Joint Evaluation of Reduced Feedback Scheme, Scheduling, and Rate Adaptation in OFDMA Systems with Feedback Delays

Orthogonal frequency division multiple access (OFDMA) systems exploit multiuser diversity and frequency-selectivity to achieve high spectral efficiencies. However, they require considerable feedback for scheduling and rate adaptation, and are sensitive to feedback delays. We develop a comprehensive analysis of the OFDMA system throughput as a function of the feedback scheme, frequency-domain scheduler, and discrete rate adaptation rule in the presence of feedback delays. We analyze the popular best-n and threshold-based feedback schemes. We show that for both the greedy and round-robin schedulers, the throughput degradation, given a feedback delay, depends primarily on the fraction of feedback reduced by the feedback scheme and not the feedback scheme itself. Even small feedback delays at low vehicular speeds are shown to significantly degrade the throughput. We also show that optimizing the link adaptation thresholds as a function of the feedback delay can effectively counteract the detrimental effect of delays.

Joint Routing, Scheduling and Power Control in Multihop MIMO Networks with MAC and Broadcast Links

We consider the problem of joint routing, scheduling and power control in a multihop wireless network when the nodes have multiple antennas. We focus on exploiting the multiple degrees-of-freedom available at each transmitter and receiver due to multiple antennas. Specifically we use multiple antennas at each node to form multiple access and broadcast links in the network rather than just point to point links. We show that such a generic transmission model improves the system performance significantly. Since the complexity of the resulting optimization problem is very high, we also develop efficient suboptimal solutions for joint routing, scheduling and power control in this setup.

Optimal Joint Antenna Selection and Power Adaptation in Underlay Cognitive Radios

Transmit antenna selection (AS) is a popular, low hardware complexity technique that improves the performance of an underlay cognitive radio system, in which a secondary transmitter can transmit when the primary is on but under tight constraints on the interference it causes to the primary. The underlay interference constraint fundamentally changes the criterion used to select the antenna because the channel gains to the secondary and primary receivers must be both taken into account. We develop a novel and optimal joint AS and transmit power adaptation policy that minimizes a Chernoff upper bound on the symbol error probability (SEP) at the secondary receiver subject to an average transmit power constraint and an average primary interference constraint. Explicit expressions for the optimal antenna and power are provided in terms of the channel gains to the primary and secondary receivers. The SEP of the optimal policy is at least an order of magnitude lower than that achieved by several ad hoc selection rules proposed in the literature and even the optimal antenna selection rule for the case where the transmit power is either zero or a fixed value.

Joint estimation of synchronization impairments in MIMO-OFDM system

A joint Maximum Likelihood (ML) estimation algorithm for the synchronization impairments such as Carrier Frequency Offset (CFO), Sampling Frequency Offset (SFO) and Symbol Timing Error (STE) in single user MIMO-OFDM system is investigated in this work. A received signal model that takes into account the nonlinear effects of CFO, SFO, STE and Channel Impulse Response (CIR) is formulated. Based on the signal model, a joint ML estimation algorithm is proposed. Cramer-Rao Lower Bound (CRLB) for the continuous parameters CFO and SFO is derived for the cases of with and without channel response effects and is used to compare the effect of coupling between different estimated parameters. The performance of the estimation method is studied through numerical simulations.

Joint Scheduling & Jamming for Data Secrecy in Wireless Networks

The broadcast nature of the wireless medium jeopardizes secure transmissions. Cryptographic measures fail to ensure security when eavesdroppers have superior computational capability; however, it can be assured from information theoretic security approaches. We use physical layer security to guarantee non-zero secrecy rate in single source, single destination multi-hop networks with eavesdroppers for two cases: when eavesdropper locations and channel gains are known and when their positions are unknown. We propose a two-phase solution which consists of finding activation sets and then obtaining transmit powers subject to SINR constraints for the case when eavesdropper locations are known. We introduce methods to find activation sets and compare their performance. Necessary but reasonable approximations are made in power minimization formulations for tractability reasons. For scenarios with no eavesdropper location information, we suggest vulnerability region (the area having zero secrecy rate) minimization over the network. Our results show that in the absence of location information average number of eavesdroppers who have access to data is reduced.

