Abstract-Telecommunications networks, and in particular optical WDM networks, are vulnerable to large-scale failures of their physical infrastructure, resulting from physical attacks (such as an Electromagnetic Pulse attack) or natural disasters (such as solar flares, earthquakes, and floods). Such events happen at specific geographical locations and disrupt specific parts of the network but their effects are not deterministic. Therefore, we provide a unified framework to model the network vulnerability when the event has a probabilistic nature, defined by an arbitrary probability density function. Our framework captures scenarios with a number of simultaneous attacks, in which network components consist of several dependent subcomponents, and in which either a 1+1 or a 1:1 protection plan is in place. We use computational geometric tools to provide efficient algorithms to identify vulnerable points within the network under various metrics. Then, we obtain numerical results for specific backbone networks, thereby demonstrating the applicability of our algorithms to real-world scenarios. Our novel approach allows for identifying locations which require additional protection efforts (e.g., equipment shielding). Overall, the paper demonstrates that using computational geometric techniques can significantly contribute to our understanding of network resilience.
This paper studies two problems that arise in optimization of sensor networks: First, we devise provable approximation schemes for locating a base station and constructing a network among a set of sensors each of which has a data stream to get to the base station. Subject to power constraints at the sensors, our goal is to locate the base station and establish a network in order to maximize the lifespan of the network.Second, we study optimal sensor placement problems for quality coverage of given domains cluttered with obstacles. We assume "line-of-site", sensors, that sense a point only if the straight segment connecting the sensor to this point (the "line-of-site") does not cross any obstacle. so obstacles occludes area from Using line-of-site sensors, the goal is to minimize the number of sensors required in order to have each point "well covered" according to precise criteria (e.g., that each point is seen by two sensors that form at least angle α, or that each point is seen by three sensors that form a triangle containing the point).
Abstract. We consider the problem of simultaneous embedding of planar graphs. There are two variants of this problem, one in which the mapping between the vertices of the two graphs is given and another in which the mapping is not given. In particular, given a mapping, we show how to embed two paths on an n × n grid, and two caterpillar graphs on a 3n × 3n grid. We show that it is not always possible to simultaneously embed three paths. If the mapping is not given, we show that any number of outerplanar graphs can be embedded simultaneously on an O(n) × O(n) grid, and an outerplanar and general planar graph can be embedded simultaneously on an O(n 2 ) × O(n 2 ) grid.
Subtle cellular phenotypes in the CNS may evade detection by routine histopathology. Here, we demonstrate the value of primary culture for revealing genetically determined neuronal phenotypes at high resolution. Gamma neurons of Drosophila melanogaster mushroom bodies (MBs) are remodeled during metamorphosis under the control of the steroid hormone 20-hydroxyecdysone (20E). In vitro, wild-type ␥ neurons retain characteristic morphogenetic features, notably a single axon-like dominant primary process and an arbor of short dendrite-like processes, as determined with microtubule-polarity markers. We found three distinct genetically determined phenotypes of cultured neurons from grossly normal brains, suggesting that subtle in vivo attributes are unmasked and amplified in vitro. First, the neurite outgrowth response to 20E is sexually dimorphic, being much greater in female than in male ␥ neurons. Second, the ␥ neuron-specific "naked runt" phenotype results from transgenic insertion of an MB-specific promoter. Third, the recessive, panneuronal "filagree" phenotype maps to singed, which encodes the actin-bundling protein fascin. Fascin deficiency does not impair the 20E response, but neurites fail to maintain their normal, nearly straight trajectory, instead forming curls and hooks. This is accompanied by abnormally distributed filamentous actin. This is the first demonstration of fascin function in neuronal morphogenesis. Our findings, along with the regulation of human Fascin1 (OMIM 602689) by CREB (cAMP response element-binding protein) binding protein, suggest FSCN1 as a candidate gene for developmental brain disorders. We developed an automated method of computing neurite curvature and classifying neurons based on curvature phenotype. This will facilitate detection of genetic and pharmacological modifiers of neuronal defects resulting from fascin deficiency.
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