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Register a new userCriticality of spreading dynamics in hierarchical cluster networks without inhibition
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An essential requirement for the representation of functional patterns in complex neural networks, such as the mammalian cerebral cortex, is the existence of stable network activations within a limited critical range. In this range, the activity of neural populations in the network persists between the extremes of quickly dying out, or activating the whole network. The nerve fiber network of the mammalian cerebral cortex possesses a modular organization extending across several levels of organization. Using a basic spreading model without inhibition, we investigated how functional activations of nodes propagate through such a hierarchically clustered network. The simulations demonstrated that persistent and scalable activation could be produced in clustered networks, but not in random networks of the same size. Moreover, the parameter range yielding critical activations was substantially larger in hierarchical cluster networks than in small-world networks of the same size. These findings indicate that a hierarchical cluster architecture may provide the structural basis for the stable and diverse functional patterns observed in cortical networks.
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The collective dynamics of a network of excitable nodes changes dramatically when inhibitory nodes are introduced. We consider inhibitory nodes which may be activated just like excitatory nodes but, upon activating, decrease the probability of activation of network neighbors. We show that, although the direct effect of inhibitory nodes is to decrease activity, the collective dynamics becomes self-sustaining. We explain this counterintuitive result by defining and analyzing a branching function which may be thought of as an activity-dependent branching ratio. The shape of the branching function implies that for a range of global coupling parameters dynamics are self-sustaining. Within the self-sustaining region of parameter space lies a critical line along which dynamics take the form of avalanches with universal scaling of size and duration, embedded in ceaseless timeseries of activity. Our analyses, confirmed by numerical simulation, suggest that inhibition may play a counterintuitive role in excitable networks.
We investigate the dynamics of a broad class of stochastic copying processes on a network that includes examples from population genetics (spatially-structured Wright-Fisher models), ecology (Hubbell-type models), linguistics (the utterance selection model) and opinion dynamics (the voter model) as special cases. These models all have absorbing states of fixation where all the nodes are in the same state. Earlier studies of these models showed that the mean time when this occurs can be made to grow as different powers of the network size by varying the the degree distribution of the network. Here we demonstrate that this effect can also arise if one varies the asymmetry of the copying dynamics whilst holding the degree distribution constant. In particular, we show that the mean time to fixation can be accelerated even on homogeneous networks when certain nodes are very much more likely to be copied from than copied to. We further show that there is a complex interplay between degree distribution and asymmetry when they may co-vary; and that the results are robust to correlations in the network or the initial condition.
Networks are widely used to model the contact structure within a population and in the resulting models of disease spread. While networks provide a high degree of realism, the analysis of the exact model is out of reach and even numerical methods fail for modest network size. Hence, mean-field models (e.g. pairwise) focusing on describing the evolution of some summary statistics from the exact model gained a lot of traction over the last few decades. In this paper we revisit the problem of deriving triple closures for pairwise models and we investigate in detail the assumptions behind some of the well-known closures as well as their validity. Using a top-down approach we start at the level of the entire graph and work down to the level of triples and combine this with information around nodes and pairs. We use our approach to derive many of the existing closures and propose new ones and theoretically connect the two well-studied models of multinomial link and Poisson link selection. The theoretical work is backed up by numerical examples to highlight where the commonly used assumptions may fail and provide some recommendations for how to choose the most appropriate closure when using graphs with no or modest degree heterogeneity.
Understanding and predicting outbreaks of contagious diseases are crucial to the development of society and public health, especially for underdeveloped countries. However, challenging problems are encountered because of complex epidemic spreading dynamics influenced by spatial structure and human dynamics (including both human mobility and human interaction intensity). We propose a systematical model to depict nationwide epidemic spreading in C^{o}te dIvoire, which integrates multiple factors, such as human mobility, human interaction intensity, and demographic features. We provide insights to aid in modeling and predicting the epidemic spreading process by data-driven simulation and theoretical analysis, which is otherwise beyond the scope of local evaluation and geometrical views. We show that the requirement that the average local basic reproductive number to be greater than unity is not necessary for outbreaks of epidemics. The observed spreading phenomenon can be roughly explained as a heterogeneous diffusion-reaction process by redefining mobility distance according to the human mobility volume between nodes, which is beyond the geometrical viewpoint. However, the heterogeneity of human dynamics still poses challenges to precise prediction.
The $1/f$-like decay observed in the power spectrum of electro-physiological signals, along with scale-free statistics of the so-called neuronal avalanches, constitute evidences of criticality in neuronal systems. Recent in vitro studies have shown that avalanche dynamics at criticality corresponds to some specific balance of excitation and inhibition, thus suggesting that this is a basic feature of the critical state of neuronal networks. In particular, a lack of inhibition significantly alters the temporal structure of the spontaneous avalanche activity and leads to an anomalous abundance of large avalanches. Here we study the relationship between network inhibition and the scaling exponent $beta$ of the power spectral density (PSD) of avalanche activity in a neuronal network model inspired in Self-Organized Criticality (SOC). We find that this scaling exponent depends on the percentage of inhibitory synapses and tends to the value $beta = 1$ for a percentage of about 30%. More specifically, $beta$ is close to $2$, namely brownian noise, for purely excitatory networks and decreases towards values in the interval $[1,1.4]$ as the percentage of inhibitory synapses ranges between 20 and 30%, in agreement with experimental findings. These results indicate that the level of inhibition affects the frequency spectrum of resting brain activity and suggest the analysis of the PSD scaling behavior as a possible tool to study pathological conditions.
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