Queue-length synchronization in a communication networks

We study synchronization in the context of network traffic on a $2-d$ communication network with local clustering and geographic separations. The network consists of nodes and randomly distributed hubs where the top five hubs ranked according to their coefficient of betweenness centrality (CBC) are connected by random assortative and gradient mechanisms. For multiple message traffic, messages can trap at the high CBC hubs, and congestion can build up on the network with long queues at the congested hubs. The queue lengths are seen to synchronize in the congested phase. Both complete and phase synchronization is seen, between pairs of hubs. In the decongested phase, the pairs start clearing, and synchronization is lost. A cascading master-slave relation is seen between the hubs, with the slower hubs (which are slow to decongest) driving the faster ones. These are usually the hubs of high CBC. Similar results are seen for traffic of constant density. Total synchronization between the hubs of high CBC is also seen in the congested regime. Similar behavior is seen for traffic on a network constructed using the Waxman random topology generator. We also demonstrate the existence of phase synchronization in real Internet traffic data.Comment: 13 Pages, 15 figure

Emotion Based Music Player - XBeats

This paper showcases the development of an Android platform based application named XBeats which acts as a Music Player working on Image Processing fundamentals to capture, analyze and present music as per the emotion or mood of the user using this application. The Android application was developed using the Android SDK software and OpenCV software was used to implement facial recognition algorithms and cascades. The unique aspect of this project is that it focuses on facial recognition on the Android platform unlike that on Computer systems which use commonly available softwares for the same. This paper also provides comparison between use of various classification algorithms used for facial detection

Activation of PTHrP-cAMP-CREB1 signaling following p53 loss is essential for osteosarcoma initiation and maintenance

Mutations in the P53 pathway are a hallmark of human cancer. The identification of pathways upon which p53-deficient cells depend could reveal therapeutic targets that may spare normal cells with intact p53. In contrast to P53 point mutations in other cancer, complete loss of P53 is a frequent event in osteosarcoma (OS), the most common cancer of bone. The consequences of p53 loss for osteoblastic cells and OS development are poorly understood. Here we use murine OS models to demonstrate that elevated Pthlh (Pthrp), cAMP levels and signalling via CREB1 are characteristic of both p53-deficient osteoblasts and OS. Normal osteoblasts survive depletion of both PTHrP and CREB1. In contrast, p53-deficient osteoblasts and OS depend upon continuous activation of this pathway and undergo proliferation arrest and apoptosis in the absence of PTHrP or CREB1. Our results identify the PTHrP-cAMP-CREB1 axis as an attractive pathway for therapeutic inhibition in OS.Mannu K Walia, Patricia MW Ho, Scott Taylor, Alvin JM Ng, Ankita Gupte, Alistair M Chalk, Andrew CW Zannettino, T John Martin, Carl R Walkle

Glucose-6-phosphate dehydrogenase-derived NADPH fuels superoxide production in the failing heart.

In the failing heart, NADPH oxidase and uncoupled NO synthase utilize cytosolic NADPH to form superoxide. NADPH is supplied principally by the pentose phosphate pathway, whose rate-limiting enzyme is glucose 6-phosphate dehydrogenase (G6PD). Therefore, we hypothesized that cardiac G6PD activation drives part of the excessive superoxide production implicated in the pathogenesis of heart failure. Pacing-induced heart failure was performed in eight chronically instrumented dogs. Seven normal dogs served as control. End-stage failure occurred after 28 +/- 1 days of pacing, when left ventricular end-diastolic pressure reached 25 mm Hg. In left ventricular tissue homogenates, spontaneous superoxide generation measured by lucigenin (5 microM) chemiluminescence was markedly increased in heart failure (1338 +/- 419 vs. 419 +/- 102 AU/mg protein, P < 0.05), as were NADPH levels (15.4 +/- 1.5 vs. 7.5 +/- 1.5 micromol/gww, P < 0.05). Superoxide production was further stimulated by the addition of NADPH. The NADPH oxidase inhibitor gp91(ds-tat) (50 microM) and the NO synthase inhibitor L-NAME (1 mM) both significantly lowered superoxide generation in failing heart homogenates by 80% and 76%, respectively. G6PD was upregulated and its activity higher in heart failure compared to control (0.61 +/- 0.10 vs. 0.24 +/- 0.03 nmol/min/mg protein, P < 0.05), while superoxide production decreased to normal levels in the presence of the G6PD inhibitor 6-aminonicotinamide. We conclude that the activation of myocardial G6PD is a novel mechanism that enhances NADPH availability and fuels superoxide-generating enzymes in heart failure

Training safer surgeons: How do patients view the role of simulation in orthopaedic training?