NOD2-Nitric Oxide-responsive MicroRNA-146a Activates Sonic Hedgehog Signaling to Orchestrate Inflammatory Responses in Murine Model of Inflammatory Bowel Disease

Background: Genetic variants of NOD2 are linked to inflammatory bowel disease (IBD) etiology. Results: DSS model of colitis in wild-type and inducible nitric-oxide synthase (iNOS) null mice revealed that NOD2-iNOS/NO-responsive microRNA-146a targets NUMB gene facilitating Sonic hedgehog (SHH) signaling. Conclusion: miR-146a-mediated NOD2-SHH signaling regulates gut inflammation. Significance: Identification of novel regulators of IBD provides new insights into pathophysiology and development of new therapy concepts. Inflammatory bowel disease (IBD) is a debilitating chronic inflammatory disorder of the intestine. The interactions between enteric bacteria and genetic susceptibilities are major contributors of IBD etiology. Although genetic variants with loss or gain of NOD2 functions have been linked to IBD susceptibility, the mechanisms coordinating NOD2 downstream signaling, especially in macrophages, during IBD pathogenesis are not precisely identified. Here, studies utilizing the murine dextran sodium sulfate model of colitis revealed the crucial roles for inducible nitric-oxide synthase (iNOS) in regulating pathophysiology of IBDs. Importantly, stimulation of NOD2 failed to activate Sonic hedgehog (SHH) signaling in iNOS null macrophages, implicating NO mediated cross-talk between NOD2 and SHH signaling. NOD2 signaling up-regulated the expression of a NO-responsive microRNA, miR-146a, that targeted NUMB gene and alleviated the suppression of SHH signaling. In vivo and ex vivo studies confirmed the important roles for miR-146a in amplifying inflammatory responses. Collectively, we have identified new roles for miR-146a that established novel cross-talk between NOD2-SHH signaling during gut inflammation. Potential implications of these observations in therapeutics could increase the possibility of defining and developing better regimes to treat IBD pathophysiology.

Crystal structures of SCP2-thiolases of Trypanosomatidae, human pathogens causing widespread tropical diseases: the importance for catalysis of the cysteine of the unique HDCF loop

Thiolases are essential CoA-dependent enzymes in lipid metabolism. In the present study we report the crystal structures of trypanosomal and leishmanial SCP2 (sterol carrier protein, type-2)-thiolases. Trypanosomatidae cause various widespread devastating (sub)-tropical diseases, for which adequate treatment is lacking. The structures reveal the unique geometry of the active site of this poorly characterized subfamily of thiolases. The key catalytic residues of the classical thiolases are two cysteine residues, functioning as a nucleophile and an acid/base respectively. The latter cysteine residue is part of a CxG motif. Interestingly, this cysteine residue is not conserved in SCP2-thiolases. The structural comparisons now show that in SCP2-thiolases the catalytic acid/base is provided by the cysteine residue of the HDCF motif, which is unique for this thiolase subfamily. This HDCF cysteine residue is spatially equivalent to the CxG cysteine residue of classical thiolases. The HDCF cysteine residue is activated for acid/base catalysis by two main chain NH-atoms, instead of two water molecules, as present in the CxG active site. The structural results have been complemented with enzyme activity data, confirming the importance of the HDCF cysteine residue for catalysis. The data obtained suggest that these trypanosomatid SCP2-thiolases are biosynthetic thiolases. These findings provide promise for drug discovery as biosynthetic thiolases catalyse the first step of the sterol biosynthesis pathway that is essential in several of these parasites.

Low complexity joint estimation of synchronization impairments in sparse channel for MIMO-OFDM system

Low complexity joint estimation of synchronization impairments and channel in a single-user MIMO-OFDM system is presented in this paper. Based on a system model that takes into account the effects of synchronization impairments such as carrier frequency offset, sampling frequency offset, and symbol timing error, and channel, a Maximum Likelihood (ML) algorithm for the joint estimation is proposed. To reduce the complexity of ML grid search, the number of received signal samples used for estimation need to be reduced. The conventional channel estimation techniques using Least-Squares (LS) or Maximum a posteriori (MAP) methods fail for the reduced sample under-determined system, which results in poor performance of the joint estimator. The proposed ML algorithm uses Compressed Sensing (CS) based channel estimation method in a sparse fading scenario, where the received samples used for estimation are less than that required for an LS or MAP based estimation. The performance of the estimation method is studied through numerical simulations, and it is observed that CS based joint estimator performs better than LS and MAP based joint estimator. (C) 2013 Elsevier GmbH. All rights reserved.

