Cluster and group synchronization in delay-coupled networks

We investigate the stability of synchronized states in delay-coupled networks where synchronization takes place in groups of different local dynamics or in cluster states in networks with identical local dynamics. Using a master stability approach, we find that the master stability function shows a discrete rotational symmetry depending on the number of groups. The coupling matrices that permit solutions on group or cluster synchronization manifolds show a very similar symmetry in their eigenvalue spectrum, which helps to simplify the evaluation of the master stability function. Our theory allows for the characterization of stability of different patterns of synchronized dynamics in networks with multiple delay times, multiple coupling functions, but also with multiple kinds of local dynamics in the networks' nodes. We illustrate our results by calculating stability in the example of delay-coupled semiconductor lasers and in a model for neuronal spiking dynamics.Comment: 11 pages, 7 figure

Adaptive synchronization in delay-coupled networks of Stuart-Landau oscillators

We consider networks of delay-coupled Stuart-Landau oscillators. In these systems, the coupling phase has been found to be a crucial control parameter. By proper choice of this parameter one can switch between different synchronous oscillatory states of the network. Applying the speed-gradient method, we derive an adaptive algorithm for an automatic adjustment of the coupling phase such that a desired state can be selected from an otherwise multistable regime. We propose goal functions based on both the difference of the oscillators and a generalized order parameter and demonstrate that the speed-gradient method allows one to find appropriate coupling phases with which different states of synchronization, e.g., in-phase oscillation, splay or various cluster states, can be selected.Comment: 8 pages, 7 figure

Controlling cluster synchronization by adapting the topology

We suggest an adaptive control scheme for the control of zero-lag and cluster synchronization in delay-coupled networks. Based on the speed-gradient method, our scheme adapts the topology of a network such that the target state is realized. It is robust towards different initial condition as well as changes in the coupling parameters. The emerging topology is characterized by a delicate interplay of excitatory and inhibitory links leading to the stabilization of the desired cluster state. As a crucial parameter determining this interplay we identify the delay time. Furthermore, we show how to construct networks such that they exhibit not only a given cluster state but also with a given oscillation frequency. We apply our method to coupled Stuart-Landau oscillators, a paradigmatic normal form that naturally arises in an expansion of systems close to a Hopf bifurcation. The successful and robust control of this generic model opens up possible applications in a wide range of systems in physics, chemistry, technology, and life science

Heterogeneous Delays in Neural Networks

We investigate heterogeneous coupling delays in complex networks of excitable elements described by the FitzHugh-Nagumo model. The effects of discrete as well as of uni- and bimodal continuous distributions are studied with a focus on different topologies, i.e., regular, small-world, and random networks. In the case of two discrete delay times resonance effects play a major role: Depending on the ratio of the delay times, various characteristic spiking scenarios, such as coherent or asynchronous spiking, arise. For continuous delay distributions different dynamical patterns emerge depending on the width of the distribution. For small distribution widths, we find highly synchronized spiking, while for intermediate widths only spiking with low degree of synchrony persists, which is associated with traveling disruptions, partial amplitude death, or subnetwork synchronization, depending sensitively on the network topology. If the inhomogeneity of the coupling delays becomes too large, global amplitude death is induced

Chandra Observation of the Edge-on Spiral NGC 5775: Probing the Hot Galactic Disk/Halo Connection

We study the edge-on galaxy NGC 5775, utilizing a 58.2 ks {\sl Chandra} ACIS-S observation together with complementary {\sl HST} ACS, {\sl Spitzer} IRAC and other multi-wavelength data sets. This edge-on galaxy, with its disk-wide active star formation, is particularly well-suited for studying the disk/halo interaction on sub-galactic scales. We detect 27 discrete X-ray sources within the $D_{25}$ region of the galaxy, including an ultra-luminous source with a 0.3-7 keV luminosity of $\sim7\times10^{40}\rm ergs s^{-1}$. The source-removed diffuse X-ray emission shows several prominent extraplanar features, including a $\sim10\rm kpc$ diameter ``shell-like'' feature and a ``blob'' reaching a projected distance of $\sim25\rm kpc$ from the galactic disk. The bulk of the X-ray emission in the halo has a scale height of $\sim$1.5 kpc and can be characterized by a two-temperature optically thin thermal plasma with temperatures of $\sim$ 0.2 and 0.6 keV and a total 0.3-2 keV luminosity of $\sim3.5\times10^{39}\rm ergs s^{-1}$. The high-resolution, multi-wavelength data reveal the presence of several extraplanar features around the disk, which appear to be associated with the in-disk star formation. We suggest that hot gas produced with different levels of mass loading can have different temperatures, which may explain the characteristic temperatures of hot gas in the halo. We have obtained a sub-galactic scale X-ray-intensity-star formation relation, which is consistent with the integrated version in other star forming galaxies.Comment: 25 pages, 10 figures, 4 tables, accepted for publication in MNRA

Influenza A (H10N7) virus causes respiratory tract disease in harbor seals and ferrets

Avian influenza viruses sporadically cross the species barrier to mammals, including humans, in which they may cause epidemic disease. Recently such an epidemic occurred due to the emergence of avian influenza virus of the subtype H10N7 (Seal/H10N7) in harbor seals (Phoca vitulina). This epidemic caused high mortality in seals along the north-west coast of Europe and represented a potential risk for human health. To characterize the spectrum of lesions and to identify the target cells and viral distribution, findings in 16 harbor seals spontaneously infected with Seal/H10N7 are described. The seals had respiratory tract inflammation extending from the nasal cavity to bronchi associated with intralesional virus antigen in respiratory epithelial cells. Virus infection was restricted to the respiratory tract. The fatal outcome of the viral infection in seals was most likely caused by secondary bacterial infections. To investigate the pathogenic potential of H10N7 infection for humans, we inoculated the seal virus intratracheally into six ferrets and performed pathological and virological analyses at 3 and 7 days post inoculation. These experimentally inoculated ferrets displayed mild clinical signs, virus excretion from the pharynx and respiratory tract inflammation extending from bronchi to alveoli that was associated with virus antigen expression exclusively in the respiratory epithelium. Virus was isolated only from the respiratory tract. In conclusion, Seal/H10N7 infection in naturally infected harbor seals and experimentally infected ferrets shows that respiratory epithelial cells are the permissive cells for viral replication. Fatal outcome in seals was caused by secondary bacterial pneumonia similar to that in fatal human cases during influenza pandemics. Productive infection of ferrets indicates that seal/H10N7 may possess a zoonotic potential. This outbreak of LPAI from wild birds to seals demonstrates the risk of such occasions for mammals and thus humans