Achievable sum-rate of multiuser massive MIMO downlink in ricean fading channels

We investigate the achievable ergodic sum-rate of multi-user multiple-input multiple-output systems in Ricean fading channels. We first derive a lower bound on the average signal-to-leakage-and-noise ratio by utilizing the Mullen's inequality, which is then used to analyze the effect of channel mean information on the achievable sum-rate. With these results, a novel statistical-eigenmode space-division multipleaccess downlink transmission scheme is proposed. For this scheme, we derive an exact closed-form expression for the achievable ergodic sum-rate. Our results show that the achievable ergodic sum-rate converges to a saturation value in the high signal-to-noise ratio (SNR) region and reaches to a lower limit value in the lower Ricean K-factor range. In addition, we present tractable upper and lower bounds, which are shown to be tight for any SNR and Ricean K-factor value. Finally, the theoretical analysis is validated via numerical simulations.

Energy efficiency analysis of rank-1 Ricean fading MIMO channels

This paper studies the energy efficiency (EE) of a point-to-point rank-1 Ricean fading multiple-input-multiple-output (MIMO) channel. In particular, a tight lower bound and an asymptotic approximation for the EE of the considered MIMO system are presented, under the assumption that the channel is unknown at the transmitter and perfectly known at the receiver. Moreover, the effects of different system parameters, namely, transmit power, spectral efficiency (SE), and number of transmit and receive antennas, on the EE are analytically investigated. An important observation is that, in the high signal-to-noise ratio regime and with the other system parameters fixed, the optimal transmit power that maximizes the EE increases as the Ricean-K factor increases. On the contrary, the optimal SE and the optimal number of transmit antennas decrease as K increases.

Massive MIMO in sparse channels

Massive multi-user multiple-input multiple-output (MU-MIMO) systems are cellular networks where the base stations (BSs) are equipped with hundreds of antennas, N, and communicate with tens of mobile stations (MSs), K, such that, N ≫ K ≫ 1. Contrary to most prior works, in this paper, we consider the uplink of a single-cell massive MIMO system operating in sparse channels with limited scattering. This case is of particular importance in most propagation scenarios, where the prevalent Rayleigh fading assumption becomes idealistic. We derive analytical approximations for the achievable rates of maximum-ratio combining (MRC) and zero-forcing (ZF) receivers. Furthermore, we study the asymptotic behavior of the achievable rates for both MRC and ZF receivers, when N and K go to infinity under the condition that N/K → c ≥ 1. Our results indicate that the achievable rate of MRC receivers reaches an asymptotic saturation limit, whereas the achievable rate of ZF receivers grows logarithmically with the number of MSs.

TRPV2 Channels Contribute to Stretch-Activated Cation Currents and Myogenic Constriction in Retinal Arterioles

<p>Purpose: Activation of the transient receptor potential channels, TRPC6, TRPM4, and TRPP1 (PKD2), has been shown to contribute to the myogenic constriction of cerebral arteries. In the present study we sought to determine the potential role of various mechanosensitive TRP channels to myogenic signaling in arterioles of the rat retina.</p><p>Methods: Rat retinal arterioles were isolated for RT-PCR, Fura-2 Ca2+ microfluorimetry, patch-clamp electrophysiology, and pressure myography studies. In some experiments, confocal immunolabeling of wholemount preparations was used to examine the localization of specific mechanosensitive TRP channels in retinal vascular smooth muscle cells (VSMCs).</p><p>Results: Reverse transcription-polymerase chain reaction analysis demonstrated mRNA expression for TRPC1, M7, V1, V2, V4, and P1, but not TRPC6 or M4, in isolated retinal arterioles. Immunolabeling revealed plasma membrane, cytosolic and nuclear expression of TRPC1, M7, V1, V2, V4, and P1 in retinal VSMCs. Hypoosmotic stretch-induced Ca2+ influx in retinal VSMCs was reversed by the TRPV2 inhibitor tranilast and the nonselective TRPP1/V2 antagonist amiloride. Inhibitors of TRPC1, M7, V1, and V4 had no effect. Hypoosmotic stretch-activated cation currents were similar in Na+ and Cs+ containing solutions suggesting no contribution by TRPP1 channels. Direct plasma membrane stretch triggered cation current activity that was blocked by tranilast and specific TRPV2 pore-blocking antibodies and mimicked by the TRPV2 activator, Δ9-tetrahydrocannabinol. Preincubation of retinal arterioles with TRPV2 blocking antibodies prevented the development of myogenic tone.</p><p>Conclusions: Our results suggest that retinal VSMCs express a range of mechanosensitive TRP channels, but only TRPV2 appears to contribute to myogenic signaling in this vascular bed.</p>