Mitigating Cross-Network Interference in Cognitive Spectrum Sharing with Opportunistic Relaying

We examine the impact of primary and secondary interference on opportunistic relaying in cognitive spectrum sharing networks. In particular, new closed-form exact and asymptotic expressions for the outage probability of cognitive opportunistic relaying are derived over Rayleigh and Nakagami-m fading channels. Our analysis presents revealing insights into the diversity and array gains, diversity-multiplexing tradeoff, impact of primary transceivers' positions, and the optimal position of relays. We highlight that cognitive opportunistic relaying achieves the full diversity gain which is a product of the number of relays and the minimum Nakagami-m fading parameter in the secondary network. Furthermore, we confirm that the diversity gain reduces to zero when the peak interference constraint in the secondary network is proportional to the interference power from the primary network.

Full-Duplex Spectrum Sharing in Cooperative Single Carrier Systems

In this paper, we propose cyclic prefix single carrier (CP-SC) full-duplex transmission in cooperative spectrum sharing to achieve multipath diversity gain and full-duplex spectral efficiency. Integrating full-duplex transmission into cooperative spectrum sharing systems results in two intrinsic problems: 1) the peak interference power constraint at the PUs are concurrently inflicted on the transmit power at the secondary source (SS) and the secondary relays (SRs); and 2) the residual loop interference occurs between the transmit and the receive antennas at the secondary relays. Thus, examining the effects of residual loop interference under peak interference power constraint at the primary users and maximum transmit power constraints at the SS and the SRs is a particularly challenging problem in frequency selective fading channels. To do so, we derive and quantitatively evaluate the exact and the asymptotic outage probability for several relay selection policies in frequency selective fading channels. Our results manifest that a zero diversity gain is obtained with full-duplex.

Full-Duplex Spectrum Sharing in Cooperative Single Carrier Systems

We propose cyclic prefix single carrier full-duplex transmission in amplify-and-forward cooperative spectrum sharing networks to achieve multipath diversity and full-duplex spectral efficiency. Integrating full-duplex transmission into cooperative spectrum sharing systems results in two intrinsic problems: 1) the residual loop interference occurs between the transmit and the receive antennas at the secondary relays and 2) the primary users simultaneously suffer interference from the secondary source (SS) and the secondary relays (SRs). Thus, examining the effects of residual loop interference under peak interference power constraint at the primary users and maximum transmit power constraints at the SS and the SRs is a particularly challenging problem in frequency selective fading channels. To do so, we derive and quantitatively compare the lower bounds on the outage probability and the corresponding asymptotic outage probability for max–min relay selection, partial relay selection, and maximum interference relay selection policies in frequency selective fading channels. To facilitate comparison, we provide the corresponding analysis for half-duplex. Our results show two complementary regions, named as the signal-to-noise ratio (SNR) dominant region and the residual loop interference dominant region, where the multipath diversity and spatial diversity can be achievable only in the SNR dominant region, however the diversity gain collapses to zero in the residual loop interference dominant region.

Secure Transmission in Spectrum Sharing MIMO Networks with Generalized Antenna Selection over Nakagami-m Channels

In this paper, we investigate the secrecy outage performance of spectrum sharing multiple-input multiple-output networks using generalized transmit antenna selection with maximal ratio combining over Nakagami-m channels. In particular, the outdated channel state information is considered at the process of antenna selection due to feedback delay. Considering a practical passive eavesdropper scenario, we derive the exact and asymptotic closed-form expressions of secrecy outage probability, which enable us to evaluate the secrecy performance with high efficiency and present a new design insight into the impact of key parameters on the secrecy performance. In addition, the analytical results demonstrate that the achievable secrecy diversity order is only determined by the parameters of the secondary network, while other parameters related to primary or eavesdropper’s channels have a significantly impact on the secrecy coding gain. 

Association of antipsychotic drug-induced weight gain with a 5-HT2C receptor gene polymorphism

A side-effect of treatment with antipsychotic drugs for schizophrenia is increased body fat, which leads to further morbidity and poor adherence to treatment. The 5-hydroxytryptamine 2C receptor (5-HT2C) has been associated with this effect; we aimed to establish whether a genetic polymorphism of the promoter region of this receptor affects weight gain after drug treatment in first-episode patients with schizophrenia. We noted significantly less weight gain in patients with the -759T variant allele (p=0.0003) than in those without this allele, who were more likely to have substantial (>7%) weight gain (p=0.002). We have identified a genetic factor that is associated with antipsychotic drug-induced weight gain.

A gain-of-function mutation in the HIF2A gene in familial erythrocytosis

Hypoxia-inducible factor (HIF) a, which has three isoforms, is central to the continuous balancing of the supply and demand of oxygen throughout the body. HIF-a is a transcription factor that modulates a wide range of processes, including erythropoiesis, angiogenesis, and cellular metabolism. We describe a family with erythrocytosis and a mutation in the HIF2A gene, which encodes the HIF-2a protein. Our functional studies indicate that this mutation leads to stabilization of the HIF-2a protein and suggest that wild-type HIF-2a regulates erythropoietin production in adults.