Transmit Antenna Selection in Cognitive MIMO Relaying with Multiple Primary Transceivers

We consider transmit antenna selection (TAS) in cognitive multiple-input multiple-output (MIMO) relay networks, as an interference-aware design for secondary users (SUs) to ensure power and interference constraints of multiple primary users (PUs). In doing so, we derive new exact and asymptotic expressions for the outage probability of TAS with maximal ratio combining (TAS/MRC) and with selection combining (TAS/SC) over Rayleigh fading. The proposed analysis and simulations highlight that TAS/MRC and TAS/SC with decode-and-forward relaying achieve the same diversity order in cognitive MIMO networks, which scales with the minimum number of antennas at the SUs. Furthermore, we accurately characterize the outage gap between TAS/MRC and TAS/SC relaying as a concise ratio of their array gains.

Relay Selection for Security Enhancement in Cognitive Relay Networks

This letter proposes several relay selection policies for secure communication in cognitive decode-and-forward (DF) relay networks, where a pair of cognitive relays are opportunistically selected for security protection against eavesdropping. The first relay transmits the secrecy information to the destination,
and the second relay, as a friendly jammer, transmits the jamming signal to confound the eavesdropper. We present new exact closed-form expressions for the secrecy outage probability. Our analysis and simulation results strongly support our conclusion that the proposed relay selection policies can enhance the performance of secure cognitive radio. We also confirm that the error floor phenomenon is created in the absence of jamming.

On the Security of Cognitive Radio Networks

Cognitive radio has emerged as an essential recipe for future high-capacity high-coverage multi-tier hierarchical networks. Securing data transmission in these networks is of utmost importance. In this paper, we consider the cognitive wiretap channel and propose multiple antennas to secure the transmission at the physical layer, where the eavesdropper overhears the transmission from the secondary transmitter to the secondary receiver. The secondary receiver and the eavesdropper are equipped with multiple antennas, and passive eavesdropping is considered where the channel state information of the eavesdropper’s channel is not available at the secondary transmitter. We present new closedform expressions for the exact and asymptotic secrecy outage probability. Our results reveal the impact of the primary network on the secondary network in the presence of a multi-antenna wiretap channel.

Cognitive amplify-and-forward relay networks with beamforming under primary user power constraint over Nakagami-m fading channels

In this paper, we analyze the performance of cognitive amplify-and-forward (AF) relay networks with beamforming under the peak interference power constraint of the primary user (PU). We focus on the scenario that beamforming is applied at the multi-antenna secondary transmitter and receiver. Also, the secondary relay network operates in channel state information-assisted AF mode, and the signals undergo independent Nakagami-m fading. In particular, closed-form expressions for the outage probability and symbol error rate (SER) of the considered network over Nakagami-m fading are presented. More importantly, asymptotic closed-form expressions for the outage probability and SER are derived. These tractable closed-form expressions for the network performance readily enable us to evaluate and examine the impact of network parameters on the system performance. Specifically, the impact of the number of antennas, the fading severity parameters, the channel mean powers, and the peak interference power is addressed. The asymptotic analysis manifests that the peak interference power constraint imposed on the secondary relay network has no effect on the diversity gain. However, the coding gain is affected by the fading parameters of the links from the primary receiver to the secondary relay network

Secure D2D Communication in Large-Scale Cognitive Cellular Networks with Wireless Power Transfer

In this paper, we investigate secure device-to-device (D2D) communication in energy harvesting large-scale cognitive cellular networks. The energy constrained D2D transmitter harvests energy from multi-antenna equipped power beacons (PBs), and communicates with the corresponding receiver using the spectrum of the cellular base stations (BSs). We introduce a power transfer model and an information signal model to enable wireless energy harvesting and secure information transmission. In the power transfer model, we propose a new power transfer policy, namely, best power beacon (BPB) power transfer. To characterize the power transfer reliability of the proposed policy, we derive new closed-form expressions for the exact power outage probability and the asymptotic power outage probability with large antenna arrays at PBs. In the information signal model, we present a new comparative framework with two receiver selection schemes: 1) best receiver selection (BRS), and 2) nearest receiver selection (NRS). To assess the secrecy performance, we derive new expressions for the secrecy throughput considering the two receiver selection schemes using the BPB power transfer policies. We show that secrecy performance improves with increasing densities of PBs and D2D receivers because of a larger multiuser diversity gain. A pivotal conclusion is reached that BRS achieves better secrecy performance than NRS but demands more instantaneous feedback and overhead.

Multiuser Scheduling for Cognitive MIMO with Channel Estimation Errors and Feedback Delay

A multiuser scheduling multiple-input multiple-output (MIMO) cognitive radio network (CRN) with space-time block coding (STBC) is considered in this paper, where one secondary base station (BS) communicates with one secondary user (SU) selected from K candidates. The joint impact of imperfect channel state information (CSI) in BS → SUs and BS → PU due to channel estimation errors and feedback delay on the outage performance is firstly investigated. We obtain the exact outage probability expressions for the considered network under the peak interference power IP at PU and maximum transmit power Pm at BS which cover perfect/imperfect CSI scenarios in BS → SUs and BS → PU. In addition, asymptotic expressions of outage probability in high SNR region are also derived from which we obtain several important insights into the system design. For example, only with perfect CSIs in BS → SUs, i.e., without channel estimation errors and feedback delay, the multiuser diversity can be exploited. Finally, simulation results confirm the correctness of our analysis.

