Self-segregation in heterogeneous metapopulation landscapes.

Complex interactions are at the root of the population dynamics of many natural systems, particularly for being responsible for the allocation of species and individuals across apposite niches of the ecological landscapes. On the other side, the randomness that unavoidably characterises complex systems has increasingly challenged the niche paradigm providing alternative neutral theoretical models. We introduce a network-inspired metapopulation individual-based model (IBM), hereby named self-segregation, where the density of individuals in the hosting patches (local habitats) drives the individuals spatial assembling while still constrained by nodes' saturation. In particular, we prove that the core-periphery structure of the networked landscape triggers the spontaneous emergence of vacant habitat patches, which segregate the population in multistable patterns of isolated (sub)communities separated by empty patches. Furthermore, a quantisation effect in the number of vacant patches is observed once the total system mass varies continuously, emphasising thus a striking feature of the robustness of population stationary distributions. Notably, our model reproduces the patch vacancy found in the fragmented habitat of the Glanville fritillary butterfly Melitaea cinxia, an endemic species of the Åland islands. We argue that such spontaneous breaking of the natural habitat supports the concept of the highly contentious (Grinnellian) niche vacancy and also suggests a new mechanism for the endogeneous habitat fragmentation and consequently the peripatric speciation.

Symmetry-breaking mechanism for the formation of cluster chimera patterns.

The emergence of order in collective dynamics is a fascinating phenomenon that characterizes many natural systems consisting of coupled entities. Synchronization is such an example where individuals, usually represented by either linear or nonlinear oscillators, can spontaneously act coherently with each other when the interactions' configuration fulfills certain conditions. However, synchronization is not always perfect, and the coexistence of coherent and incoherent oscillators, broadly known in the literature as chimera states, is also possible. Although several attempts have been made to explain how chimera states are created, their emergence, stability, and robustness remain a long-debated question. We propose an approach that aims to establish a robust mechanism through which cluster synchronization and chimera patterns originate. We first introduce a stability-breaking method where clusters of synchronized oscillators can emerge. At variance with the standard approach where synchronization arises as a collective behavior of coupled oscillators, in our model, the system initially sets on a homogeneous fixed-point regime, and, only due to a global instability principle, collective oscillations emerge. Following a combination of the network modularity and the model's parameters, one or more clusters of oscillators become incoherent within yielding a particular class of patterns that we here name cluster chimera states.

Role of modularity in self-organization dynamics in biological networks.

Interconnected ensembles of biological entities are perhaps some of the most complex systems that modern science has encountered so far. In particular, scientists have concentrated on understanding how the complexity of the interacting structure between different neurons, proteins, or species influences the functioning of their respective systems. It is well established that many biological networks are constructed in a highly hierarchical way with two main properties: short average paths that join two apparently distant nodes (neuronal, species, or protein patches) and a high proportion of nodes in modular aggregations. Although several hypotheses have been proposed so far, still little is known about the relation of the modules with the dynamical activity in such biological systems. Here we show that network modularity is a key ingredient for the formation of self-organizing patterns of functional activity, independently of the topological peculiarities of the structure of the modules. In particular, we propose a self-organizing mechanism which explains the formation of macroscopic spatial patterns, which are homogeneous within modules. This may explain how spontaneous order in biological networks follows their modular structural organization. We test our results on real-world networks to confirm the important role of modularity in creating macroscale patterns.

Synchronization Dynamics in Non-Normal Networks: The Trade-Off for Optimality.

Synchronization is an important behavior that characterizes many natural and human made systems that are composed by several interacting units. It can be found in a broad spectrum of applications, ranging from neuroscience to power-grids, to mention a few. Such systems synchronize because of the complex set of coupling they exhibit, with the latter being modeled by complex networks. The dynamical behavior of the system and the topology of the underlying network are strongly intertwined, raising the question of the optimal architecture that makes synchronization robust. The Master Stability Function (MSF) has been proposed and extensively studied as a generic framework for tackling synchronization problems. Using this method, it has been shown that, for a class of models, synchronization in strongly directed networks is robust to external perturbations. Recent findings indicate that many real-world networks are strongly directed, being potential candidates for optimal synchronization. Moreover, many empirical networks are also strongly non-normal. Inspired by this latter fact in this work, we address the role of the non-normality in the synchronization dynamics by pointing out that standard techniques, such as the MSF, may fail to predict the stability of synchronized states. We demonstrate that, due to a transient growth that is induced by the structure's non-normality, the system might lose synchronization, contrary to the spectral prediction. These results lead to a trade-off between non-normality and directedness that should be properly considered when designing an optimal network, enhancing the robustness of synchronization.

