Publications by authors named "Arcangelis L"

The identification of patterns in space, time, and magnitude, which could potentially encode the subsequent earthquake magnitude, represents a significant challenge in earthquake forecasting. A pivotal aspect of this endeavor involves the search for correlations between earthquake magnitudes, a task greatly hindered by the incompleteness of instrumental catalogs. A novel strategy to address this challenge is provided by the groundbreaking observation by Van der Elst (Journal of Geophysical Research: Solid Earth, 2021) that positive magnitude differences, under specific conditions, remain unaffected by catalog incompleteness.

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Recent results have evidenced that spontaneous brain activity signals are organized in bursts with scale free features and long-range spatio-temporal correlations. These observations have stimulated a theoretical interpretation of results inspired in critical phenomena. In particular, relying on maximum entropy arguments, certain aspects of time-averaged experimental neuronal data have been recently described using Ising-like models, allowing the study of neuronal networks under an analogous thermodynamical framework.

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We analyze time-averaged experimental data from in vitro activities of neuronal networks. Through a Pairwise Maximum-Entropy method, we identify through an inverse binary Ising-like model the local fields and interaction couplings which best reproduce the average activities of each neuron as well as the statistical correlations between the activities of each pair of neurons in the system. The specific information about the type of neurons is mainly stored in the local fields, while a symmetric distribution of interaction constants seems generic.

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Alpha oscillations are a distinctive feature of the awake resting state of the human brain. However, their functional role in resting-state neuronal dynamics remains poorly understood. Here we show that, during resting wakefulness, alpha oscillations drive an alternation of attenuation and amplification bouts in neural activity.

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The relation between spontaneous and stimulated brain activity is a fundamental question in neuroscience which has received wide attention in experimental studies. Recently, it has been suggested that the evoked response to external stimuli can be predicted from temporal correlations of spontaneous activity. Previous theoretical results, confirmed by the comparison with magnetoencephalography data for human brains, were obtained for the Wilson-Cowan model in the condition of balance of excitation and inhibition, a signature of a healthy brain.

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The identification of the transmission parameters of a virus is fundamental to identify the optimal public health strategy. These parameters can present significant changes over time caused by genetic mutations or viral recombination, making their continuous monitoring fundamental. Here we present a method, suitable for this task, which uses as unique information the daily number of reported cases.

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The power spectrum of brain activity is composed by peaks at characteristic frequencies superimposed to a background that decays as a power law of the frequency, [Formula: see text], with an exponent [Formula: see text] close to 1 (pink noise). This exponent is predicted to be connected with the exponent [Formula: see text] related to the scaling of the average size with the duration of avalanches of activity. "Mean field" models of neural dynamics predict exponents [Formula: see text] and [Formula: see text] equal or near 2 at criticality (brown noise), including the simple branching model and the fully-connected stochastic Wilson-Cowan model.

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Many systems in nature exhibit avalanche dynamics with scale-free features. A general scaling theory has been proposed for critical avalanche profiles in crackling noise, predicting the collapse onto a universal avalanche shape, as well as the scaling behavior of the activity power spectrum as Brown noise. Recently, much attention has been given to the profile of neuronal avalanches, measured in neuronal systems in vitro and in vivo.

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The transmissibility of an infectious disease is usually quantified in terms of the reproduction number [Formula: see text] representing, at a given time, the average number of secondary cases caused by an infected individual. Recent studies have enlightened the central role played by w(z), the distribution of generation times z, namely the time between successive infections in a transmission chain. In standard approaches this quantity is usually substituted by the distribution of serial intervals, which is obtained by contact tracing after measuring the time between onset of symptoms in successive cases.

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Spontaneous brain activity is characterized by bursts and avalanche-like dynamics, with scale-free features typical of critical behaviour. The stochastic version of the celebrated Wilson-Cowan model has been widely studied as a system of spiking neurons reproducing non-trivial features of the neural activity, from avalanche dynamics to oscillatory behaviours. However, to what extent such phenomena are related to the presence of a genuine critical point remains elusive.

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Local anaxonic neurons with graded potential release are important ingredients of nervous systems, present in the olfactory bulb system of mammalians and in the human visual system, as well as in arthropods and nematodes. We develop a neuronal network model including both axonic and anaxonic neurons and monitor the activity tuned by the following parameters: the decay length of the graded potential in local neurons, the fraction of local neurons, the largest eigenvalue of the adjacency matrix, and the range of connections of the local neurons. Tuning the fraction of local neurons, we derive the phase diagram including two transition lines: a critical line separating subcritical and supercritical regions, characterized by power-law distributions of avalanche sizes and durations, and a bifurcation line.

