60 research outputs found

    Energy Efficient Mobile Routing in Actuator and Sensor Networks with Connectivity Preservation

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    International audienceIn mobile wireless sensor networks, flows sent from data col- lecting sensors to a sink could traverse inefficient resource expensive paths. Such paths may have several negative effects such as devices bat- tery depletion that may cause the network to be disconnected and packets to experience arbitrary delays. This is particularly problematic in event- based sensor networks (deployed in disaster recovery missions) where flows are of great importance. In this paper, we use node mobility to im- prove energy consumption of computed paths. Mobility is a two-sword edge, however. Moving a node may render the network disconnected and useless. We propose CoMNet (Connectivity preservation Mobile routing protocol for actuator and sensor NETworks), a localized mechanism that modifies the network topology to support resource efficient transmissions. To the best of our knowledge, CoMNet is the first georouting algorithm which considers controlled mobility to improve routing energy consump- tion while ensuring network connectivity. CoMNet is based on (i) a cost to progress metric which optimizes both sending and moving costs, (ii) the use of a connected dominating set to maintain network connectivity. CoMNet is general enough to be applied to various networks (actuator, sensor). Our simulations show that CoMNet guarantees network connec- tivity and is effective in achieving high delivery rates and substantial energy savings compared to traditional approaches

    Association of angiotensin II type 1 receptor gene polymorphism with essential hypertension

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    The renin-angiotensin system is involved in control of blood pressure and salt and fluid homeostasis. Genes for components of this system have been of major focus in research on the causation of the common, complex, polygenic trait, essential hypertension (HT). Association of an A-->C variant at nucleotide 1166 of the angiotensin II type 1 receptor (AT(1)R) gene with HT, but an absence of linkage of this locus with this disease, has been reported recently. Since cofirmation in a different setting is imperative, we performed a cross-sectional case-control study of the Al166C variant in a well-characterized group of 108 Caucasian HT subjects with a strong family history (two affected parents) and early onset disease. Genotyping was by mismatch polymerase chain reaction/BfrI restriction fragment length polymorphism analysis. Frequency of the C-1166 allele was 0.40 in HTs and 0.29 in normotensives. The difference in genotype (chi(2) = 13, P = 0.0015) and allele (chi(2) = 5.3, P = 0.02) frequencies between the two groups was significant (odds ratio for CC vs AA + AC = 7.3 [95% CI, 1.9-31.9). The present results implicate the AT(1)R gene, or a locus in linkage disequilibrium with the variant tested, in the causation of essential HT
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