The dynamics of power-grid networks is becoming an increasingly active area of research within the physics and network science communities. The results from such studies are typically insightful and illustrative, but are often based on simplifying as
sumptions that can be either difficult to assess or not fully justified for realistic applications. Here we perform a comprehensive comparative analysis of three leading models recently used to study synchronization dynamics in power-grid networks -- a fundamental problem of practical significance given that frequency synchronization of all power generators in the same interconnection is a necessary condition for a power grid to operate. We show that each of these models can be derived from first principles within a common framework based on the classical model of a generator, thereby clarifying all assumptions involved. This framework allows us to view power grids as complex networks of coupled second-order phase oscillators with both forcing and damping terms. Using simple illustrative examples, test systems, and real power-grid datasets, we study the inherent frequencies of the oscillators as well as their coupling structure, comparing across the different models. We demonstrate, in particular, that if the network structure is not homogeneous, generators with identical parameters need to be modeled as non-identical oscillators in general. We also discuss an approach to estimate the required (dynamical) parameters that are unavailable in typical power-grid datasets, their use for computing the constants of each of the three models, and an open-source MATLAB toolbox that we provide for these computations.
An imperative condition for the functioning of a power-grid network is that its power generators remain synchronized. Disturbances can prompt desynchronization, which is a process that has been involved in large power outages. Here we derive a condit
ion under which the desired synchronous state of a power grid is stable, and use this condition to identify tunable parameters of the generators that are determinants of spontaneous synchronization. Our analysis gives rise to an approach to specify parameter assignments that can enhance synchronization of any given network, which we demonstrate for a selection of both test systems and real power grids. Because our results concern spontaneous synchronization, they are relevant both for reducing dependence on conventional control devices, thus offering an additional layer of protection given that most power outages involve equipment or operational errors, and for contributing to the development of smart grids that can recover from failures in real time.
The metabolic network of a living cell involves several hundreds or thousands of interconnected biochemical reactions. Previous research has shown that under realistic conditions only a fraction of these reactions is concurrently active in any given
cell. This is partially determined by nutrient availability, but is also strongly dependent on the metabolic function and network structure. Here, we establish rigorous bounds showing that the fraction of active reactions is smaller (rather than larger) in metabolic networks evolved or engineered to optimize a specific metabolic task, and we show that this is largely determined by the presence of thermodynamically irreversible reactions in the network. We also show that the inactivation of a certain number of reactions determined by irreversibility can generate a cascade of secondary reaction inactivations that propagates through the network. The mathematical results are complemented with numerical simulations of the metabolic networks of the bacterium Escherichia coli and of human cells, which show, counterintuitively, that even the maximization of the total reaction flux in the network leads to a reduced number of active reactions.
To understand the formation, evolution, and function of complex systems, it is crucial to understand the internal organization of their interaction networks. Partly due to the impossibility of visualizing large complex networks, resolving network str
ucture remains a challenging problem. Here we overcome this difficulty by combining the visual pattern recognition ability of humans with the high processing speed of computers to develop an exploratory method for discovering groups of nodes characterized by common network properties, including but not limited to communities of densely connected nodes. Without any prior information about the nature of the groups, the method simultaneously identifies the number of groups, the group assignment, and the properties that define these groups. The results of applying our method to real networks suggest the possibility that most group structures lurk undiscovered in the fast-growing inventory of social, biological, and technological networks of scientific interest.
Synchronization, in which individual dynamical units keep in pace with each other in a decentralized fashion, depends both on the dynamical units and on the properties of the interaction network. Yet, the role played by the network has resisted compr
ehensive characterization within the prevailing paradigm that interactions facilitating pair-wise synchronization also facilitate collective synchronization. Here we challenge this paradigm and show that networks with best complete synchronization, least coupling cost, and maximum dynamical robustness, have arbitrary complexity but quantized total interaction strength that constrains the allowed number of connections. It stems from this characterization that negative interactions as well as link removals can be used to systematically improve and optimize synchronization properties in both directed and undirected networks. These results extend the recently discovered compensatory perturbations in metabolic networks to the realm of oscillator networks and demonstrate why less can be more in network synchronization.
Metabolic reactions of single-cell organisms are routinely observed to become dispensable or even incapable of carrying activity under certain circumstances. Yet, the mechanisms as well as the range of conditions and phenotypes associated with this b
ehavior remain very poorly understood. Here we predict computationally and analytically that any organism evolving to maximize growth rate, ATP production, or any other linear function of metabolic fluxes tends to significantly reduce the number of active metabolic reactions compared to typical non-optimal states. The reduced number appears to be constant across the microbial species studied and just slightly larger than the minimum number required for the organism to grow at all. We show that this massive spontaneous reaction silencing is triggered by the irreversibility of a large fraction of the metabolic reactions and propagates through the network as a cascade of inactivity. Our results help explain existing experimental data on intracellular flux measurements and the usage of latent pathways, shedding new light on microbial evolution, robustness, and versatility for the execution of specific biochemical tasks. In particular, the identification of optimal reaction activity provides rigorous ground for an intriguing knockout-based method recently proposed for the synthetic recovery of metabolic function.
Previous work on undirected small-world networks established the paradigm that locally structured networks tend to have high density of short loops. On the other hand, many realistic networks are directed. Here we investigate the local organization o
f directed networks and find, surprisingly, that real networks often have very few short loops as compared to random models. We develop a theory and derive conditions for determining if a given network has more or less loops than its randomized counterpart. These findings carry broad implications for structural and dynamical processes sustained by directed networks.
An important goal of medical research is to develop methods to recover the loss of cellular function due to mutations and other defects. Many approaches based on gene therapy aim to repair the defective gene or to insert genes with compensatory funct
ion. Here, we propose an alternative, network-based strategy that aims to restore biological function by forcing the cell to either bypass the functions affected by the defective gene, or to compensate for the lost function. Focusing on the metabolism of single-cell organisms, we computationally study mutants that lack an essential enzyme, and thus are unable to grow or have a significantly reduced growth rate. We show that several of these mutants can be turned into viable organisms through additional gene deletions that restore their growth rate. In a rather counterintuitive fashion, this is achieved via additional damage to the metabolic network. Using flux balance-based approaches, we identify a number of synthetically viable gene pairs, in which the removal of one enzyme-encoding gene results in a nonviable phenotype, while the deletion of a second enzyme-encoding gene rescues the organism. The systematic network-based identification of compensatory rescue effects may open new avenues for genetic interventions.
