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    Delays-induced Phase Transitions in Active Matter

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    We consider the patterns of collective motion emerging when many aligning, self-propelling units move in two dimensions while interacting through a repulsive potential and are also subject to delays and random perturbations. In this approach, delay plays the role analogous to reaction time so that a given particle is influenced by the information about the velocity and the position of the other particles in its vicinity with some time delay. To get insight into the involved complex flows and the transitions between them we use a simple model allowing, by fine-tuning of its few parameters, the observation and analysis of behaviours that are less accessible by experiments or analytic calculations and at the same time make the reproduction of experimental results possible. We report for the first time about a transition from an ordered, polarized collective motion to disorder as a function of the increasing time delay. For a fixed intermediate value of the delay similar transition (from order to disorder) is obtained as the repulsion radius is increased. Our simulations show a transition from total polarization to two kinds of states: fully disordered and a kind of state which is a mixture of patches of fully disordered motion in the background of orderly moving other particles. The transition occurs as the delay time is increased and is sharp, indicating that the nature of this order-disorder transition is either of first-order or is described by a sharply decreasing linear function. Our model is a simplified version of a practical situation of quickly growing interest because time delays are expected to play an increasingly important role when the traffic of many, densely distributed autonomous drones will move around in a quasi-two-dimensional air space

    Protein kinase C-dependent signaling controls the midgut epithelial barrier to malaria parasite infection in anopheline mosquitoes.

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    Anopheline mosquitoes are the primary vectors of parasites in the genus Plasmodium, the causative agents of malaria. Malaria parasites undergo a series of complex transformations upon ingestion by the mosquito host. During this process, the physical barrier of the midgut epithelium, along with innate immune defenses, functionally restrict parasite development. Although these defenses have been studied for some time, the regulatory factors that control them are poorly understood. The protein kinase C (PKC) gene family consists of serine/threonine kinases that serve as central signaling molecules and regulators of a broad spectrum of cellular processes including epithelial barrier function and immunity. Indeed, PKCs are highly conserved, ranging from 7 isoforms in Drosophila to 16 isoforms in mammals, yet none have been identified in mosquitoes. Despite conservation of the PKC gene family and their potential as targets for transmission-blocking strategies for malaria, no direct connections between PKCs, the mosquito immune response or epithelial barrier integrity are known. Here, we identify and characterize six PKC gene family members--PKCδ, PKCε, PKCζ, PKD, PKN, and an indeterminate conventional PKC--in Anopheles gambiae and Anopheles stephensi. Sequence and phylogenetic analyses of the anopheline PKCs support most subfamily assignments. All six PKCs are expressed in the midgut epithelia of A. gambiae and A. stephensi post-blood feeding, indicating availability for signaling in a tissue that is critical for malaria parasite development. Although inhibition of PKC enzymatic activity decreased NF-κB-regulated anti-microbial peptide expression in mosquito cells in vitro, PKC inhibition had no effect on expression of a panel of immune genes in the midgut epithelium in vivo. PKC inhibition did, however, significantly increase midgut barrier integrity and decrease development of P. falciparum oocysts in A. stephensi, suggesting that PKC-dependent signaling is a negative regulator of epithelial barrier function and a potential new target for transmission-blocking strategies
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