Deterministic equivalent performance analysis of time-varying massive MIMO systems

© 2015 IEEE. Personal use of this material is permitted. Permission from IEEE must be obtained for all other uses, in any current or future media, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works, for resale or redistribution to servers or lists, or reuse of any copyrighted component of this work in other works.Delayed channel state information at the transmitter (CSIT) due to time variation of the channel, coming from the users' relative movement with regard to the BS antennas, is an inevitable degrading performance factor in practical systems. Despite its importance, little attention has been paid to the literature of multi-cellular multiple-input massive multiple-output (MIMO) system by investigating only the maximal ratio combining (MRC) receiver and the maximum ratio transmission (MRT) precoder. Hence, the contribution of this work is designated by the performance analysis/comparison of/with more sophisticated linear techniques, i.e., a minimum-mean-square-error (MMSE) detector for the uplink and a regularized zero-forcing (RZF) precoder for the downlink are assessed. In particular, we derive the deterministic equivalents of the signal-to-interference-plus-noise ratios (SINRs), which capture the effect of delayed CSIT, and make the use of lengthy Monte Carlo simulations unnecessary. Furthermore, prediction of the current CSIT after applying a Wiener filter allows to evaluate the mitigation capabilities of MMSE and RZF. Numerical results depict that the proposed achievable SINRs (MMSE/RZF) are more efficient than simpler solutions (MRC/MRT) in delayed CSIT conditions, and yield a higher prediction at no special computational cost due to their deterministic nature. Nevertheless, it is shown that massive MIMO are preferable even in time-varying channel conditions.Peer reviewe

Performance of massive MIMO uplink with zero-forcing receivers under delayed channels

© 2016 IEEE. Personal use of this material is permitted. Permission from IEEE must be obtained for all other uses, in any current or future media, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works, for resale or redistribution to servers or lists, or reuse of any copyrighted component of this work in other works.In this paper, we analyze the performance of the uplink communication of massive multicell multiple-input multiple-output (MIMO) systems under the effects of pilot contamination and delayed channels because of terminal mobility. The base stations (BSS) estimate the channels through the uplink training and then use zero-forcing (ZF) processing to decode the transmit signals from the users. The probability density function (pdf) of the signal-to-interference-plus-noise ratio (SINR) is derived for any finite number of antennas. From this pdf, we derive an achievable ergodic rate with a finite number of BS antennas in closed form. Insights into the impact of the Doppler shift (due to terminal mobility) at the low signal-to-noise ratio (SNR) regimes are exposed. In addition, the effects on the outage probability are investigated. Furthermore, the power scaling law and the asymptotic performance result by infinitely increasing the numbers of antennas and terminals (while their ratio is fixed) are provided. The numerical results demonstrate the performance loss for various Doppler shifts. Among the interesting observations revealed is that massive MIMO is favorable even under channel aging conditions.Peer reviewe

A Minorization-Maximization Method for Optimizing Sum Rate in Non-Orthogonal Multiple Access Systems

Non-orthogonal multiple access (NOMA) systems have the potential to deliver higher system throughput, compared to contemporary orthogonal multiple access techniques. For a linearly precoded multiple-input multiple-output (MISO) system, we study the downlink sum rate maximization problem, when the NOMA principles are applied. Being a non-convex and intractable optimization problem,we resort to approximate it with a minorization-maximization algorithm (MMA), which is a widely used tool in statistics. In each step of the MMA, we solve a second-order cone program, such that the feasibility set in each step contains that of the previous one, and is always guaranteed to be a subset of the feasibility set of the original problem. It should be noted that the algorithm takes a few iterations to converge. Furthermore, we study the conditions under which the achievable rates maximization can be further simplified to a low complexity design problem, and we compute the probability of occurrence of this event. Numerical examples are conducted to show a comparison of the proposed approach against conventional multiple access systems. NOMA is reported to provide better spectral and power efficiency with a polynomial time computational complexity.Comment: Submitted for journal publicatio

Transcription cofactor GRIP1 differentially affects myeloid cell-driven neuroinflammation and response to IFN-β therapy.

