Sink-oriented Dynamic Location Service Protocol for Mobile Sinks with an Energy Efficient Grid-Based Approach

Sensor nodes transmit the sensed information to the sink through wireless sensor networks (WSNs). They have limited power, computational capacities and memory. Portable wireless devices are increasing in popularity. Mechanisms that allow information to be efficiently obtained through mobile WSNs are of significant interest. However, a mobile sink introduces many challenges to data dissemination in large WSNs. For example, it is important to efficiently identify the locations of mobile sinks and disseminate information from multi-source nodes to the multi-mobile sinks. In particular, a stationary dissemination path may no longer be effective in mobile sink applications, due to sink mobility. In this paper, we propose a Sink-oriented Dynamic Location Service (SDLS) approach to handle sink mobility. In SDLS, we propose an Eight-Direction Anchor (EDA) system that acts as a location service server. EDA prevents intensive energy consumption at the border sensor nodes and thus provides energy balancing to all the sensor nodes. Then we propose a Location-based Shortest Relay (LSR) that efficiently forwards (or relays) data from a source node to a sink with minimal delay path. Our results demonstrate that SDLS not only provides an efficient and scalable location service, but also reduces the average data communication overhead in scenarios with multiple and moving sinks and sources

Experimental studies of strong dipolar interparticle interaction in monodisperse Fe3O4 nanoparticles

Interparticle interaction of monodisperse Fe3 O4 nanoparticles has been experimentally investigated by dispersing the nanoparticles in solvents. With increasing the interparticle distances to larger than 100 nm in a controlled manner, the authors found that the blocking temperature (TB) of the nanoparticles drops continuously and eventually gets saturated with a total drop in TB of 7-17 K observed for 3, 5, and 7 nm samples, compared with their respective nanopowder samples. By carefully studying the dependence of TB on the interparticle distance, the authors could demonstrate that the experimental dependence of TB follows the theoretical curve of the dipole-dipole interaction. © 2007 American Institute of Physics.open313

Boosting hot electron flux and catalytic activity at metal-oxide interfaces of PtCo bimetallic nanoparticles

Despite numerous studies, the origin of the enhanced catalytic performance of bimetallic nanoparticles (NPs) remains elusive because of the ever-changing surface structures, compositions, and oxidation states of NPs under reaction conditions. An effective strategy for obtaining critical clues for the phenomenon is real-time quantitative detection of hot electrons induced by a chemical reaction on the catalysts. Here, we investigate hot electrons excited on PtCo bimetallic NPs during H-2 oxidation by measuring the chemicurrent on a catalytic nanodiode while changing the Pt composition of the NPs. We reveal that the presence of a CoO/Pt interface enables efficient transport of electrons and higher catalytic activity for PtCo NPs. These results are consistent with theoretical calculations suggesting that lower activation energy and higher exothermicity are required for the reaction at the CoO/Pt interfac

CDKL Family Kinases Have Evolved Distinct Structural Features and Ciliary Function

Various kinases, including a cyclin-dependent kinase (CDK) family member, regulate the growth and functions of primary cilia, which perform essential roles in signaling and development. Neurological disorders linked to CDK-Like (CDKL) proteins suggest that these underexplored kinases may have similar functions. Here, we present the crystal structures of human CDKL1, CDKL2, CDKL3, and CDKL5, revealing their evolutionary divergence from CDK and mitogen-activated protein kinases (MAPKs), including an unusual ?J helix important for CDKL2 and CDKL3 activity. C. elegans CDKL-1, most closely related to CDKL1-4 and localized to neuronal cilia transition zones, modulates cilium length; this depends on its kinase activity and ?J helix-containing C terminus. Human CDKL5, linked to Rett syndrome, also localizes to cilia, and it impairs ciliogenesis when overexpressed. CDKL5 patient mutations modeled in CDKL-1 cause localization and/or cilium length defects. Together, our studies establish a disease model system suggesting cilium length defects as a pathomechanism for neurological disorders, including epilepsy

Efficient calculation of a partial-derivative wavefield using reciprocity for seismic imaging and inversion

Linearized inversion of surface seismic data for a model of the earths subsurface requires estimating the sensitivity of the seismic response to perturbations in the earths subsurface. This sensitivity, or Jacobian, matrix is usually quite expensive to estimate for all but the simplest model parameterizations.We exploit the numerical structure of the finite-element method, modern sparse matrix technology, and source–receiver reciprocity to develop an algorithm that explicitly calculates the Jacobian matrix at only the cost of a forward model solution. Furthermore, we show that we can achieve improved subsurface images using only one inversion iteration through proper scaling of the image by a diagonal approximation of the Hessian matrix, as predicted by the classical Gauss-Newton method. Our method is applicable to the full suite of wave scattering problems amenable to finiteelement forward modeling.We demonstrate our method through some simple 2-D synthetic examples