Generalized Selection Combining for Cognitive Relay Networks over Nakagami-m Fading

We consider transmit antenna selection with receive generalized selection combining (TAS/GSC) for cognitive decodeand-forward (DF) relaying in Nakagami-m fading channels. In an effort to assess the performance, the probability density function and the cumulative distribution function of the endto-end SNR are derived using the moment generating function, from which new exact closed-form expressions for the outage probability and the symbol error rate are derived. We then derive a new closed-form expression for the ergodic capacity. More importantly, by deriving the asymptotic expressions for the outage probability and the symbol error rate, as well as the high SNR approximations of the ergodic capacity, we establish new design insights under the two distinct constraint scenarios: 1) proportional interference power constraint, and 2) fixed interference power constraint. Several pivotal conclusions are reached. For the first scenario, the full diversity order of the
outage probability and the symbol error rate is achieved, and the high SNR slope of the ergodic capacity is 1/2. For the second scenario, the diversity order of the outage probability and the symbol error rate is zero with error floors, and the high SNR slope of the ergodic capacity is zero with capacity ceiling.

Simulation using novel equipment designed to explain spirometric abnormalities in respiratory disease enhances learning in higher cognitive domains

Simulation of disorders of respiratory mechanics shown by spirometry provides insight into the pathophysiology of disease but some clinically important disorders have not been simulated and none have been formally evaluated for education. We have designed simple mechanical devices which, along with existing simulators, enable all the main dysfunctions which have diagnostic value in spirometry to be simulated and clearly explained with visual and haptic feedback. We modelled the airways as Starling resistors by a clearly visible mechanical action to simulate intra- and extra-thoracic obstruction. A narrow tube was used to simulate fixed large airway obstruction and inelastic bands to simulate restriction. We hypothesized that using simulators whose action explains disease promotes learning especially in higher domain educational objectives. The main features of obstruction and restriction were correctly simulated. Simulation of variable extra-thoracic obstruction caused blunting and plateauing of inspiratory flow, and simulation of intra-thoracic obstruction caused limitation of expiratory flow with marked dynamic compression. Multiple choice tests were created with questions allocated to lower (remember and understand) or higher cognitive domains (apply, analyse and evaluate). In a cross-over design, overall mean scores increased after 1½ h simulation spirometry (43-68 %, effect size 1.06, P < 0.0001). In higher cognitive domains the mean score was lower before and increased further than lower domains (Δ 30 vs 20 %, higher vs lower effect size 0.22, P < 0.05). In conclusion, the devices successfully simulate various patterns of obstruction and restriction. Using these devices medical students achieved marked enhancement of learning especially in higher cognitive domains.

Untargeted Metabolomic Analysis of Human Plasma Indicates Differentially Affected Polyamine and L-Arginine Metabolism in Mild Cognitive Impairment Subjects Converting to Alzheimer’s Disease

This study combined high resolution mass spectrometry (HRMS), advanced chemometrics and pathway enrichment analysis to analyse the blood metabolome of patients attending the memory clinic: cases of mild cognitive impairment (MCI; n = 16), cases of MCI who upon subsequent follow-up developed Alzheimer's disease (MCI_AD; n = 19), and healthy age-matched controls (Ctrl; n = 37). Plasma was extracted in acetonitrile and applied to an Acquity UPLC HILIC (1.7μm x 2.1 x 100 mm) column coupled to a Xevo G2 QTof mass spectrometer using a previously optimised method. Data comprising 6751 spectral features were used to build an OPLS-DA statistical model capable of accurately distinguishing Ctrl, MCI and MCI_AD. The model accurately distinguished (R2 = 99.1%; Q2 = 97%) those MCI patients who later went on to develop AD. S-plots were used to shortlist ions of interest which were responsible for explaining the maximum amount of variation between patient groups. Metabolite database searching and pathway enrichment analysis indicated disturbances in 22 biochemical pathways, and excitingly it discovered two interlinked areas of metabolism (polyamine metabolism and L-Arginine metabolism) were differentially disrupted in this well-defined clinical cohort. The optimised untargeted HRMS methods described herein not only demonstrate that it is possible to distinguish these pathologies in human blood but also that MCI patients 'at risk' from AD could be predicted up to 2 years earlier than conventional clinical diagnosis. Blood-based metabolite profiling of plasma from memory clinic patients is a novel and feasible approach in improving MCI and AD diagnosis and, refining clinical trials through better patient stratification.

Plasma Clusterin Levels and the rs11136000 Genotype in Individuals with Mild Cognitive Impairment and Alzheimer's Disease

Aim: Substantial evidence links atherosclerosis and Alzheimer's disease (AD). Apolipoproteins, such as apolipoprotein E, have a causal relationship with both diseases. The rs11136000 SNP within the CLU gene, which encodes clusterin (apolipoprotein J), is also associated with increased AD risk. The aim of this study was to investigate the relationship between plasma clusterin and the rs11136000 genotype in mild cognitive impairment (MCI) and AD.

Methods: Plasma and DNA samples were collected from control, MCI and AD subjects (n=142, 111, 154, respectively). Plasma clusterin was determined by ELISA and DNA samples were genotyped for rs11136000 by TaqMan assay.

Results: Plasma clusterin levels were higher in MCI and AD subjects vs. controls (222.3 +/- 61.3 and 193.6 +/- 58.2 vs. 178.6 +/- 52.3 mu g/ml, respectively; p

Conclusion: This study examined control, MCI and AD subjects, identifying for the first time that plasma clusterin levels were influenced, not only by the presence of AD, but also the transitional stage of MCI, while rs11136000 genotype only influenced plasma clusterin levels in the control group. The increase in plasma clusterin in MCI and AD subjects may occur in response to the disease process and would be predicted to increase binding capacity for amyloid-beta peptides in plasma, enhancing their removal from the brain.