Guided-wave-based damage detection in a composite T-joint using 3D scanning laser Doppler vibrometer

Composite T-joints are commonly used in modern composite airframe, pressure vessels and piping structures, mainly to increase the bending strength of the joint and prevents buckling of plates and shells, and in multi-cell thin-walled structures. Here we report a detailed study on the propagation of guided ultrasonic wave modes in a composite T-joint and their interactions with delamination in the co-cured co-bonded flange. A well designed guiding path is employed wherein the waves undergo a two step mode conversion process, one is due to the web and joint filler on the back face of the flange and the other is due to the delamination edges close to underneath the accessible surface of the flange. A 3D Laser Doppler Vibrometer is used to obtain the three components of surface displacements/velocities of the accessible face of the flange of the T-joint. The waves are launched by a piezo ceramic wafer bonded on to the back surface of the flange. What is novel in the proposed method is that the location of any change in material/geometric properties can be traced by computing a frequency domain power flow along a scan line. The scan line can be chosen over a grid either during scan or during post-processing of the scan data off-line. The proposed technique eliminates the necessity of baseline data and disassembly of structure for structural interrogation.

Evaluation of benzothiophene carboxamides as analgesics and anti-inflammatory agents

Nonsteroid anti-inflammatory drugs (NSAIDs) represent standard therapy for the alleviation of pain and inflammation. At present various classes of compounds have been reported as selective inhibitors of cyclooxygenase-2 (COX-2). However, they are associated with adverse side effects. To address these issues, we report here a new class of compounds that exhibit potent analgesic and anti-inflammatory response. Substituted bromo-benzothiophene carboxamides (4-11) were examined for their analgesic and anti-inflammatory properties. Our findings demonstrate that newly synthesized bromo-benzothiophene carboxamide derivatives 4, 6, and 8 attenuate nociception and inflammation at lower concentration than classical NSAIDs, such as ibuprofen. These compounds act by selectively inhibiting COX-2 and by disrupting the prostaglandin-E2-dependent positive feedback of COX-2 regulation, which was further substantiated by reduction in the levels of cytokines, chemokines, neutrophil accumulation, synthesis of prostaglandin-E2, expression of COX-2, and neutrophil activation at lower concentration than the classic NSAID ibuprofen. Toxicological study reveals that these compounds are well tolerated and metabolized to avoid any toxicity. Thus, these molecules represent a new class of analgesic and anti-inflammatory agents. (c) 2014 IUBMB Life, 66(3):201-211, 2014

A Stochastic Chemical Dynamic Approach to Correlate Autoimmunity and Optimal Vitamin-D Range

Motivated by several recent experimental observations that vitamin-D could interact with antigen presenting cells (APCs) and T-lymphocyte cells (T-cells) to promote and to regulate different stages of immune response, we developed a coarse grained but general kinetic model in an attempt to capture the role of vitamin-D in immunomodulatory responses. Our kinetic model, developed using the ideas of chemical network theory, leads to a system of nine coupled equations that we solve both by direct and by stochastic (Gillespie) methods. Both the analyses consistently provide detail information on the dependence of immune response to the variation of critical rate parameters. We find that although vitamin-D plays a negligible role in the initial immune response, it exerts a profound influence in the long term, especially in helping the system to achieve a new, stable steady state. The study explores the role of vitamin-D in preserving an observed bistability in the phase diagram (spanned by system parameters) of immune regulation, thus allowing the response to tolerate a wide range of pathogenic stimulation which could help in resisting autoimmune diseases. We also study how vitamin-D affects the time dependent population of dendritic cells that connect between innate and adaptive immune responses. Variations in dose dependent response of anti-inflammatory and pro-inflammatory T-cell populations to vitamin-D correlate well with recent experimental results. Our kinetic model allows for an estimation of the range of optimum level of vitamin-D required for smooth functioning of the immune system and for control of both hyper-regulation and inflammation. Most importantly, the present study reveals that an overdose or toxic level of vitamin-D or any steroid analogue could give rise to too large a tolerant response, leading to an inefficacy in adaptive immune function.