Secure Transmission in MIMO Wiretap Channels Using General-Order Transmit Antenna Selection with Outdated CSI

In this paper, we propose general-order transmit antenna selection to enhance the secrecy performance of multiple-input–multiple-output multieavesdropper channels with outdated channel state information (CSI) at the transmitter. To evaluate the effect of the outdated CSI on the secure transmission of the system, we investigate the secrecy performance for two practical scenarios, i.e., Scenarios I and II, where the eavesdropper's CSI is not available at the transmitter and is available at the transmitter, respectively. For Scenario I, we derive exact and asymptotic closed-form expressions for the secrecy outage probability in Nakagami- m fading channels. In addition, we also derive the probability of nonzero secrecy capacity and the \varepsilon -outage secrecy capacity, respectively. Simple asymptotic expressions for the secrecy outage probability reveal that the secrecy diversity order is reduced when the CSI is outdated at the transmitter, and it is independent of the number of antennas at each eavesdropper N_text\rm{E} , the fading parameter of the eavesdropper's channel m_text\rm{E} , and the number of eavesdroppers M . For Scenario II, we make a comprehensive analysis of the average secrecy capacity obtained by the system. Specifically, new closed-form expressions for the exact and asymptotic average secrecy capacity are derived, which are valid for general systems with an arbitrary number of antennas, number of eavesdroppers, and fading severity parameters. Resorting to these results, we also determine a high signal-to-noise ratio power offset to explicitly quantify the impact of the main c- annel and the eavesdropper's channel on the average secrecy capacity.

Hyperglycemia and Diabetes Downregulate the Functional Expression of TRPV4 Channels in Retinal Microvascular Endothelium

Retinal endothelial cell dysfunction is believed to play a key role in the etiology and pathogenesis of diabetic retinopathy. Numerous studies have shown that TRPV4 channels are critically involved in maintaining normal endothelial cell function. In the current paper, we demonstrate that TRPV4 is functionally expressed in the endothelium of the retinal microcirculation and that both channel expression and activity is downregulated by hyperglycaemia. Quantitative PCR and immunostaining demonstrated molecular expression of TRPV4 in cultured bovine retinal microvascular endothelial cells (RMECs). Functional TRPV4 activity was assessed in cultured RMECs from endothelial Ca2+-responses recorded using fura-2 microfluorimetry and electrophysiological recordings of membrane currents. The TRPV4 agonist 4α-phorbol 12,13-didecanoate (4-αPDD) increased [Ca2+]i in RMECs and this response was largely abolished using siRNA targeted against TRPV4. These Ca2+-signals were completely inhibited by removal of extracellular Ca2+, confirming their dependence on influx of extracellular Ca2+. The 4-αPDD Ca2+-response recorded in the presence of cyclopiazonic acid (CPA), which depletes the intracellular stores preventing any signal amplification through store release, was used as a measure of Ca2+-influx across the cell membrane. This response was blocked by HC067047, a TRPV4 antagonist. Under voltage clamp conditions, the TRPV4 agonist GSK1016790A stimulated a membrane current, which was again inhibited by HC067047. Following incubation with 25mM D-glucose TRPV4 expression was reduced in comparison with RMECs cultured under control conditions, as were 4αPDD-induced Ca2+-responses in the presence of CPA and ion currents evoked by GSK1016790A. Molecular expression of TRPV4 in the retinal vascular endothelium of 3 months' streptozotocin-induced diabetic rats was also reduced in comparison with that in age-matched controls. We conclude that hyperglycaemia and diabetes reduce the molecular and functional expression of TRPV4 channels in retinal microvascular endothelial cells. These changes may contribute to diabetes induced endothelial dysfunction and retinopathy.

CaV3.1 T-Type Ca2+ Channels Contribute to Myogenic Signalling in Rat Retinal Arterioles

Purpose: Although L-type Ca2+ channels are known to play a key role in the myogenic reactivity of retinal arterial vessels, the involvement of other types of voltage-gated Ca2+ channels in this process remains unknown. In the present study we have investigated the contribution of T-type Ca2+ channels to myogenic signalling in arterioles of the rat retinal microcirculation.