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Stroke is one of the main causes of human disabilities. Experimental observations indicate that several mechanisms are activated during the recovery of functional activity after a stroke. Here we unveil how the brain recovers by explaining the role played by three mechanisms: Plastic adaptation, hyperexcitability and synaptogenesis.

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Pattern recognition is a fundamental neuronal process which enables a cortical system to interpret visual stimuli. How the brain learns to recognize patterns is, however, an unsolved problem. The frequently employed method of back propagation excels at this task but has been found to be unbiological in many aspects.

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An increase of seismic activity is often observed before large earthquakes. Events responsible for this increase are usually named foreshock and their occurrence probably represents the most reliable precursory pattern. Many foreshocks statistical features can be interpreted in terms of the standard mainshock-to-aftershock triggering process and are recovered in the Epidemic Type Aftershock Sequence ETAS model.

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The frictional properties of disordered systems are affected by external perturbations. These perturbations usually weaken the system by reducing the macroscopic friction coefficient. This friction reduction is of particular interest in the case of disordered systems composed of granular particles confined between two plates, as this is a simple model of seismic fault.

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In recent years self organized critical neuronal models have provided insights regarding the origin of the experimentally observed avalanching behavior of neuronal systems. It has been shown that dynamical synapses, as a form of short-term plasticity, can cause critical neuronal dynamics. Whereas long-term plasticity, such as Hebbian or activity dependent plasticity, have a crucial role in shaping the network structure and endowing neural systems with learning abilities.

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We experimentally investigate the fluidization of a granular material subject to mechanical vibrations by monitoring the angular velocity of a vane suspended in the medium and driven by an external motor. On increasing the frequency, we observe a reentrant transition, as a jammed system first enters a fluidized state, where the vane rotates with high constant velocity, and then returns to a frictional state, where the vane velocity is much lower. While the fluidization frequency is material independent, the viscosity recovery frequency shows a clear dependence on the material that we rationalize by relating this frequency to the balance between dissipative and inertial forces in the system.

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According to the acoustic fluidization hypothesis, elastic waves at a characteristic frequency form inside seismic faults even in the absence of an external perturbation. These waves are able to generate a normal stress which contrasts the confining pressure and promotes failure. Here, we study the mechanisms responsible for this wave activation via numerical simulations of a granular fault model.

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Particle detachment bursts during the flow of suspensions through porous media are a phenomenon that can severely affect the efficiency of deep bed filters. Despite the relevance in several industrial fields, little is known about the statistical properties and the temporal organization of these events. We present experiments of suspensions of deionized water carrying quartz particles pushed with a peristaltic pump through a filter of glass beads measuring simultaneously the pressure drop, flux, and suspension solid fraction.

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Granular materials jam when developing a network of contact forces able to resist the applied stresses. Through numerical simulations of the dynamics of the jamming process, we show that the jamming transition does not occur when the kinetic energy vanishes. Rather, as the system jams, the kinetic energy becomes dominated by rattler particles, which scatter within their cages.

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Recent studies have proposed that the diffusion of messenger molecules, such as monoamines, can mediate the plastic adaptation of synapses in supervised learning of neural networks. Based on these findings we developed a model for neural learning, where the signal for plastic adaptation is assumed to propagate through the extracellular space. We investigate the conditions allowing learning of Boolean rules in a neural network.

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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, constitutes evidence 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.

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Neuronal avalanches measured in vitro and in vivo in different cortical networks consistently exhibit power law behaviour for the size and duration distributions with exponents typical for a mean field self-organized branching process. These exponents are also recovered in neuronal network simulations implementing various neuronal dynamics on different network topologies. They can therefore be considered a very robust feature of spontaneous neuronal activity.

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Ongoing cortical activity consists of sequences of synchronized bursts, named neuronal avalanches, whose size and duration are power law distributed. These features have been observed in a variety of systems and conditions, at all spatial scales, supporting scale invariance, universality and therefore criticality. However, the mechanisms leading to burst triggering, as well as the relationship between bursts and quiescence, are still unclear.

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Aftershocks are the most striking evidence of earthquake interactions and the physical mechanisms at the origin of their occurrence are still intensively debated. Novel insights stem from recent results on the influence of the faulting style on the aftershock organisation in magnitude and time. Our study shows that the size of the aftershock zone depends on the fault geometry.

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