Ranking of Nodal Infection Probability in Susceptible-Infected-Susceptible Epidemic.
ABSTRACT: The prevalence, which is the average fraction of infected nodes, has been studied to evaluate the robustness of a network subject to the spread of epidemics. We explore the vulnerability (infection probability) of each node in the metastable state with a given effective infection rate ?. Specifically, we investigate the ranking of the nodal vulnerability subject to a susceptible-infected-susceptible epidemic, motivated by the fact that the ranking can be crucial for a network operator to assess which nodes are more vulnerable. Via both theoretical and numerical approaches, we unveil that the ranking of nodal vulnerability tends to change more significantly as ? varies when ? is smaller or in Barabási-Albert than Erd?s-Rényi random graphs.
Project description:Controllability of complex networks has attracted much attention, and understanding the robustness of network controllability against potential attacks and failures is of practical significance. In this paper, we systematically investigate the attack vulnerability of network controllability for the canonical model networks as well as the real-world networks subject to attacks on nodes and edges. The attack strategies are selected based on degree and betweenness centralities calculated for either the initial network or the current network during the removal, among which random failure is as a comparison. It is found that the node-based strategies are often more harmful to the network controllability than the edge-based ones, and so are the recalculated strategies than their counterparts. The Barabási-Albert scale-free model, which has a highly biased structure, proves to be the most vulnerable of the tested model networks. In contrast, the Erd?s-Rényi random model, which lacks structural bias, exhibits much better robustness to both node-based and edge-based attacks. We also survey the control robustness of 25 real-world networks, and the numerical results show that most real networks are control robust to random node failures, which has not been observed in the model networks. And the recalculated betweenness-based strategy is the most efficient way to harm the controllability of real-world networks. Besides, we find that the edge degree is not a good quantity to measure the importance of an edge in terms of network controllability.
Project description:The vulnerability to real-life networks against small initial attacks has been one of outstanding challenges in the study of interrelated networks. We study cascading failures in two interrelated networks S and B composed from dependency chains and connectivity links respectively. This work proposes a realistic model for cascading failures based on the redistribution of traffic flow. We study the Barabási-Albert networks (BA) and Erdős-Rényi graphs (ER) with such structure, and found that the efficiency sharply decreases with increasing percentages of the dependency nodes for removing a node randomly. Furthermore, we study the robustness of interrelated traffic networks, especially the subway and bus network in Beijing. By analyzing different attacking strategies, we uncover that the efficiency of the city traffic system has a non-equilibrium phase transition at low capacity of the networks. This explains why the pressure of the traffic overload is relaxed by singly increasing the number of small buses during rush hours. We also found that the increment of some buses may release traffic jam caused by removing a node of the bus network randomly if the damage is limited. However, the efficiencies to transfer people flow will sharper increase when the capacity of the subway network α(S) > α0.
Project description:Residue networks representing 595 nonhomologous proteins are studied. These networks exhibit universal topological characteristics as they belong to the topological class of modular networks formed by several highly interconnected clusters separated by topological cavities. There are some networks that tend to deviate from this universality. These networks represent small-size proteins having <200 residues. This article explains such differences in terms of the domain structure of these proteins. On the other hand, the topological cavities characterizing proteins residue networks match very well with protein binding sites. This study investigates the effect of the cutoff value used in building the residue network. For small cutoff values, <5 A, the cavities found are very large corresponding almost to the whole protein surface. On the contrary, for large cutoff value, >10.0 A, only very large cavities are detected and the networks look very homogeneous. These findings are useful for practical purposes as well as for identifying protein-like complex networks. Finally, this article shows that the main topological class of residue networks is not reproduced by random networks growing according to Erdös-Rényi model or the preferential attachment method of Barabási-Albert. However, the Watts-Strogatz model reproduces very well the topological class as well as other topological properties of residue network. A more biologically appealing modification of the Watts-Strogatz model to describe residue networks is proposed.
