Energy Management in Wireless Sensor Networks: A Crosslayer,Channel Adaptive Approach Towards Performance Optimization

The proliferation of wireless sensor networks in a large spectrum of applications had been spurered by the rapid advances in MEMS(micro-electro mechanical systems )based sensor technology coupled with low power,Low cost digital signal processors and radio frequency circuits.A sensor network is composed of thousands of low cost and portable devices bearing large sensing computing and wireless communication capabilities. This large collection of tiny sensors can form a robust data computing and communication distributed system for automated information gathering and distributed sensing.The main attractive feature is that such a sensor network can be deployed in remote areas.Since the sensor node is battery powered,all the sensor nodes should collaborate together to form a fault tolerant network so as toprovide an efficient utilization of precious network resources like wireless channel,memory and battery capacity.The most crucial constraint is the energy consumption which has become the prime challenge for the design of long lived sensor nodes.

Channel Adaptive MAC Protocol with Traffic-Aware Distributed Power Management in Wireless Sensor Networks-Some Performance Issues

In Wireless Sensor Networks (WSN), neglecting the effects of varying channel quality can lead to an unnecessary wastage of precious battery resources and in turn can result in the rapid depletion of sensor energy and the partitioning of the network. Fairness is a critical issue when accessing a shared wireless channel and fair scheduling must be employed to provide the proper flow of information in a WSN. In this paper, we develop a channel adaptive MAC protocol with a traffic-aware dynamic power management algorithm for efficient packet scheduling and queuing in a sensor network, with time varying characteristics of the wireless channel also taken into consideration. The proposed protocol calculates a combined weight value based on the channel state and link quality. Then transmission is allowed only for those nodes with weights greater than a minimum quality threshold and nodes attempting to access the wireless medium with a low weight will be allowed to transmit only when their weight becomes high. This results in many poor quality nodes being deprived of transmission for a considerable amount of time. To avoid the buffer overflow and to achieve fairness for the poor quality nodes, we design a Load prediction algorithm. We also design a traffic aware dynamic power management scheme to minimize the energy consumption by continuously turning off the radio interface of all the unnecessary nodes that are not included in the routing path. By Simulation results, we show that our proposed protocol achieves a higher throughput and fairness besides reducing the delay

Influence of occupation number of single particle levels on K - K charge transfer in collisions of 90 keV - Ne{^9+} on Ne

The influence of the occupation of the single particle levels on the impact parameter dependent K - K charge transfer occuring in collisions of 90 keV Ne{^9+} on Ne was studied using coupled channel calculations. The energy eigenvalues and matrixelements for the single particle levels were taken from ab initio self consistent MO-LCAO-DIRAC-FOCK-SLATER calculations with occupation numbers corresponding to the single particle amplitudes given by the coupled channel calculations.

Inclusive probability calculations for the K-vacancy transfer in collisions of S{^15+} on Ar

Using the single-particle amplitudes from a 20-level coupled-channel calculation with ab initio relativistic self consistent LCAO-MO Dirac-Fock-Slater energy eigenvalues and matrix elements we calculate within the frame of the inclusive probability formalism impact-parameter-dependent K-hole transfer probabilities. As an example we show results for the heavy asymmetric collision system S{^15+} on Ar for impact energies from 4.7 to 16 MeV. The inclusive probability formalism which reinstates the many-particle aspect of the collision system permits a qualitative and quantitative agreement with the experiment which is not achieved by the single-particle picture.

Realistic many electron coupled channel calculations in heavy ion scattering

The time dependent Dirac equation which describes a heavy ion-atom collision system is solved via a set of coupled channel equations with energy eigenvalues and matrix elements which are given by a selfconsistent field many electron calculation. After a brief discussion of the theoretical approximations and the connection of the many particle with the one particle interpretation we discuss first results for the systems F{^8+} - Ne and F{^6+} - Ne. The resulting P(b) curves for the creation of a Ne K-hole are in good agreement with the experimental results.

Many electron coupled channel calculations for the system F{^8+} - Ne

To describe the time dependence of an atomic collision system the Dirac equation usually is rewritten in a coupled channel equation. We first discuss part of the approximation used in this approach and the connection of the many particle with the one particle interpretation. The coupled channel equations are solved for the system F{^8+} - Ne using static selfconsistent many electron Dirac-Fock-Slater wavefunctions as basis. The resulting P(b) curves for the creation of a Ne K-hole are in reasonable agreement with the experimental results.

Observations on the effects of a single-channel cochlear implant on a seven year old

This paper presents observations on the effects of a single-channel cochlear implant on a seven year-old hearing impaired child.

