Bifractality of fractal scale-free networks.

The presence of large-scale real-world networks with various architectures has motivated active research towards a unified understanding of diverse topologies of networks. Such studies have revealed that many networks with scale-free and fractal properties exhibit the structural multifractality, some of which are actually bifractal. Bifractality is a particular case of the multifractal property, where only two local fractal dimensions d_{f}^{min} and d_{f}^{max}(>d_{f}^{min}) suffice to explain the structural inhomogeneity of a network. In this work we investigate analytically and numerically the multifractal property of a wide range of fractal scale-free networks (FSFNs) including deterministic hierarchical, stochastic hierarchical, nonhierarchical, and real-world FSFNs. Then we demonstrate how commonly FSFNs exhibit the bifractal property. The results show that all these networks possess the bifractal nature. We conjecture from our findings that any FSFN is bifractal. Furthermore, we find that in the thermodynamic limit the lower local fractal dimension d_{f}^{min} describes substructures around infinitely high-degree hub nodes and finite-degree nodes at finite distances from these hub nodes, whereas d_{f}^{max} characterizes local fractality around finite-degree nodes infinitely far from the infinite-degree hub nodes. Since the bifractal nature of FSFNs may strongly influence time-dependent phenomena on FSFNs, our results will be useful for understanding dynamics such as information diffusion and synchronization on FSFNs from a unified perspective.

A general model of hierarchical fractal scale-free networks.

We propose a general model of unweighted and undirected networks having the scale-free property and fractal nature. Unlike the existing models of fractal scale-free networks (FSFNs), the present model can systematically and widely change the network structure. In this model, an FSFN is iteratively formed by replacing each edge in the previous generation network with a small graph called a generator. The choice of generators enables us to control the scale-free property, fractality, and other structural properties of hierarchical FSFNs. We calculate theoretically various characteristic quantities of networks, such as the exponent of the power-law degree distribution, fractal dimension, average clustering coefficient, global clustering coefficient, and joint probability describing the nearest-neighbor degree correlation. As an example of analyses of phenomena occurring on FSFNs, we also present the critical point and critical exponents of the bond-percolation transition on infinite FSFNs, which is related to the robustness of networks against edge removal. By comparing the percolation critical points of FSFNs whose structural properties are the same as each other except for the clustering nature, we clarify the effect of the clustering on the robustness of FSFNs. As demonstrated by this example, the present model makes it possible to elucidate how a specific structural property influences a phenomenon occurring on FSFNs by varying systematically the structures of FSFNs. Finally, we extend our model for deterministic FSFNs to a model of non-deterministic ones by introducing asymmetric generators and reexamine all characteristic quantities and the percolation problem for such non-deterministic FSFNs.

Identification of intrinsic long-range degree correlations in complex networks.

Many real-world networks exhibit degree-degree correlations between nodes separated by more than one step. Such long-range degree correlations (LRDCs) can be fully described by one joint and four conditional probability distributions with respect to degrees of two randomly chosen nodes and shortest path distance between them. While LRDCs are induced by nearest-neighbor degree correlations (NNDCs) between adjacent nodes, some networks possess intrinsic LRDCs which cannot be generated by NNDCs. Here we develop a method to extract intrinsic LRDC in a correlated network by comparing the probability distributions for the given network with those for nearest-neighbor correlated random networks. We also demonstrate the utility of our method by applying it to several real-world networks.

General formulation of long-range degree correlations in complex networks.

We provide a general framework for analyzing degree correlations between nodes separated by more than one step (i.e., beyond nearest neighbors) in complex networks. One joint and four conditional probability distributions are introduced to fully describe long-range degree correlations with respect to degrees k and k^{'} of two nodes and shortest path length l between them. We present general relations among these probability distributions and clarify the relevance to nearest-neighbor degree correlations. Unlike nearest-neighbor correlations, some of these probability distributions are meaningful only in finite-size networks. Furthermore, as a baseline to determine the existence of intrinsic long-range degree correlations in a network other than inevitable correlations caused by the finite-size effect, the functional forms of these probability distributions for random networks are analytically evaluated within a mean-field approximation. The utility of our argument is demonstrated by applying it to real-world networks.

Structural instability of large-scale functional networks.

We study how large functional networks can grow stably under possible cascading overload failures and evaluated the maximum stable network size above which even a small-scale failure would cause a fatal breakdown of the network. Employing a model of cascading failures induced by temporally fluctuating loads, the maximum stable size nmax has been calculated as a function of the load reduction parameter r that characterizes how quickly the total load is reduced during the cascade. If we reduce the total load sufficiently fast (r ≥ rc), the network can grow infinitely. Otherwise, nmax is finite and increases with r. For a fixed r(< rc), nmax for a scale-free network is larger than that for an exponential network with the same average degree. We also discuss how one detects and avoids the crisis of a fatal breakdown of the network from the relation between the sizes of the initial network and the largest component after an ordinarily occurring cascading failure.