Macrophages (MФ) and microglia (MG) are critical in the pathogenesis of multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). Glucocorticoids (GCs) and interferon β (IFN-β) are frontline treatments for MS, and disrupting each pathway in mice aggravates EAE. Glucocorticoid receptor-interacting protein 1 (GRIP1) facilitates both GR and type I IFN transcriptional actions; hence, we evaluated the role of GRIP1 in neuroinflammation. Surprisingly, myeloid cell-specific loss of GRIP1 dramatically reduced EAE severity, immune cell infiltration of the CNS, and MG activation and demyelination specifically during the neuroinflammatory phase of the disease, yet also blunted therapeutic properties of IFN-β. MФ/MG transcriptome analyses at the bulk and single-cell levels revealed that GRIP1 deletion attenuated nuclear receptor, inflammatory and, interestingly, type I IFN pathways and promoted the persistence of a homeostatic MG signature. Together, these results uncover the multifaceted function of type I IFN in MS/EAE pathogenesis and therapy, and an unexpectedly permissive role of myeloid cell GRIP1 in neuroinflammation

Radiolysis of NaCl at high and low temperatures: development of size distribution of bubbles and colloids

New experimental results are presented on low temperature irradiation (18 °C) of rock-salt samples which had been exposed to initial doses up to 320 GRad at 100 °C. Differential scanning calorimetry (DSC) shows that the latent heat of melting (LHM) of sodium colloids decreases during subsequent low-temperature irradiation, whereas the stored energy (SE) increases slowly, indicating that the process of radiolysis continues. The decrease of the LHM is due to dissolution of large colloids, because the intensities of the melting peaks decrease during the second stage irradiation at low temperature. The model is formulated to describe the nucleation kinetics and the evolution of the size distribution of chlorine precipitates and sodium colloids in NaCl under high dose irradiation. It is shown that the mechanism of dissolution of large Na colloids during low temperature irradiation can be related to melting of sodium colloids.

Electrostatically Shielded Quantum Confined Stark Effect Inside Polar Nanostructures

The effect of electrostatic shielding of the polarization fields in nanostructures at high carrier densities is studied. A simplified analytical model, employing screened, exponentially decaying polarization potentials, localized at the edges of a QW, is introduced for the ES-shielded quantum confined Stark effect (QCSE). Wave function trapping within the Debye-length edge-potential causes blue shifting of energy levels and gradual elimination of the QCSE red-shifting with increasing carrier density. The increase in the e−h wave function overlap and the decrease of the radiative emission time are, however, delayed until the “edge-localization” energy exceeds the peak-voltage of the charged layer. Then the wave function center shifts to the middle of the QW, and behavior becomes similar to that of an unbiased square QW. Our theoretical estimates of the radiative emission time show a complete elimination of the QCSE at doping densities ≥1020 cm−3, in quantitative agreement with experimental measurements

Inhibitor of Kappa B Epsilon (IκBε) Is a Non-Redundant Regulator of c-Rel-Dependent Gene Expression in Murine T and B Cells

Inhibitors of kappa B (IκBs) -α, -β and -ε effect selective regulation of specific nuclear factor of kappa B (NF-κB) dimers according to cell lineage, differentiation state or stimulus, in a manner that is not yet precisely defined. Lymphocyte antigen receptor ligation leads to degradation of all three IκBs but activation only of subsets of NF-κB-dependent genes, including those regulated by c-Rel, such as anti-apoptotic CD40 and BAFF-R on B cells, and interleukin-2 (IL-2) in T cells. We report that pre-culture of a mouse T cell line with tumour necrosis factor-α (TNF) inhibits IL-2 gene expression at the level of transcription through suppressive effects on NF-κB, AP-1 and NFAT transcription factor expression and function. Selective upregulation of IκBε and suppressed nuclear translocation of c-Rel were very marked in TNF-treated, compared to control cells, whether activated via T cell receptor (TCR) pathway or TNF receptor. IκBε associated with newly synthesised c-Rel in activated cells and, in contrast to IκBα and -β, showed enhanced association with p65/c-Rel in TNF-treated cells relative to controls. Studies in IκBε-deficient mice revealed that basal nuclear expression and nuclear translocation of c-Rel at early time-points of receptor ligation were higher in IκBε−/− T and B cells, compared to wild-type. IκBε−/− mice exhibited increased lymph node cellularity and enhanced basal thymidine incorporation by lymphoid cells ex vivo. IκBε−/− T cell blasts were primed for IL-2 expression, relative to wild-type. IκBε−/− splenic B cells showed enhanced survival ex vivo, compared to wild-type, and survival correlated with basal expression of CD40 and induced expression of CD40 and BAFF-R. Enhanced basal nuclear translocation of c-Rel, and upregulation of BAFF-R and CD40 occurred despite increased IκBα expression in IκBε−/− B cells. The data imply that regulation of these c-Rel-dependent lymphoid responses is a non-redundant function of IκBε