Phase chimera states on nonlocal hyperrings.

Chimera states are dynamical states where regions of synchronous trajectories coexist with incoherent ones. A significant amount of research has been devoted to studying chimera states in systems of identical oscillators, nonlocally coupled through pairwise interactions. Nevertheless, there is increasing evidence, also supported by available data, that complex systems are composed of multiple units experiencing many-body interactions that can be modeled by using higher-order structures beyond the paradigm of classic pairwise networks. In this work we investigate whether phase chimera states appear in this framework, by focusing on a topology solely involving many-body, nonlocal, and nonregular interactions, hereby named nonlocal d-hyperring, (d+1) being the order of the interactions. We present the theory by using the paradigmatic Stuart-Landau oscillators as node dynamics, and we show that phase chimera states emerge in a variety of structures and with different coupling functions. For comparison, we show that, when higher-order interactions are "flattened" to pairwise ones, the chimera behavior is weaker and more elusive.

Higher-order interactions induce anomalous transitions to synchrony.

We analyze the simplest model of identical coupled phase oscillators subject to two-body and three-body interactions with permutation symmetry and phase lags. This model is derived from an ensemble of weakly coupled nonlinear oscillators by phase reduction, where the first and second harmonic interactions with phase lags naturally appear. Our study indicates that the higher-order interactions induce anomalous transitions to synchrony. Unlike the conventional Kuramoto model, higher-order interactions lead to anomalous phenomena such as multistability of full synchronization, incoherent, and two-cluster states, and transitions to synchrony through slow switching and clustering. Phase diagrams of the dynamical regimes are constructed theoretically and verified by direct numerical simulations. We also show that similar transition scenarios are observed even if a small heterogeneity in the oscillators' frequency is included.

Diffusion-driven instability of topological signals coupled by the Dirac operator.

The study of reaction-diffusion systems on networks is of paramount relevance for the understanding of nonlinear processes in systems where the topology is intrinsically discrete, such as the brain. Until now, reaction-diffusion systems have been studied only when species are defined on the nodes of a network. However, in a number of real systems including, e.g., the brain and the climate, dynamical variables are not only defined on nodes but also on links, faces, and higher-dimensional cells of simplicial or cell complexes, leading to topological signals. In this work, we study reaction-diffusion processes of topological signals coupled through the Dirac operator. The Dirac operator allows topological signals of different dimension to interact or cross-diffuse as it projects the topological signals defined on simplices or cells of a given dimension to simplices or cells of one dimension up or one dimension down. By focusing on the framework involving nodes and links, we establish the conditions for the emergence of Turing patterns and we show that the latter are never localized only on nodes or only on links of the network. Moreover, when the topological signals display a Turing pattern their projection does as well. We validate the theory hereby developed on a benchmark network model and on square lattices with periodic boundary conditions.

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.

The common message of constraint-based optimization approaches: overflow metabolism is caused by two growth-limiting constraints.

Living cells can express different metabolic pathways that support growth. The criteria that determine which pathways are selected in which environment remain unclear. One recurrent selection is overflow metabolism: the simultaneous usage of an ATP-efficient and -inefficient pathway, shown for example in Escherichia coli, Saccharomyces cerevisiae and cancer cells. Many models, based on different assumptions, can reproduce this observation. Therefore, they provide no conclusive evidence which mechanism is causing overflow metabolism. We compare the mathematical structure of these models. Although ranging from flux balance analyses to self-fabricating metabolism and expression models, we can rewrite all models into one standard form. We conclude that all models predict overflow metabolism when two, model-specific, growth-limiting constraints are hit. This is consistent with recent theory. Thus, identifying these two constraints is essential for understanding overflow metabolism. We list all imposed constraints by these models, so that they can hopefully be tested in future experiments.

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.