Nerve terminal GABAA receptors activate Ca2+/calmodulin-dependent signaling to inhibit voltage-gated Ca2+ influx and glutamate release

-Aminobutyric acid type A (GABAA) receptors, a family of Cl-permeable ion channels, mediate fast synaptic inhibition as postsynaptically enriched receptors for -aminobutyric acid at GABAergic synapses. Here we describe an alternative type of inhibition mediated byGABAA receptors present on neocortical glutamatergic nerve terminals and examine the underlying signaling mechanism(s). By monitoring the activity of the presynaptic CaM kinase II/synapsin I signaling pathway in isolated nerve terminals, we demonstrate that GABAA receptor activation correlated with an increase in basal intraterminal [Ca2]i. Interestingly, this activation of GABAA receptors resulted in a reduction of subsequent depolarization-evoked Ca2 influx, which thereby led to an inhibition of glutamate release. To investigate how the observed GABAA receptor-mediated modulation operates, we determined the sensitivity of this process to the Na-K-2Cl cotransporter 1 antagonist bumetanide, as well as substitution of Ca2 with Ba2, or Ca2/calmodulin inhibition by W7. All of these treatments abolished the modulation by GABAA receptors. Application of selective antagonists of voltage-gated Ca2 channels (VGCCs) revealed that the GABAA receptor-mediated modulation of glutamate release required the specific activity of L- and R-type VGCCs. Crucially, the inhibition of release by these receptors was abolished in terminals isolated from R-type VGCC knock-out mice. Together, our results indicate that a functional coupling between nerve terminal GABAA receptors and L- or R-type VGCCs is mediated by Ca2/calmodulin-dependent signaling. This mechanism provides a GABA-mediated control of glutamatergic synaptic activity by a direct inhibition of glutamate release.

Remote sensing of intertidal morphological change in Morecambe Bay, U.K., between 1991 and 2007

Tidal Flats are important examples of extensive areas of natural environment that remain relatively unaffected by man. Monitoring of tidal flats is required for a variety of purposes. Remote sensing has become an established technique for the measurement of topography over tidal flats. A further requirement is to measure topographic changes in order to measure sediment budgets. To date there have been few attempts to make quantitative estimates of morphological change over tidal flat areas. This paper illustrates the use of remote sensing to measure quantitative and qualitative changes in the tidal flats of Morecambe Bay during the relatively long period 1991–2007. An understanding of the patterns of sediment transport within the Bay is of considerable interest for coastal management and defence purposes. Tidal asymmetry is considered to be the dominant cause of morphological change in the Bay, with the higher currents associated with the flood tide being the main agency moulding the channel system. Quantitative changes were measured by comparing a Digital Elevation Model (DEM) of the intertidal zone formed using the waterline technique applied to satellite Synthetic Aperture Radar (SAR) images from 1991–1994, to a second DEM constructed from airborne laser altimetry data acquired in 2005. Qualitative changes were studied using additional SAR images acquired since 2003. A significant movement of sediment from below Mean Sea Level (MSL) to above MSL was detected by comparing the two Digital Elevation Models, though the proportion of this change that could be ascribed to seasonal effects was not clear. Between 1991 and 2004 there was a migration of the Ulverston channel of the river Leven north-east by about 5 km, followed by the development of a straighter channel to the west, leaving the previous channel decoupled from the river. This is thought to be due to independent tidal and fluvial forcing mechanisms acting on the channel. The results demonstrate the effectiveness of remote sensing for measurement of long-term morphological change in tidal flat areas. An alternative use of waterlines as partial bathymetry for assimilation into a morphodynamic model of the coastal zone is also discussed.

Upwind solution of singular differential equations arising from steady channel flows

We study ordinary nonlinear singular differential equations which arise from steady conservation laws with source terms. An example of steady conservation laws which leads to those scalar equations is the Saint–Venant equations. The numerical solution of these scalar equations is sought by using the ideas of upwinding and discretisation of source terms. Both the Engquist–Osher scheme and the Roe scheme are used with different strategies for discretising the source terms.

