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Societies are complex systems which tend to polarize into sub-groups of individuals with dramatically opposite perspectives. This phenomenon is reflected -- and often amplified -- in online social networks where, however, humans are no more the only players, and co-exist alongside with social bots, i.e., software-controlled accounts. Analyzing large-scale social data collected during the Catalan referendum for independence on October 1, 2017, consisting of nearly 4 millions Twitter posts generated by almost 1 million users, we identify the two polarized groups of Independentists and Constitutionalists and quantify the structural and emotional roles played by social bots. We show that bots act from peripheral areas of the social system to target influential humans of both groups, bombarding Independentists with violent contents, increasing their exposure to negative and inflammatory narratives and exacerbating social conflict online. Our findings stress the importance of developing countermeasures to unmask these forms of automated social manipulation., Comment: 8 pages, 5 figures

Assessing the navigability of interconnected networks (transporting information, people, or goods) under eventual random failures is of utmost importance to design and protect critical infrastructures. Random walks are a good proxy to determine this navigability, specifically the coverage time of random walks, which is a measure of the dynamical functionality of the network. Here, we introduce the theoretical tools required to describe random walks in interconnected networks accounting for structure and dynamics inherent to real systems. We develop an analytical approach for the covering time of random walks in interconnected networks and compare it with extensive Monte Carlo simulations. Generally speaking, interconnected networks are more resilient to random failures than their individual layers per se, and we are able to quantify this effect. As an application––which we illustrate by considering the public transport of London––we show how the efficiency in exploring the multiplex critically depends on layers’ topology, interconnection strengths, and walk strategy. Our findings are corroborated by data-driven simulations, where the empirical distribution of check-ins and checks-out is considered and passengers travel along fastest paths in a network affected by real disruptions. These findings are fundamental for further development of searching and navigability strategies in real interconnected systems.

Hepcidin is a hormone secreted in response to iron loading and inflammation. Hepcidin binds to the iron exporter ferroportin, inducing its degradation and thus preventing iron entry into plasma. We determined that hepcidin binding to ferroportin leads to the binding and activation of the protein Janus Kinase2 (Jak2), which is required for phosphorylation of ferroportin. Ferroportin is a dimer and both monomers must be capable of binding hepcidin for Jak2 to bind to ferroportin. Once Jak2 is bound to the ferroportin dimer, both ferroportin monomers must be functionally competent to activate Jak2 and for ferroportin to be phosphorylated. These results show that cooperativity between the ferroportin monomers is required for hepcidin-mediated Jak2 activation and ferroportin down-regulation. These results provide a molecular explanation for the dominant inheritance of hepcidin resistant iron overload disease.

Angiogenesis, the synthesis of new blood vessels from preexisting vessels, plays a critical role in normal wound healing and tumor growth. HKa (cleaved high molecular weight kininogen) is an endogenous inhibitor of angiogenesis formed by the cleavage of kininogen on endothelial cells. Ferritin is a protein principally known for its central role in iron storage. Here, we demonstrate that ferritin binds to HKa with high affinity (Kd 13 nM). Further, ferritin antagonizes the antiangiogenic effects of HKa, enhancing the migration, assembly, and survival of HKa-treated endothelial cells. Effects of ferritin were independent of its iron content. Peptide mapping revealed that ferritin binds to a 22-aa subdomain of HKa that is critical to its antiangiogenic activity. In vivo, ferritin opposed HKa's antiangiogenic effects in a human prostate cancer xenograft, restoring tumor-dependent vessel growth. Ferritin-mediated regulation of angiogenesis represents a new angiogenic regulatory pathway, and identifies a new role for ferritin in cell biology.