Traveltime and amplitude calculation using a perturbation approach

Accurate amplitudes and correct traveltimes are critical factors that govern the quality of prestack migration images. Because we never know the correct velocity initially, recomputing traveltimes and amplitudes of updated velocity models can dominate the iterative prestack migration procedure. Most tomographic velocity updating techniques require the calculation of the change of traveltime due to local changes in velocity. For such locally updated velocity models, perturbation techniques can be a significantly more economic way of calculating traveltimes and amplitudes than recalculating the entire solutions from scratch. In this paper, we implement an iterative Born perturbation theory applied to the damped wave equation algorithm. Our iterative Born perturbation algorithm yields stable solutions for models having velocity contrasts of 30% about the initial velocity estimate, which is significantly more economic than recalculating the entire solution.This work was financially supported by National Research Laboratory Project of the Korea Ministry of Science and Technology, Brain Korea 21 project of the Korea Ministry of Education, grant No. R05-2000-00003 from the Basic Research Program of the Korea Science&Engineering Foundation, and grant No. PM10300 from Korea Ocean Research & Development Institute

EFHC1, Implicated in Juvenile Myoclonic Epilepsy, Functions at the Cilium and Synapse to Modulate Dopamine Signaling

Neurons throughout the mammalian brain possess non-motile cilia, organelles with varied functions in sensory physiology and cellular signaling. Yet, the roles of cilia in these neurons are poorly understood. To shed light into their functions, we studied EFHC1, an evolutionarily conserved protein required for motile cilia function and linked to a common form of inherited epilepsy in humans, juvenile myoclonic epilepsy (JME). We demonstrate that C. elegans EFHC-1 functions within specialized non-motile mechanosensory cilia, where it regulates neuronal activation and dopamine signaling. EFHC-1 also localizes at the synapse, where it further modulates dopamine signaling in cooperation with the orthologue of an R-type voltage-gated calcium channel. Our findings unveil a previously undescribed dual-regulation of neuronal excitability at sites of neuronal sensory input (cilium) and neuronal output (synapse). Such a distributed regulatory mechanism may be essential for establishing neuronal activation thresholds under physiological conditions, and when impaired, may represent a novel pathomechanism for epilepsy

Cilium length regulation in Caenorhabditis elegans

Nearly all vertebrate cells possess a primary cilium, akin to a cellular antenna, that plays essential roles in various physiological and developmental processes. Cilium length is tightly regulated to provide the optimal functions for each type of cell and tissue, such as the eye and kidney. Impairment of this regulation can result in cilium-associated disorders, collectively termed ciliopathies. The intraflagellar transport (IFT) system, involved in cilium assembly, and microtubule depolymerizing kinesins, which participate in cilium disassembly, play key roles in cilium length regulation. Additionally, several classes of kinases, including CDKL5, modify IFT components and/or depolymerizing kinesins to modulate ciliary length. We therefore hypothesized that the entire family of cyclin-dependent kinase-like (CDKL) proteins (CDKL1-5) may have similar ciliary functions. To test this hypothesis, we undertook studies in C. elegans. This nematode has one CDKL protein (CDKL-1) closely related to CDKL1-4 and more distantly related to CDKL5. We find that CDKL-1 localizes to cilia, including the transition zone (TZ), and negatively regulates cilium length by controlling IFT flux. Cilium length regulation by CDKL-1 is distinct from that of other kinases, namely DYF-18 (mammalian CCRK ortholog), DYF-5 (MAK) and NEKL-1 (NEK8/9). It also occurs independently from the depolymerizing kinesin-13 family, KLP-7 (KIF2A), which positively controls cilium length at the TZ. To query the molecular etiologies of human diseases caused by mutations in CDKL5 (epilepsy and atypical Rett syndrome) or KIF2A (brain malformations), we introduced corresponding patient mutations in C. elegans CDKL-1 and KLP-7, respectively. The mutations cause mislocalization and ciliary length defects. In addition, we find that disrupting C. elegans cdkl-1 results in sensory (CO2 avoidance) and developmental (body size) phenotypes, possibly resulting from anomalies in signaling pathway(s), including cGMP signaling. These data suggest that human ailments such as Rett syndrome and brain anomalies may arise from cilium length misregulation, and consequently, disruption of signaling pathways. In summary, our findings provide evidence that CDKL-1 works cooperatively with other kinases, and independently from a depolymerizing kinesin, to maintain correct ciliary length. Our work also suggests links between ciliary length control and potential ciliopathies, which provides potentially useful experimental avenues of exploration