Arda Halu

Connect and win: The role of social networks in political elections

Many networks do not live in isolation but are strongly interacting, with profound consequences on their dynamics. Here, we consider the case of two interacting social networks and, in the context of a simple model, we address the case of political elections. Each network represents a competing party and every agent on the election day can choose to be either active in one of the two networks (vote for the corresponding party) or to be inactive in both (not vote). The opinion dynamics during the election campaign is described through a simulated annealing algorithm. We find that for a large region of the parameter space the result of the competition between the two parties allows for the existence of pluralism in the society, where both parties have a finite share of the votes. The central result is that a densely connected social network is key for the final victory of a party. However, small committed minorities can play a crucial role, and even reverse the election outcome.

Emergence of overlap in ensembles of spatial multiplexes and statistical mechanics of spatial interacting network ensembles.

Spatial networks range from the brain networks, to transportation networks and infrastructures. Recently interacting and multiplex networks are attracting great attention because their dynamics and robustness cannot be understood without treating at the same time several networks. Here we present maximal entropy ensembles of spatial multiplex and spatial interacting networks that can be used in order to model spatial multilayer network structures and to build null models of real data sets. We show that spatial multiplexes naturally develop a significant overlap of the links, a noticeable property of many multiplexes that can affect significantly the dynamics taking place on them. Additionally, we characterize ensembles of spatial interacting networks and we analyze the structure of interacting airport and railway networks in India, showing the effect of space in determining the link probability.

PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation.

Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that PARP9 and PARP14 regulate macrophage activation. In primary macrophages, PARP9 and PARP14 have opposing roles in macrophage activation. PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells, whereas it suppresses anti-inflammatory gene expression and STAT6 phosphorylation in M(IL-4) cells. PARP9 silencing suppresses pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells. PARP14 induces ADP-ribosylation of STAT1, which is suppressed by PARP9. Mutations at these ADP-ribosylation sites lead to increased phosphorylation. Network analysis links PARP9–PARP14 with human coronary artery disease. PARP14 deficiency in haematopoietic cells accelerates the development and inflammatory burden of acute and chronic arterial lesions in mice. These findings suggest that PARP9 and PARP14 cross-regulate macrophage activation.

Data-driven modeling of solar-powered urban microgrids

A modeling framework for citywide solar microgrids with real hourly consumption, and the interplay between spatial costs and resilience. Distributed generation takes center stage in today’s rapidly changing energy landscape. Particularly, locally matching demand and generation in the form of microgrids is becoming a promising alternative to the central distribution paradigm. Infrastructure networks have long been a major focus of complex networks research with their spatial considerations. We present a systemic study of solar-powered microgrids in the urban context, obeying real hourly consumption patterns and spatial constraints of the city. We propose a microgrid model and study its citywide implementation, identifying the self-sufficiency and temporal properties of microgrids. Using a simple optimization scheme, we find microgrid configurations that result in increased resilience under cost constraints. We characterize load-related failures solving power flows in the networks, and we show the robustness behavior of urban microgrids with respect to optimization using percolation methods. Our findings hint at the existence of an optimal balance between cost and robustness in urban microgrids.

Phase diagram of the Bose-Hubbard model on complex networks

Critical phenomena can show unusual phase diagrams when defined in complex network topologies. The case of classical phase transitions such as the classical Ising model and the percolation transition has been studied extensively in the last decade. Here we show that the phase diagram of the Bose-Hubbard model, an exclusively quantum mechanical phase transition, also changes significantly when defined on random scale-free networks. We present a mean-field calculation of the model in annealed networks and we show that when the second moment of the average degree diverges, the Mott-insulator phase disappears in the thermodynamic limit. Moreover we study the model on quenched networks and we show that the Mott-insulator phase disappears in the thermodynamic limit as long as the maximal eigenvalue of the adjacency matrix diverges. Finally we study the phase diagram of the model on Apollonian scale-free networks that can be embedded in 2 dimensions showing the extension of the results also to this case.

Phase transition of light on complex quantum networks.

Recent advances in quantum optics and atomic physics allow for an unprecedented level of control over light-matter interactions, which can be exploited to investigate new physical phenomena. In this work we are interested in the role played by the topology of quantum networks describing coupled optical cavities and local atomic degrees of freedom. In particular, using a mean-field approximation, we study the phase diagram of the Jaynes-Cummings-Hubbard model on complex networks topologies, and we characterize the transition between a Mott-like phase of localized polaritons and a superfluid phase. We found that, for complex topologies, the phase diagram is nontrivial and well defined in the thermodynamic limit only if the hopping coefficient scales like the inverse of the maximal eigenvalue of the adjacency matrix of the network. Furthermore we provide numerical evidences that, for some complex network topologies, this scaling implies an asymptotically vanishing hopping coefficient in the limit of large network sizes. The latter result suggests the interesting possibility of observing quantum phase transitions of light on complex quantum networks even with very small couplings between the optical cavities.