Project description:A network is scale-free if its connectivity density function is proportional to a power-law distribution. It has been suggested that scale-free networks may provide an explanation for the robustness observed in certain physical and biological phenomena, since the presence of a few highly connected hub nodes and a large number of small-degree nodes may provide alternate paths between any two nodes on average-such robustness has been suggested in studies of metabolic networks, gene interaction networks and protein folding. A theoretical justification for why many networks appear to be scale-free has been provided by Barabási and Albert, who argue that expanding networks, in which new nodes are preferentially attached to highly connected nodes, tend to be scale-free. In this paper, we provide the first efficient algorithm to compute the connectivity density function for the ensemble of all homopolymer secondary structures of a user-specified length-a highly nontrivial result, since the exponential size of such networks precludes their enumeration. Since existent power-law fitting software, such as powerlaw, cannot be used to determine a power-law fit for our exponentially large RNA connectivity data, we also implement efficient code to compute the maximum likelihood estimate for the power-law scaling factor and associated Kolmogorov-Smirnov p value. Hypothesis tests strongly indicate that homopolymer RNA secondary structure networks are not scale-free; moreover, this appears to be the case for real (non-homopolymer) RNA networks.
Project description:Public opinion is often affected by the presence of committed groups of individuals dedicated to competing points of view. Using a model of pairwise social influence, we study how the presence of such groups within social networks affects the outcome and the speed of evolution of the overall opinion on the network. Earlier work indicated that a single committed group within a dense social network can cause the entire network to quickly adopt the group's opinion (in times scaling logarithmically with the network size), so long as the committed group constitutes more than about 10% of the population (with the findings being qualitatively similar for sparse networks as well). Here we study the more general case of opinion evolution when two groups committed to distinct, competing opinions A and B, and constituting fractions pA and pB of the total population respectively, are present in the network. We show for stylized social networks (including Erdös-Rényi random graphs and Barabási-Albert scale-free networks) that the phase diagram of this system in parameter space (pA,pB) consists of two regions, one where two stable steady-states coexist, and the remaining where only a single stable steady-state exists. These two regions are separated by two fold-bifurcation (spinodal) lines which meet tangentially and terminate at a cusp (critical point). We provide further insights to the phase diagram and to the nature of the underlying phase transitions by investigating the model on infinite (mean-field limit), finite complete graphs and finite sparse networks. For the latter case, we also derive the scaling exponent associated with the exponential growth of switching times as a function of the distance from the critical point.
Project description:There has been tremendous development in linear controllability of complex networks. Real-world systems are fundamentally nonlinear. Is linear controllability relevant to nonlinear dynamical networks? We identify a common trait underlying both types of control: the nodal "importance". For nonlinear and linear control, the importance is determined, respectively, by physical/biological considerations and the probability for a node to be in the minimum driver set. We study empirical mutualistic networks and a gene regulatory network, for which the nonlinear nodal importance can be quantified by the ability of individual nodes to restore the system from the aftermath of a tipping-point transition. We find that the nodal importance ranking for nonlinear and linear control exhibits opposite trends: for the former large-degree nodes are more important but for the latter, the importance scale is tilted towards the small-degree nodes, suggesting strongly the irrelevance of linear controllability to these systems. The recent claim of successful application of linear controllability to Caenorhabditis elegans connectome is examined and discussed.
Project description:Models of the spread of disease in a population often make the simplifying assumption that the population is homogeneously mixed, or is divided into homogeneously mixed compartments. However, human populations have complex structures formed by social contacts, which can have a significant influence on the rate of epidemic spread. Contact network models capture this structure by explicitly representing each contact which could possibly lead to a transmission. We developed a method based on approximate Bayesian computation (ABC), a likelihood-free inference strategy, for estimating structural parameters of the contact network underlying an observed viral phylogeny. The method combines adaptive sequential Monte Carlo for ABC, Gillespie simulation for propagating epidemics though networks, and a kernel-based tree similarity score. We used the method to fit the Barabási-Albert network model to simulated transmission trees, and also applied it to viral phylogenies estimated from ten published HIV sequence datasets. This model incorporates a feature called preferential attachment (PA), whereby individuals with more existing contacts accumulate new contacts at a higher rate. On simulated data, we found that the strength of PA and the number of infected nodes in the network can often be accurately estimated. On the other hand, the mean degree of the network, as well as the total number of nodes, was not estimable with ABC. We observed sub-linear PA power in all datasets, as well as higher PA power in networks of injection drug users. These results underscore the importance of considering contact structures when performing phylodynamic inference. Our method offers the potential to quantitatively investigate the contact network structure underlying viral epidemics.
