Lazaros K. Gallos

Identification of influential spreaders in complex networks

Spreading of information, ideas or diseases can be conveniently modelled in the context of complex networks. An analysis now reveals that the most efficient spreaders are not always necessarily the most connected agents in a network. Instead, the position of an agent relative to the hierarchical topological organization of the network might be as important as its connectivity.

A small world of weak ties provides optimal global integration of self-similar modules in functional brain networks

The human brain is organized in functional modules. Such an organization presents a basic conundrum: Modules ought to be sufficiently independent to guarantee functional specialization and sufficiently connected to bind multiple processors for efficient information transfer. It is commonly accepted that small-world architecture of short paths and large local clustering may solve this problem. However, there is intrinsic tension between shortcuts generating small worlds and the persistence of modularity, a global property unrelated to local clustering. Here, we present a possible solution to this puzzle. We first show that a modified percolation theory can define a set of hierarchically organized modules made of strong links in functional brain networks. These modules are “large-world” self-similar structures and, therefore, are far from being small-world. However, incorporating weaker ties to the network converts it into a small world preserving an underlying backbone of well-defined modules. Remarkably, weak ties are precisely organized as predicted by theory maximizing information transfer with minimal wiring cost. This trade-off architecture is reminiscent of the “strength of weak ties” crucial concept of social networks. Such a design suggests a natural solution to the paradox of efficient information flow in the highly modular structure of the brain.

Stability and Topology of Scale-Free Networks under Attack and Defense Strategies

We study tolerance and topology of random scale-free networks under attack and defense strategies that depend on the degree k of the nodes. This situation occurs, for example, when the robustness of a node depends on its degree or in an intentional attack with insufficient knowledge of the network. We determine, for all strategies, the critical fraction p(c) of nodes that must be removed for disintegrating the network. We find that, for an intentional attack, little knowledge of the well-connected sites is sufficient to strongly reduce p(c). At criticality, the topology of the network depends on the removal strategy, implying that different strategies may lead to different kinds of percolation transitions.

How to calculate the fractal dimension of a complex network: the box covering algorithm

Covering a network with the minimum possible number of boxes can reveal interesting features for the network structure, especially in terms of self-similar or fractal characteristics. Considerable attention has been recently devoted to this problem, with the finding that many real networks are self-similar fractals. Here we present, compare and study in detail a number of algorithms that we have used in previous papers towards this goal. We show that this problem can be mapped to the well-known graph colouring problem and then we simply can apply well-established algorithms. This seems to be the most efficient method, but we also present two other algorithms based on burning which provide a number of other benefits. We argue that the algorithms presented provide a solution close to optimal and that another algorithm that can significantly improve this result in an efficient way does not exist. We offer to anyone that finds such a method to cover his/her expenses for a one-week trip to our lab in New York (details in http://jamlab.org).

Scaling theory of transport in complex biological networks

Transport is an important function in many network systems and understanding its behavior on biological, social, and technological networks is crucial for a wide range of applications. However, it is a property that is not well understood in these systems, probably because of the lack of a general theoretical framework. Here, based on the finding that renormalization can be applied to bionetworks, we develop a scaling theory of transport in self-similar networks. We demonstrate the networks invariance under length scale renormalization, and we show that the problem of transport can be characterized in terms of a set of critical exponents. The scaling theory allows us to determine the influence of the modular structure on transport in metabolic and protein-interaction networks. We also generalize our theory by presenting and verifying scaling arguments for the dependence of transport on microscopic features, such as the degree of the nodes and the distance between them. Using transport concepts such as diffusion and resistance, we exploit this invariance, and we are able to explain, based on the topology of the network, recent experimental results on the broad flow distribution in metabolic networks.

Improving immunization strategies.

We introduce an immunization method where the percentage of required vaccinations for immunity are close to the optimal value of a targeted immunization scheme of highest degree nodes. Our strategy retains the advantage of being purely local, without the need for knowledge on the global network structure or identification of the highest degree nodes. The method consists of selecting a random node and asking for a neighbor that has more links than himself or more than a given threshold and immunizing him. We compare this method to other efficient strategies on three real social networks and on a scale-free network model and find it to be significantly more effective.

The Effect of Disease-Induced Mortality on Structural Network Properties

As the understanding of the importance of social contact networks in the spread of infectious diseases has increased, so has the interest in understanding the feedback process of the disease altering the social network. While many studies have explored the influence of individual epidemiological parameters and/or underlying network topologies on the resulting disease dynamics, we here provide a systematic overview of the interactions between these two influences on population-level disease outcomes. We show that the sensitivity of the population-level disease outcomes to the combination of epidemiological parameters that describe the disease are critically dependent on the topological structure of the population’s contact network. We introduce a new metric for assessing disease-driven structural damage to a network as a population-level outcome. Lastly, we discuss how the expected individual-level disease burden is influenced by the complete suite of epidemiological characteristics for the circulating disease and the ongoing process of network compromise. Our results have broad implications for prediction and mitigation of outbreaks in both natural and human populations.

The Conundrum of Functional Brain Networks: Small-World Efficiency or Fractal Modularity

The human brain has been studied at multiple scales, from neurons, circuits, areas with well-defined anatomical and functional boundaries, to large-scale functional networks which mediate coherent cognition. In a recent work, we addressed the problem of the hierarchical organization in the brain through network analysis. Our analysis identified functional brain modules of fractal structure that were inter-connected in a small-world topology. Here, we provide more details on the use of network science tools to elaborate on this behavior. We indicate the importance of using percolation theory to highlight the modular character of the functional brain network. These modules present a fractal, self-similar topology, identified through fractal network methods. When we lower the threshold of correlations to include weaker ties, the network as a whole assumes a small-world character. These weak ties are organized precisely as predicted by theory maximizing information transfer with minimal wiring costs.

Collective behavior in the spatial spreading of obesity.

Obesity prevalence is increasing in many countries at alarming levels. A difficulty in the conception of policies to reverse these trends is the identification of the drivers behind the obesity epidemics. Here, we implement a spatial spreading analysis to investigate whether obesity shows spatial correlations, revealing the effect of collective and global factors acting above individual choices. We find a regularity in the spatial fluctuations of their prevalence revealed by a pattern of scale-free long-range correlations. The fluctuations are anomalous, deviating in a fundamental way from the weaker correlations found in the underlying population distribution indicating the presence of collective behavior, i.e., individual habits may have negligible influence in shaping the patterns of spreading. Interestingly, we find the same scale-free correlations in economic activities associated with food production. These results motivate future interventions to investigate the causality of this relation providing guidance for the implementation of preventive health policies.

Explosive percolation in the human protein homology network

AbstractWe study the explosive character of the percolation transition in a real-world network. We show that the emergence of a spanning cluster in the Human Protein Homology Network (H-PHN) exhibits similar features to an Achlioptas-type process and is markedly different from regular random percolation. The underlying mechanism of this transition can be described by slow-growing clusters that remain isolated until the later stages of the process, when the addition of a small number of links leads to the rapid interconnection of these modules into a giant cluster. Our results indicate that the evolutionary-based process that shapes the topology of the H-PHN through duplication-divergence events may occur in sudden steps, similarly to what is seen in first-order phase transitions.