BACKGROUND: Simulation allows training without posing risk to patient safety. It has developed in response to the demand for patient safety and the reduced training times for surgeons. Whilst there is an increasing role of simulation in orthopaedic training, the perception of patients and the general public of this novel method is yet unknown. Patients and the public were given the opportunity to perform a diagnostic knee arthroscopy on a virtual reality ARTHRO Mentor simulator. After their practice session, participants answered a validated questionnaire based on a 5-point Likert Scale assessing their opinions on arthroscopic simulation. Primary objective was observing perception of patients on orthopaedic virtual reality simulation. FINDINGS: There were a total of 159 respondents, of which 86% were of the opinion that simulators are widely used in surgical training and 94% felt that they should be compulsory. 91% would feel safer having an operation by a surgeon trained on simulators, 87% desired their surgeon to be trained on simulators and 72% believed that additional simulator training resulted in better surgeons. Moreover, none of the respondents would want their operation to be performed by a surgeon who had not trained on a simulator. Cronbach's alpha was 0.969. CONCLUSIONS: There is also a clear public consensus for this method of training to be more widely utilised and it would enhance public perception of safer training of orthopaedic surgeons. This study of public perception provides a mandate to increase investment and infrastructure in orthopaedic simulation as part of promoting clinical governance

Evidence for directed percolation universality at the onset of spatiotemporal intermittency in coupled circle maps

We consider a lattice of coupled circle maps, a model arising naturally in descriptions of solid state phenomena such as Josephson junction arrays. We find that the onset of spatiotemporal intermittency (STI) in this system is analogous to directed percolation (DP), with the transition being to an unique absorbing state for low nonlinearities, and to weakly chaotic absorbing states for high nonlinearities. We find that the complete set of static exponents and spreading exponents at all critical points match those of DP very convincingly. Further, hyperscaling relations are fulfilled, leading to independent controls and consistency checks of the values of all the critical exponents. These results lend strong support to the conjecture that the onset of STI in deterministic models belongs to the DP universality class.Comment: Submitted to Physical Review

Coupled Maps on Trees

We study coupled maps on a Cayley tree, with local (nearest-neighbor) interactions, and with a variety of boundary conditions. The homogeneous state (where every lattice site has the same value) and the node-synchronized state (where sites of a given generation have the same value) are both shown to occur for particular values of the parameters and coupling constants. We study the stability of these states and their domains of attraction. As the number of sites that become synchronized is much higher compared to that on a regular lattice, control is easier to effect. A general procedure is given to deduce the eigenvalue spectrum for these states. Perturbations of the synchronized state lead to different spatio-temporal structures. We find that a mean-field like treatment is valid on this (effectively infinite dimensional) lattice.Comment: latex file (25 pages), 4 figures included. To be published in Phys. Rev.

Effect of hydrogen on ground state structures of small silicon clusters

We present results for ground state structures of small Si$_{n}$H (2 \leq \emph{n} \leq 10) clusters using the Car-Parrinello molecular dynamics. In particular, we focus on how the addition of a hydrogen atom affects the ground state geometry, total energy and the first excited electronic level gap of an Si$_{n}$ cluster. We discuss the nature of bonding of hydrogen in these clusters. We find that hydrogen bonds with two silicon atoms only in Si$_{2}$H, Si$_{3}$H and Si$_{5}$H clusters, while in other clusters (i.e. Si$_{4}$H, Si$_{6}$H, Si$_{7}$H, Si$_{8}$H, Si$_{9}$H and Si$_{10}$H) hydrogen is bonded to only one silicon atom. Also in the case of a compact and closed silicon cluster hydrogen bonds to the cluster from outside. We find that the first excited electronic level gap of Si$_{n}$ and Si$_{n}$H fluctuates as a function of size and this may provide a first principles basis for the short-range potential fluctuations in hydrogenated amorphous silicon. Our results show that the addition of a single hydrogen can cause large changes in the electronic structure of a silicon cluster, though the geometry is not much affected. Our calculation of the lowest energy fragmentation products of Si$_{n}$H clusters shows that hydrogen is easily removed from Si$_{n}$H clusters.Comment: one latex file named script.tex including table and figure caption. Six postscript figure files. figure_1a.ps and figure_1b.ps are files representing Fig. 1 in the main tex