Robustness of scale-free networks to cascading failures induced by fluctuating loads.

Taking into account the fact that overload failures in real-world functional networks are usually caused by extreme values of temporally fluctuating loads that exceed the allowable range, we study the robustness of scale-free networks against cascading overload failures induced by fluctuating loads. In our model, loads are described by random walkers moving on a network and a node fails when the number of walkers on the node is beyond the node capacity. Our results obtained by using the generating function method show that scale-free networks are more robust against cascading overload failures than Erdos-Rényi random graphs with homogeneous degree distributions. This conclusion is contrary to that predicted by previous works, which neglect the effect of fluctuations of loads.

Catalytic reaction dynamics in inhomogeneous networks.

Biochemical reactions in a cell can be modeled by a catalytic reaction network (CRN). It has been reported that catalytic chain reactions occur intermittently in the CRN with a homogeneous random-graph topology and its avalanche-size distribution obeys a power law with the exponent 4/3 [A. Awazu and K. Kaneko, Phys. Rev. E 80, 010902(R) (2009)]. This fact indicates that the catalytic reaction dynamics in homogeneous CRNs exhibits self-organized criticality (SOC). Structures of actual CRNs are, however, known to be highly inhomogeneous. We study the influence of various types of inhomogeneities found in real-world metabolic networks on the universality class of SOC. Our numerical results clarify that SOC keeps its universality class even for networks possessing structural inhomogeneities such as the scale-free property, community structures, and degree correlations. In contrast, if the CRN has inhomogeneous catalytic functionality, the universality class of SOC depends on how widely distributed the number of reaction paths catalyzed by a single chemical species is.

Structural robustness of scale-free networks against overload failures.

We study the structural robustness of scale-free networks against overload failures induced by loads exceeding the node capacity, based on analytical and numerical approaches to the percolation problem in which a fixed number of nodes are removed according to the overload probability. Modeling fluctuating loads by random walkers in a network, we find that the degree dependence of the overload probability drastically changes with respect to the total load. We also elucidate that there exist two types of structural robustness of networks against overload failures. One is measured by the critical total load W(c) and the other is by the critical node removal fraction f(c). Enhancing the scale-free property, networks become fragile in both senses of W(c) and f(c). By contrast, increasing the node tolerance, scale-free networks become robust in the sense of the critical total load, while they come to be fragile in the sense of the critical node removal fraction. Furthermore, we show that these trends are not affected by degree-degree correlations, although assortative mixing makes networks robust in both senses of W(c) and f(c).

Multifractality of complex networks.

We demonstrate analytically and numerically the possibility that the fractal property of a scale-free network cannot be characterized by a unique fractal dimension and the network takes a multifractal structure. It is found that the mass exponents τ(q) for several deterministic, stochastic, and real-world fractal scale-free networks are nonlinear functions of q, which implies that structural measures of these networks obey the multifractal scaling. In addition, we give a general expression of τ(q) for some class of fractal scale-free networks by a mean-field approximation. The multifractal property of network structures is a consequence of large fluctuations of local node density in scale-free networks.

Topological factors in placental surface arteries correlate with neonatal birth weight.

OBJECTIVES: There has been no study concerning association between topological factors of placental vascularization and neonatal growth in humans. The aim of study was to assess whether any network index of placental surface arteries was associated with neonatal birth weight. MATERIALS AND METHODS: Twenty-six placentas were randomly selected between 34 and 41 weeks of gestational ages. Placental weights ranged 385 to 770 g; and neonatal weights ranged 1960 to 3680 g. After visualization of placental surface arteries by a milk injection method, network indices including the number of nodes, network density, network diameter, average distance of nodes, and the degree centralization were determined. These network indices and placental weights were compared with neonatal birth weights. RESULTS: The number of nodes, network density, network diameter, average distance of nodes, and the degree centralization were found to be as follows (Mean +/- SD); 84.7 +/- 29.3, 0.0262 +/- 0.0088, 15.8 +/- 2.77, 7.83 +/- 1.13, 0.0263 +/- 0.0091, respectively. We found that neonatal birth weights correlated with the number of nodes of placental surface arteries (correlation coefficient R = 0.40) and placental weights (R = 0.52) both. However, the number of nodes of placental surface arteries was not associated with the placental weights or the gestational age. CONCLUSIONS: We for the first time found that a topological factor, i.e., the number of nodes of placental surface arteries correlated with neonatal growth. There was no correlation between numbers of nodes and placental weights. This suggests that the number of nodes affects fetal growth independent of placental weights. A topological factor of placental vascularization might significantly affect fetal growth in utero and determine risks of vascular diseases in their future lives.