Resilience for stochastic systems interacting via a quasi-degenerate network.

A stochastic reaction-diffusion model is studied on a networked support. In each patch of the network, two species are assumed to interact following a non-normal reaction scheme. When the interaction unit is replicated on a directed linear lattice, noise gets amplified via a self-consistent process, which we trace back to the degenerate spectrum of the embedding support. The same phenomenon holds when the system is bound to explore a quasidegenerate network. In this case, the eigenvalues of the Laplacian operator, which governs species diffusion, accumulate over a limited portion of the complex plane. The larger the network, the more pronounced the amplification. Beyond a critical network size, a system deemed deterministically stable, hence resilient, can develop seemingly regular patterns in the concentration amount. Non-normality and quasidegenerate networks may, therefore, amplify the inherent stochasticity and so contribute to altering the perception of resilience, as quantified via conventional deterministic methods.

Patterns of non-normality in networked systems.

Several mechanisms have been proposed to explain the spontaneous generation of self-organised patterns, hypothesised to play a role in the formation of many of the magnificent patterns observed in Nature. In several cases of interest, the system under scrutiny displays a homogeneous equilibrium, which is destabilised via a symmetry breaking instability which reflects the specificity of the problem being inspected. The Turing instability is among the most celebrated paradigms for pattern formation. In its original form, the diffusion constants of the two mobile species need to be quite different from each other for the instability to develop. Unfortunately, this condition limits the applicability of the theory. To overcome this impediment, and with the ambitious long term goal to eventually reconcile theory and experiments, we here propose an alternative mechanism for promoting the onset of pattern. To this end a multi-species reactive model is studied, assuming a generalized transport on a discrete and directed network-like support: the instability is triggered by the non-normality of the embedding network. The non-normal character of the dynamics instigates a short time amplification of the imposed perturbation, thus making the system unstable for a choice of parameters that would yield stability under the conventional scenario. In other words, non-normality promotes the emergence of patterns in cases where a classical linear analysis would not predict them. The importance of our result relies also on the fact that non-normal networks are pervasively found, motivating the general interest of the mechanism discussed here.

Structure and dynamical behavior of non-normal networks.

We analyze a collection of empirical networks in a wide spectrum of disciplines and show that strong non-normality is ubiquitous in network science. Dynamical processes evolving on non-normal networks exhibit a peculiar behavior, as initial small disturbances may undergo a transient phase and be strongly amplified in linearly stable systems. In addition, eigenvalues may become extremely sensible to noise and have a diminished physical meaning. We identify structural properties of networks that are associated with non-normality and propose simple models to generate networks with a tunable level of non-normality. We also show the potential use of a variety of metrics capturing different aspects of non-normality and propose their potential use in the context of the stability of complex ecosystems.

A minimally invasive neurostimulation method for controlling abnormal synchronisation in the neuronal activity.

Many collective phenomena in Nature emerge from the -partial- synchronisation of the units comprising a system. In the case of the brain, this self-organised process allows groups of neurons to fire in highly intricate partially synchronised patterns and eventually lead to high level cognitive outputs and control over the human body. However, when the synchronisation patterns are altered and hypersynchronisation occurs, undesirable effects can occur. This is particularly striking and well documented in the case of epileptic seizures and tremors in neurodegenerative diseases such as Parkinson's disease. In this paper, we propose an innovative, minimally invasive, control method that can effectively desynchronise misfiring brain regions and thus mitigate and even eliminate the symptoms of the diseases. The control strategy, grounded in the Hamiltonian control theory, is applied to ensembles of neurons modelled via the Kuramoto or the Stuart-Landau models and allows for heterogeneous coupling among the interacting unities. The theory has been complemented with dedicated numerical simulations performed using the small-world Newman-Watts network and the random Erdos-Rényi network. Finally the method has been compared with the gold-standard Proportional-Differential Feedback control technique. Our method is shown to achieve equivalent levels of desynchronisation using lesser control strength and/or fewer controllers, being thus minimally invasive.

Topological resilience in non-normal networked systems.

