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.Comment: (6 pages, 4 figures

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

Many real systems are made of strongly interacting networks, 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

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

Multiplex PageRank

(15 pages, 6 figures

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