of player pairings that coevolve as players attempt to maximize their return. We use a node-based strategy model wherein each player follows one strategy at a time (cooperate or defect) across all of its neighbors, changing that strategy and possibly changing partners in response to local changes in the network of player pairing and in the strategies used by connected partners. We compare and contrast numerical simulations with existing pair approximation differential equations for describing this system, as well as more accurate equations developed here using the framework of approximate master equations. We explore the parameter space of the model, demonstrating the relatively high accuracy of the approximate master equations for describing the system observations made from simulations. We study two variations of this partner-switching model to investigate the system evolution, predict stationary states, and compare the total utilities and other qualitative differences between these two model variants.

Early warning signals of sudden regime shifts are a widely studied phenomenon for their ability to quantify a system\'s proximity to a tipping point to a new and contrasting dynamical regime. However, this effect has been little studied in the context of the complex interactions between disease dynamics and vaccinating behaviour. Our objective was to determine whether critical slowing down (CSD) occurs in a multiplex network that captures opinion propagation on one network layer and disease spread on a second network layer. We parameterized a network simulation model to represent a hypothetical self-limiting, acute, vaccine-preventable infection with short-lived natural immunity. We tested five different network types: random, lattice, small-world, scale-free, and an empirically derived network. For the first four network types, the model exhibits a regime shift as perceived vaccine risk moves beyond a tipping point from full vaccine acceptance and disease elimination to full vaccine refusal and disease endemicity. This regime shift is preceded by an increase in the spatial correlation in non-vaccinator opinions beginning well before the bifurcation point, indicating CSD. The early warning signals occur across a wide range of parameter values. However, the more gradual transition exhibited in the empirically-derived network underscores the need for further research before it can be determined whether trends in spatial correlation in real-world social networks represent critical slowing down. The potential upside of having this monitoring ability suggests that this is a worthwhile area for further research.