Performance analysis of contention based bandwidth request mechanisms in WiMAX networks

This article is posted here with the permission of IEEE. The official version can be obtained from the DOI below - Copyright @ 2010 IEEEWiMAX networks have received wide attention as they support high data rate access and amazing ubiquitous connectivity with great quality-of-service (QoS) capabilities. In order to support QoS, bandwidth request (BW-REQ) mechanisms are suggested in the WiMAX standard for resource reservation, in which subscriber stations send BW-REQs to a base station which can grant or reject the requests according to the available radio resources. In this paper we propose a new analytical model for the performance analysis of various contention based bandwidth request mechanisms, including grouping and no-grouping schemes, as suggested in the WiMAX standard. Our analytical model covers both unsaturated and saturated traffic load conditions in both error-free and error-prone wireless channels. The accuracy of this model is verified by various simulation results. Our results show that the grouping mechanism outperforms the no-grouping mechanism when the system load is high, but it is not preferable when the system load is light. The channel noise degrades the performance of both throughput and delay.This work was supported by the U.K. Engineering and Physical Sciences Research Council (EPSRC) under Grant EP/G070350/1 and by the Brunel University’s BRIEF Award

Simulation of Sound Absorption by Scattering Bodies Treated with Acoustic Liners Using a Time-Domain Boundary Element Method

Reducing aircraft noise is a major objective in the field of computational aeroacoustics. When designing next generation quiet aircraft, it is important to be able to accurately and efficiently predict the acoustic scattering by an aircraft body from a given noise source. Acoustic liners are an effective tool for aircraft noise reduction, and are characterized by a complex valued frequency-dependent impedance, Z(w). Converted into the time-domain using Fourier transforms, an impedance boundary condition can be used to simulate the acoustic wave scattering of geometric bodies treated with acoustic liners. This work uses an admittance boundary condition where the admittance, Y(w), is defined to be the inverse of impedance, i.e., Y(w) = 1/Z(w). An admittance boundary condition will be derived and coupled with a time domain boundary integral equation. The solution will be obtained iteratively using spatial and temporal basis functions and will allow for acoustic scattering problems to be modeled with geometries consisting of both unlined and soft surfaces. Stability will be demonstrated through eigenvalue analysis

Structural Basis for Human PECAM-1-Mediated Trans-homophilic Cell Adhesion

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HSV-2 Infection of Human Genital Epithelial Cells Upregulates TLR9 Expression Through the SP1/JNK Signaling Pathway

It is known that herpes simplex virus type 2 (HSV-2) triggers the activation of Toll-like receptor (TLR) 9 signaling pathway and the consequent production of antiviral cytokines in dendritic cells. However, the impact of HSV-2 infection on TLR9 expression and signaling in genital epithelial cells, the primary HSV-2 targets, has yet to be determined. In the current study, by using both human genital epithelial cell lines and primary genital epithelial cells as models, we found that HSV-2 infection enhances TLR9 expression at both mRNA and protein levels. Such enhancement is virus replication-dependent and CpG-independent, while the HSV-2-mediated upregulation of TLR9 does not activate TLR9 signaling pathway. Mechanistically, a SP1 binding site on TLR9 promoter appears to be essential for HSV-2-induced TLR9 transactivation. Upon HSV-2 infection, SP1 translocates from the cytoplasm to the nucleus, and consequently binds to TLR9 promoter. By using specific inhibitors, the JNK signaling pathway is shown to be involved in the HSV-2-induced TLR9 transactivation, while HSV-2 infection increases the phosphorylation but not the total level of JNK. In agreement, antagonism of JNK signaling pathway inhibits the HSV-2-induced SP1 nuclear translocation. Taken together, our study demonstrates that HSV-2 infection of human genital epithelial cells promotes TLR9 expression through SP1/JNK signaling pathway. Findings in this study provide insights into HSV-2-host interactions and potential targets for immune intervention

Investigations of the g factors and local structure for orthorhombic Cu^{2+}(1) site in fresh PrBa_{2}Cu_{3}O_{6+x} powders

The electron paramagnetic resonance (EPR) g factors g_x, g_y and g_z of the orthorhombic Cu^{2+}(1) site in fresh PrBa_{2}Cu_{3}O_{6+x} powders are theoretically investigated using the perturbation formulas of the g factors for a 3d^9 ion under orthorhombically elongated octahedra. The local orthorhombic distortion around the Cu^{2+}(1) site due to the Jahn-Teller effect is described by the orthorhombic field parameters from the superposition model. The [CuO6]^{10-} complex is found to experience an axial elongation of about 0.04 {\AA} along c axis and the relative bond length variation of about 0.09 {\AA} along a and b axes of the Jahn-Teller nature. The theoretical results of the g factors based on the above local structure are in reasonable agreement with the experimental data.Comment: 6 pages, 1 figur