Entropy rate of nonequilibrium growing networks

New entropy measures have been recently introduced for the quantification of the complexity of networks. Most of these entropy measures apply to static networks or to dynamical processes defined on static complex networks. In this paper we define the entropy rate of growing network models. This entropy rate quantifies how many labeled networks are typically generated by the growing network models. We analytically evaluate the difference between the entropy rate of growing tree network models and the entropy of tree networks that have the same asymptotic degree distribution. We find that the growing networks with linear preferential attachment generated by dynamical models are exponentially less than the static networks with the same degree distribution for a large variety of relevant growing network models. We study the entropy rate for growing network models showing structural phase transitions including models with nonlinear preferential attachment. Finally, we bring numerical evidence that the entropy rate above and below the structural phase transitions follows a different scaling with the network size.

A Systems Approach to Refine Disease Taxonomy by Integrating Phenotypic and Molecular Networks

The International Classification of Diseases (ICD) relies on clinical features and lags behind the current understanding of the molecular specificity of disease pathobiology, necessitating approaches that incorporate growing biomedical data for classifying diseases to meet the needs of precision medicine. Our analysis revealed that the heterogeneous molecular diversity of disease chapters and the blurred boundary between disease categories in ICD should be further investigated. Here, we propose a new classification of diseases (NCD) by developing an algorithm that predicts the additional categories of a disease by integrating multiple networks consisting of disease phenotypes and their molecular profiles. With statistical validations from phenotype-genotype associations and interactome networks, we demonstrate that NCD improves disease specificity owing to its overlapping categories and polyhierarchical structure. Furthermore, NCD captures the molecular diversity of diseases and defines clearer boundaries in terms of both phenotypic similarity and molecular associations, establishing a rational strategy to reform disease taxonomy.

Spatiotemporal Multi-omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease

Background: No pharmacological therapy exists for calcific aortic valve disease (CAVD), which confers a dismal prognosis without invasive valve replacement. The search for therapeutics and early diagnostics is challenging because CAVD presents in multiple pathological stages. Moreover, it occurs in the context of a complex, multi-layered tissue architecture; a rich and abundant extracellular matrix phenotype; and a unique, highly plastic, and multipotent resident cell population. Methods: A total of 25 human stenotic aortic valves obtained from valve replacement surgeries were analyzed by multiple modalities, including transcriptomics and global unlabeled and label-based tandem-mass-tagged proteomics. Segmentation of valves into disease stage–specific samples was guided by near-infrared molecular imaging, and anatomic layer-specificity was facilitated by laser capture microdissection. Side-specific cell cultures were subjected to multiple calcifying stimuli, and their calcification potential and basal/stimulated proteomes were evaluated. Molecular (protein–protein) interaction networks were built, and their central proteins and disease associations were identified. Results: Global transcriptional and protein expression signatures differed between the nondiseased, fibrotic, and calcific stages of CAVD. Anatomic aortic valve microlayers exhibited unique proteome profiles that were maintained throughout disease progression and identified glial fibrillary acidic protein as a specific marker of valvular interstitial cells from the spongiosa layer. CAVD disease progression was marked by an emergence of smooth muscle cell activation, inflammation, and calcification-related pathways. Proteins overrepresented in the disease-prone fibrosa are functionally annotated to fibrosis and calcification pathways, and we found that in vitro, fibrosa-derived valvular interstitial cells demonstrated greater calcification potential than those from the ventricularis. These studies confirmed that the microlayer-specific proteome was preserved in cultured valvular interstitial cells, and that valvular interstitial cells exposed to alkaline phosphatase–dependent and alkaline phosphatase–independent calcifying stimuli had distinct proteome profiles, both of which overlapped with that of the whole tissue. Analysis of protein–protein interaction networks found a significant closeness to multiple inflammatory and fibrotic diseases. Conclusions: A spatially and temporally resolved multi-omics, and network and systems biology strategy identifies the first molecular regulatory networks in CAVD, a cardiac condition without a pharmacological cure, and describes a novel means of systematic disease ontology that is broadly applicable to comprehensive omics studies of cardiovascular diseases.

Monochromaticity in neutral evolutionary network models.

Recent studies on epistatic networks of model organisms have unveiled a certain type of modular property called monochromaticity in which the networks are clustered into functional modules that interact with each other through the same type of epistasis. Here, we propose and study three epistatic network models that are inspired by the duplication-divergence mechanism to gain insight into the evolutionary basis of monochromaticity and to test if it can be explained as the outcome of a neutral evolutionary hypothesis. We show that the epistatic networks formed by these stochastic evolutionary models have monochromaticity conflict distributions that are centered close to zero and are statistically significantly different from their randomized counterparts. In particular, the last model we propose yields a strictly monochromatic solution. Our results agree with the monochromaticity findings in real organisms and point toward the possible role of a neutral mechanism in the evolution of this phenomenon.