Project description:We study the controllability of networks in the process of cascading failures under two different attacking strategies, random and intentional attack, respectively. For the highest-load edge attack, it is found that the controllability of Erd?s-Rényi network, that with moderate average degree, is less robust, whereas the Scale-free network with moderate power-law exponent shows strong robustness of controllability under the same attack strategy. The vulnerability of controllability under random and intentional attacks behave differently with the increasing of removal fraction, especially, we find that the robustness of control has important role in cascades for large removal fraction. The simulation results show that for Scale-free networks with various power-law exponents, the network has larger scale of cascades do not mean that there will be more increments of driver nodes. Meanwhile, the number of driver nodes in cascading failures is also related to the edges amount in strongly connected components.
Project description:A model algorithm is proposed to imitate a series of of consecutive conflicts between leaders in social groups. The leaders are represented by local hubs, i.e., nodes with highest node degrees. We simulate subsequent hierarchical partitions of a complex connected network which represents a social structure. The partitions are supposed to appear as actions of members of two conflicted groups surrounding two strongest leaders. According to the model, links at the shortest path between the rival leaders are successively removed. When the group is split into two disjoint parts then each part is further divided as the initial network. The algorithm is stopped, if in all parts a distance from a local leader to any node in his group is shorter than three links. The numerically calculated size distribution of resulting fragments of scale-free Barabási-Albert networks reveals one largest fragment which contains the original leader (hub of the network) and a number of small fragments with opponents that are described by two Weibull distributions. A mean field calculation of the size of the largest fragment is in a good agreement with numerical results. The model assumptions are validated by an application of the algorithm to the data on political blogs in U.S. (L. Adamic and N. Glance, Proc. WWW-2005). The obtained fragments are clearly polarized; either they belong to Democrats, or to Republicans. This result confirms that during conflicts, hubs are centers of polarization.
Project description:BACKGROUND:Childhood maltreatment is a major risk factor for psychopathology. However, some maltreated individuals appear remarkably resilient to the psychiatric effects while manifesting the same array of brain abnormalities as maltreated individuals with psychopathology. Hence, a critical aim is to identify compensatory brain alterations that enable resilient individuals to maintain mental well-being despite alterations in stress-susceptible regions. METHODS:Network models were constructed from diffusion tensor imaging and tractography in physically healthy unmedicated 18- to 25-year-old participants (N = 342, n = 192 maltreated) to develop network-based explanatory models. RESULTS:First, we determined that susceptible and resilient individuals had the same alterations in global fiber stream network architecture using two different definitions of resilience: 1) no lifetime history of Axis I or II disorders, and 2) no clinically significant symptoms of anxiety, depression, anger-hostility, or somatization. Second, we confirmed an a priori hypothesis that right amygdala nodal efficiency was lower in asymptomatic resilient than in susceptible participants or control subjects. Third, we identified eight other nodes with reduced nodal efficiency in resilient individuals and showed that nodal efficiency moderated the relationship between maltreatment and psychopathology. Fourth, we found that models based on global network architecture and nodal efficiency could delineate group membership (control, susceptible, resilient) with 75%, 82%, and 80% cross-validated accuracy. CONCLUSIONS:Together these findings suggest that sparse fiber networks with increased small-worldness following maltreatment render individuals vulnerable to psychopathology if abnormalities occur in specific nodes, but that decreased ability of certain nodes to propagate information throughout the network mitigates the effects and leads to resilience.