We study the robustness properties of multiplex networks consisting of multiple layers of distinct types of links, focusing on the role of correlations between degrees of a node in different layers. We use generating function formalism to address various notions of the network robustness relevant to multiplex networks, such as the resilience of ordinary and mutual connectivity under random or targeted node removals, as well as the biconnectivity. We found that correlated coupling can affect the structural robustness of multiplex networks in diverse fashion. For example, for maximally correlated duplex networks, all pairs of nodes in the giant component are connected via at least two independent paths and network structure is highly resilient to random failure. In contrast, anticorrelated duplex networks are on one hand robust against targeted attack on high-degree nodes, but on the other hand they can be vulnerable to random failure.
16 February 2015 in The European Physical Journal B
Elements of networks interact in many ways, so modeling them with graphs requires multiple types of edges (or network layers). Here we show that such multiplex networks are generically more vulnerable to global cascades than simplex networks. We generalize the threshold cascade model [Watts, Proc. Natl. Acad. Sci. USA 99, 5766 (2002)] to multiplex networks, in which a node activates if a sufficiently large fraction of neighbors in any layer are active. We show that both combining layers (i.e., realizing other interactions play a role) and splitting a network into layers (i.e., recognizing distinct kinds of interactions) facilitate cascades. Notably, layers unsusceptible to global cascades can cooperatively achieve them if coupled. On one hand, this suggests fundamental limitations on predicting cascades without full knowledge of a system's multiplexity; on the other hand, it offers feasible means to control cascades by introducing or removing sparse layers in an existing network.
Threshold cascade models have been used to describe the spread of behavior in social networks and cascades of default in financial networks. In some cases, these networks may have multiple kinds of interactions, such as distinct types of social ties or distinct types of financial liabilities; furthermore, nodes may respond in different ways to influence from their neighbors of multiple types. To start to capture such settings in a stylized way, we generalize a threshold cascade model to a multiplex network in which nodes follow one of two response rules: some nodes activate when, in at least one layer, a large enough fraction of neighbors is active, while the other nodes activate when, in all layers, a large enough fraction of neighbors is active. Varying the fractions of nodes following either rule facilitates or inhibits cascades. Near the inhibition regime, global cascades appear discontinuously as the network density increases; however, the cascade grows more slowly over time. This behavior suggests a way in which various collective phenomena in the real world could appear abruptly yet slowly.
12 October 2012 in Briefings in Functional Genomics
Advances in genome-scale molecular biology and molecular genetics have greatly elevated our knowledge on the basic components of human biology and diseases. At the same time, the importance of cellular networks between those biological components is increasingly appreciated. Built upon these recent technological and conceptual advances, a new discipline called the network medicine, an approach to understand human diseases from a network point-of-view, is about to emerge. In this review article, we will survey some recent endeavours along this direction, centred on the concept and applications of the human diseasome and the human disease network. Questions, and partial answers thereof, such as how the connectivity between molecular parts translates into the relationships between the related disorders on a global scale and how central the disease-causing genetic components are in the cellular network, will be discussed. The use of the diseasome in combination with various interactome networks and other disease-related factors is also reviewed.
Distinct channels of interaction in a complex networked system define network layers, which coexist and cooperate for the system's function. Towards understanding such multiplex systems, we propose a modeling framework based on coevolution of network layers, with a class of minimalistic growing network models as working examples. We examine how the entangled growth of coevolving layers can shape the network structure and show analytically and numerically that the coevolution can induce strong degree correlations across layers, as well as modulate degree distributions. We further show that such a coevolution-induced correlated multiplexity can alter the system's response to the dynamical process, exemplified by the suppressed susceptibility to a social cascade process.