A functional proteomic method for the enrichment of peripheral membrane proteins reveals the collagen binding protein Hsp47 is exposed on the surface of activated human platelets

Platelets are small blood cells vital for hemostasis. Following vascular damage, platelets adhere to collagens and activate, forming a thrombus that plugs the wound and prevents blood loss. Stimulation of the platelet collagen receptor glycoprotein VI (GPVI) allows recruitment of proteins to receptor-proximal signaling complexes on the inner-leaflet of the plasma membrane. These proteins are often present at low concentrations; therefore, signaling-complex characterization using mass spectrometry is limited due to high sample complexity. We describe a method that facilitates detection of signaling proteins concentrated on membranes. Peripheral membrane proteins (reversibly associated with membranes) were eluted from human platelets with alkaline sodium carbonate. Liquid-phase isoelectric focusing and gel electrophoresis were used to identify proteins that changed in levels on membranes from GPVI-stimulated platelets. Immunoblot analysis verified protein recruitment to platelet membranes and subsequent protein phosphorylation was preserved. Hsp47, a collagen binding protein, was among the proteins identified and found to be exposed on the surface of GPVI-activated platelets. Inhibition of Hsp47 abolished platelet aggregation in response to collagen, while only partially reducing aggregation in response to other platelet agonists. We propose that Hsp47 may therefore play a role in hemostasis and thrombosis.

Platelet nitric oxide synthase is activated by tyrosine dephosphorylation: possible role for SHP-1 phosphatase

Background: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli. However, the post-translational regulation of eNOS in platelets is poorly defined. Objectives: We investigated the role of tyrosine phosphorylation in the regulation of platelet eNOS activity. Methods: Tyrosine phosphorylation of eNOS and interaction with the tyrosine phosphatase SHP-1 were investigated by coimmunoprecipitation and immunoblotting. An in vitro immunoassay was used to determine eNOS activity together with the contribution of protein tyrosine phosphorylation. Results: We found platelet eNOS was tyrosine phosphorylated under basal conditions. Thrombin induced a dose- and time-dependent increase in eNOS activity without altering overall level of tyrosine phosphorylation, although we did observe evidence of minor tyrosine dephosphorylation. In vitro tyrosine dephosphorylation of platelet eNOS using a recombinant protein tyrosine phosphatase enhanced thrombin-induced activity compared to thrombin alone, but had no effect on endothelial eNOS activity either at basal or after stimulation with bradykinin. Having shown that dephosphorylation could modulate platelet eNOS activity we examined the role of potential protein phosphatases important for platelet eNOS activity. We found SHP-1 protein tyrosine phosphatase, co-associated with platelet eNOS in resting platelets, but does not associate with eNOS in endothelial cells. Stimulation of platelets with thrombin increased SHP-1 association with eNOS, while inhibition of SHP-1 abolished the ability of thrombin to induce elevated eNOS activity. Conclusions: Our data suggest a novel role for tyrosine dephosphorylation in platelet eNOS activation, which may be mediated by SHP-1.

The production, purification and characterisation of two novel alpha-D-mannosidases from Aspergillus phoenicis

1,6-alpha-D-Mannosidase from Aspergillits phoenicis was purified by anion-exchange chromatography, chromatofocussing and size-exclusion chromatography. The apparent molecular weight was 74 kDa by SDS-PAGE and 81 kDa by native-PAGE. The isoelectric point was 4.6. 1,6-alpha-D-Mannosidase had a temperature optimum of 60 degrees C, a pH optimum of 4.0-4.5. a K-m of 14 mM with alpha-D-Manp-(1 -> 6)-D-Manp as substrate. It was strongly inhibited by Mn2+ and did not need Ca2+ or any other metal cofactor of those tested. The enzyme cleaves specifically (1 -> 6)-linked mannobiose and has no activity towards any other linkages, p-nitrophenyl-alpha-D-mannopyranoside or baker's yeast mannan. 1,3(1,6)-alpha-D-Mannosidase from A. phoenicis was purified by anion-exchange chromatography, chromatofocus sing and size-exclusion chromatography. The apparent molecular weight was 97 kDa by SDS-PAGE and 110 kDa by native-PAGE. The 1,3(1,6)-alpha-D-mannosidase enzyme existed as two charge isomers or isoforms. The isoelectric points of these were 4.3 and 4.8 by isoelectric focussing. It cleaves alpha-D-Manp-(1 -> 3)-D-Manp 10 times faster than alpha-D-Manp-(1 -> 6)-D-Manp, has very low activity towards p-nitrophenyl-alpha-D-mannopyranoside and baker's yeast mannan, and no activity towards alpha-D-Manp-(1 -> 2)-D-Manp. The activity towards (1 -> 3)-linked mannobiose is strongly activated by 1 mM Ca2+ and inhibited by 10 mM EDTA, while (1 -> 6)-activity is unaffected, indicating that the two activities may be associated with different polypeptides. It is also possible that one polypeptide may have two active sites catalysing distinct activities. (c) 2005 Elsevier Ltd. All rights reserved.