The network of interactions in complex systems strongly influences their resilience and the system capability to resist external perturbations or structural damages and to promptly recover thereafter. The phenomenon manifests itself in different domains, e.g., parasitic species invasion in ecosystems or cascade failures in human-made networks. Understanding the topological features of the networks that affect the resilience phenomenon remains a challenging goal for the design of robust complex systems. We hereby introduce the concept of non-normal networks, namely networks whose adjacency matrices are non-normal, propose a generating model, and show that such a feature can drastically change the global dynamics through an amplification of the system response to exogenous disturbances and eventually impact the system resilience. This early stage transient period can induce the formation of inhomogeneous patterns, even in systems involving a single diffusing agent, providing thus a new kind of dynamical instability complementary to the Turing one. We provide, first, an illustrative application of this result to ecology by proposing a mechanism to mute the Allee effect and, second, we propose a model of virus spreading in a population of commuters moving using a non-normal transport network, the London Tube.

Hopping in the Crowd to Unveil Network Topology.

We introduce a nonlinear operator to model diffusion on a complex undirected network under crowded conditions. We show that the asymptotic distribution of diffusing agents is a nonlinear function of the nodes' degree and saturates to a constant value for sufficiently large connectivities, at variance with standard diffusion in the absence of excluded-volume effects. Building on this observation, we define and solve an inverse problem, aimed at reconstructing the a priori unknown connectivity distribution. The method gathers all the necessary information by repeating a limited number of independent measurements of the asymptotic density at a single node, which can be chosen randomly. The technique is successfully tested against both synthetic and real data and is also shown to estimate with great accuracy the total number of nodes.

Using Hamiltonian control to desynchronize Kuramoto oscillators.

Many coordination phenomena are based on a synchronization process, whose global behavior emerges from the interactions among the individual parts. Often in nature, such self-organized mechanism allows the system to behave as a whole and thus grounding its very first existence, or expected functioning, on such process. There are, however, cases where synchronization acts against the stability of the system; for instance in some neurodegenerative diseases or epilepsy or the famous case of Millennium Bridge where the crowd synchronization of the pedestrians seriously endangered the stability of the structure. In this paper we propose an innovative control method to tackle the synchronization process based on the application of the Hamiltonian control theory, by adding a small control term to the system we are able to impede the onset of the synchronization. We present our results on a generalized class of the paradigmatic Kuramoto model.

Turing instabilities on Cartesian product networks.

The problem of Turing instabilities for a reaction-diffusion system defined on a complex Cartesian product network is considered. To this end we operate in the linear regime and expand the time dependent perturbation on a basis formed by the tensor product of the eigenvectors of the discrete Laplacian operators, associated to each of the individual networks that build the Cartesian product. The dispersion relation which controls the onset of the instability depends on a set of discrete wavelengths, the eigenvalues of the aforementioned Laplacians. Patterns can develop on the Cartesian network, if they are supported on at least one of its constitutive sub-graphs. Multiplex networks are also obtained under specific prescriptions. In this case, the criteria for the instability reduce to compact explicit formulae. Numerical simulations carried out for the Mimura-Murray reaction kinetics confirm the adequacy of the proposed theory.

Turing patterns in multiplex networks.

The theory of patterns formation for a reaction-diffusion system defined on a multiplex is developed by means of a perturbative approach. The interlayer diffusion constants act as a small parameter in the expansion and the unperturbed state coincides with the limiting setting where the multiplex layers are decoupled. The interaction between adjacent layers can seed the instability of a homogeneous fixed point, yielding self-organized patterns which are instead impeded in the limit of decoupled layers. Patterns on individual layers can also fade away due to cross-talking between layers. Analytical results are compared to direct simulations.

The theory of pattern formation on directed networks.

Dynamical processes on networks have generated widespread interest in recent years. The theory of pattern formation in reaction-diffusion systems defined on symmetric networks has often been investigated, due to its applications in a wide range of disciplines. Here we extend the theory to the case of directed networks, which are found in a number of different fields, such as neuroscience, computer networks and traffic systems. Owing to the structure of the network Laplacian, the dispersion relation has both real and imaginary parts, at variance with the case for a symmetric, undirected network. The homogeneous fixed point can become unstable due to the topology of the network, resulting in a new class of instabilities, which cannot be induced on undirected graphs. Results from a linear stability analysis allow the instability region to be analytically traced. Numerical simulations show travelling waves, or quasi-stationary patterns, depending on the characteristics of the underlying graph.

Stochastic amplification of spatial modes in a system with one diffusing species.

The problem of pattern formation in a generic two species reaction-diffusion model is studied, under the hypothesis that only one species can diffuse. For such a system, the classical Turing instability cannot take place. At variance, by working in the generalized setting of a stochastic formulation to the inspected problem, spatially organized patterns can develop, seeded by finite size corrections. General conditions are given for the stochastic patterns to occur. The predictions of the theory are tested for a specific case study.