Methods: Confocal immunolabelling of wholemount preparations was used to investigate the localisation of CaV3.1-3 channels in retinal arteriolar smooth muscle cells. T-type currents and the contribution of T-type channels to myogenic signalling were assessed by whole-cell patch-clamp recording and pressure myography of isolated retinal arteriole segments.

Results: Strong immunolabelling for CaV3.1 was observed on the plasma membrane of retinal arteriolar smooth muscle cells. In contrast, no expression of CaV3.2 or CaV3.3 could be detected in retinal arterioles, although these channels were present on glial cell end feet surrounding the vessels and retinal ganglion cells, respectively. TTA-A2 sensitive T-type currents were recorded in retinal arteriolar myocytes with biophysical properties distinct from those of the L-type currents present in these cells. Inhibition of T-type channels using TTA-A2 or ML-218 dilated isolated, myogenically active, retinal arterioles.

Conclusions: CaV3.1 T-type Ca2+ channels are functionally expressed on arteriolar smooth muscle cells of retinal arterioles and play an important role in myogenic signalling in these vessels. The work has important implications concerning our understanding of the mechanisms controlling blood flow autoregulation in the retina and its disruption during ocular disease.

Functional and pharmacological characterization of volume-regulated anion channels in human normal and cystic fibrosis bronchial and nasal epithelial cells

Volume-regulated anion channels (VRACs) are widely present in various cell types and have important functions ranging from regulatory volume decrease to control of cell proliferation and apoptosis. Here we aimed to compare the biophysical features and pharmacological profiles of VRAC currents in healthy and cystic fibrosis (CF) respiratory epithelial cells in order to characterize these currents both functionally and pharmacologically. Whole-cell electrophysiology was used to characterize the VRAC current in normal (16HBE14o-; HBE) and CF cell lines (CFBE14o-; CFBE), as well as in native human nasal epithelial cells. Application of hypotonic solution produced current responses of similar sizes in both HBE and CFBE cells. Biophysical properties of VRACs, such as instantaneous activation and deactivation upon voltage step, some inactivation at potentials positive to 40 mV and outwardly-rectifying I-V curves, were indistinguishable in both cell types. Extensive pharmacological analysis of the currents revealed a similar pharmacological profile in response to three blockers--NPPB, DCPIB and DIDS. Native primary human nasal epithelial cells from both healthy and CF volunteers also showed typical VRAC responses of comparable sizes. VRACs in these cells were more sensitive to external solution hypotonicity compared to HBE and CFBE cells. In all cell types studied robust VRAC currents could be induced at constant cell volume by G-protein activation with GTPγS infusion. This study provides the first extensive comparative functional and pharmacological analysis of VRAC currents in normal and CF airway epithelial cells and shows that VRACs are unimpaired molecularly or functionally in CF.

Dual-Hop Cognitive Amplify-and-Forward Relaying Networks over η− μ Fading Channels

This paper presents a thorough performance analysis of dual-hop cognitive amplify-and-forward (AF) relaying networks under spectrum-sharing mechanism over independent non-identically distributed (i.n.i.d.) 􀀀 fading channels. In order to guarantee the quality-of-service (QoS) of primary networks, both maximum tolerable peak interference power Q at the primary users (PUs) and maximum allowable transmit power P at secondary users (SUs) are considered to constrain transmit power at the cognitive transmitters. For integer-valued fading parameters, a closed-form lower bound for the outage probability (OP) of the considered networks is obtained. Moreover, assuming arbitrary-valued fading parameters, the lower bound in integral form for the OP is derived. In order to obtain further insights on the OP performance, asymptotic expressions for the OP at high SNRs are derived, from which the diversity/coding gains and the diversity-multiplexing gain tradeoff (DMT) of the secondary network can be readily deduced. It is shown that the diversity gain and also the DMT are solely determined by the fading parameters of the secondary network whereas the primary network only affects the coding gain. The derived results include several others available in previously published works as special cases, such as those for Nakagami-m fading channels. In addition, performance evaluation results have been obtained by Monte Carlo computer simulations which have verified the accuracy of the theoretical analysis.