HEAT SHOCK PROTEINS: NOVEL THERAPEUTIC TARGETS AGAINST INSULIN RESISTANCE AND TYPE 2 DIABETES

Impaired insulin action, termed insulin resistance, is characteristic of type 2 diabetes, obesity and aging. Given the rising epidemic of diabetes, efforts to understand the mechanisms of insulin resistance and discover effective therapeutic interventions are urgent. Considerable evidence now implicates oxidative stress in the patho-physiology of insulin resistance, a condition prevalent in the elderly and obese. Oxidative stress is known to activate several signaling cascades. This includes pathways that activate the stress kinases c-Jun N-terminal kinase (JNK) and the inhibitor of kappa B kinase beta (IKK beta), which interact with and inhibit the insulin signaling cascade. The heat shock proteins HSP72 and HSP25 have been recently identified as natural inhibitors of JNK and IKK beta, respectively, and therefore represent novel therapeutic targets against insulin resistance. Overexpression of HSPs has been shown to protect against obesity-induced insulin resistance as well as age-related muscle damage. Skeletal muscle, the largest glucose disposing tissue, also contains large amounts of inducible HSPs. We hypothesized that heat shock protein overexpression in skeletal muscle could protect against insulin resistance in obesity and aging. We tested this hypothesis using aged male Fischer 344 rats (24-month-old) as the aging model of insulin resistance and male Wistar rats given a high fat diet (60% calories from fat) as the model of diet induced-insulin resistance. We examined the role of HSPs in insulin resistance by inducing HSP expression with both in vitro and in vivo heat treatments and anti-oxidant administration. Our results showed that reduced HSP expression in the aging muscles is associated with a higher degree of stress kinase activation and insulin resistance in fast-twitch muscles compared to slow-twitch muscles. Increasing HSP72 expression in the muscles of young and old animals via heat treatment inhibited JNK activation. Heat-mediated JNK inhibition was specific to HSP72 induction, as determined by HSP72-inhibition studies, and was mediated by a direct interaction between HSP72 and JNK. In contrast to the muscle, brain sections from aging rats showed a robust increase in HSP25 expression, suggesting a tissue-specific regulation of HSPs in aging. In the high fat diet model, alpha-lipoic acid (LA), a potent antioxidant, was administered to relieve oxidative stress associated with high fat feeding. LA treatment improved insulin signaling and glucose transport, reduced stress kinase activation and increased HSP expression. As another method of HSP-induction, heat treatment, given in parallel with a high fat diet, improved glucose tolerance, reduced hyperinsulinemia, and reduced epididymal fat storage. In skeletal muscles, heat treatment induced HSP72 expression, improved insulin sensitivity, and reduced stress kinase activities. Heat treatment also enhanced mitochondrial function in fast-twitch muscles, normalizing the compensatory changes in mitochondrial protein expression seen with high fat feeding. Studies in L6 myotubes showed that heat treatment improved oxygen consumption and fatty acid oxidation. Mechanistically, our results indicate that heat shock proteins can 1). improve insulin sensitivity, 2). directly inhibit stress kinase activities, and 3). protect and enhance mitochondrial function. Our studies provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for age-related and obesity-induced insulin resistance

Synchronization and directed percolation in coupled map lattices

We study a synchronization mechanism, based on one-way coupling of all-or-nothing type, applied to coupled map lattices with several different local rules. By analyzing the metric and the topological distance between the two systems, we found two different regimes: a strong chaos phase in which the transition has a directed percolation character and a weak chaos phase in which the synchronization transition occurs abruptly. We are able to derive some analytical approximations for the location of the transition point and the critical properties of the system. We propose to use the characteristics of this transition as indicators of the spatial propagation of chaoticity.Comment: 12 pages + 12 figure