MmWave Massive MIMO Based Wireless Backhaul for 5G Ultra-Dense Network

Ultra-dense network (UDN) has been considered as a promising candidate for future 5G network to meet the explosive data demand. To realize UDN, a reliable, Gigahertz bandwidth, and cost-effective backhaul connecting ultra-dense small-cell base stations (BSs) and macro-cell BS is prerequisite. Millimeter-wave (mmWave) can provide the potential Gbps traffic for wireless backhaul. Moreover, mmWave can be easily integrated with massive MIMO for the improved link reliability. In this article, we discuss the feasibility of mmWave massive MIMO based wireless backhaul for 5G UDN, and the benefits and challenges are also addressed. Especially, we propose a digitally-controlled phase-shifter network (DPSN) based hybrid precoding/combining scheme for mmWave massive MIMO, whereby the low-rank property of mmWave massive MIMO channel matrix is leveraged to reduce the required cost and complexity of transceiver with a negligible performance loss. One key feature of the proposed scheme is that the macro-cell BS can simultaneously support multiple small-cell BSs with multiple streams for each smallcell BS, which is essentially different from conventional hybrid precoding/combining schemes typically limited to single-user MIMO with multiple streams or multi-user MIMO with single stream for each user. Based on the proposed scheme, we further explore the fundamental issues of developing mmWave massive MIMO for wireless backhaul, and the associated challenges, insight, and prospect to enable the mmWave massive MIMO based wireless backhaul for 5G UDN are discussed.Comment: This paper has been accepted by IEEE Wireless Communications Magazine. This paper is related to 5G, ultra-dense network (UDN), millimeter waves (mmWave) fronthaul/backhaul, massive MIMO, sparsity/low-rank property of mmWave massive MIMO channels, sparse channel estimation, compressive sensing (CS), hybrid digital/analog precoding/combining, and hybrid beamforming. http://ieeexplore.ieee.org/stamp/stamp.jsp?tp=&arnumber=730653

REGULATION OF DENDRITIC SPINES BY 5-HT2A RECEPTOR SIGNALING PATHWAYS

Dendritic spines are small membranous protrusions from the dendrites of neuron, which are thought to serve as basic units of synaptic transmission, learning and memory. Disruptions in dendritic spine shape, size or number are associated with many brain diseases. Mounting evidence suggests that serotonin 2A (5-HT2A) receptors, the most abundant serotonin receptors in the prefrontal cortex, are involved in the regulation of dendritic spines. It has been suggested that both agonists (such as DOI) and antagonists (such as atypical antipsychotics) of 5-HT2A receptors can modulate different aspects of dendritic spines, however, the underlying mechanisms still remains unknown. In this dissertation, mechanisms underlying regulation of dendritic spines by both agonists and antagonists of 5-HT2A receptors are extensively studied and presented. I hypothesize that 5-HT2A receptor agonist regulate dendritic spines via transglutaminase- (TGase) catalyzed serotonylation of small G protein of the Rho family, whereas atypical antipsychotics change dendritic spines via activation of the Janus Kinase 2 (JAK2) signaling pathway. In the first study, the mechanisms and the functional consequences of 5-HT2A receptor-induced serotonylation of small G proteins of the Rho family were investigated in primary rat cortical neurons. Stimulation of 5-HT2A/2C receptors caused TGase-mediated transamidation and activation of Rac1 and Cdc42, but not RhoA, in both A1A1v cells and rat primary cortical culture. DOI-induced Rac1 transamidation occurs at Q61 in A1A1v cells, as demonstrated by site-directed mutagenesis at Q61 of Rac1. Furthermore, our findings were extended from 5-HT2A/2C receptors to another Gαq/11-coupled receptor, muscarinic acetylcholine receptors. In addition, stimulation of 5-HT2A/2C receptors by DOI leads to a transient dendritic spine enlargement, which was blocked by TGase inhibitor cystamine, suggesting 5-HT2A/2C receptors-induced transamidation of Rac1 and Cdc42 is involved in the regulation of dendritic spines by 5-HT2A/2C receptors. In the second study, to study the role of JAK2/ STAT pathway in the regulation of dendritic spines, Sprague-Dawley rats were pretreated with the JAK2 inhibitor AG490 or vehicle, followed by administration with olanzapine or vehicle daily for seven days. Microarray analysis of prefrontal cortices showed that 205 genes were significantly changed by AG490, olanzapine or the combination of both drugs compared to the controls. 92 of the 205 genes are changed by olanzapine via JAK2 signaling pathway. These genes are involved in the etiology of schizophrenia, neuronal signal transduction, neuronal growth factor, metabolism and energy, and synaptic plasticity. mRNA and protein levels of these genes were verified using real-time qPCR, western blot and the enzyme-linked immunosorbent assay (ELISA). Investigation on dendritic morphology shows that treatment with olanzapine induced a maturation in dendritic spines via both JAK2 dependent and independent pathways

Cascaded Cross-Module Residual Learning towards Lightweight End-to-End Speech Coding

Speech codecs learn compact representations of speech signals to facilitate data transmission. Many recent deep neural network (DNN) based end-to-end speech codecs achieve low bitrates and high perceptual quality at the cost of model complexity. We propose a cross-module residual learning (CMRL) pipeline as a module carrier with each module reconstructing the residual from its preceding modules. CMRL differs from other DNN-based speech codecs, in that rather than modeling speech compression problem in a single large neural network, it optimizes a series of less-complicated modules in a two-phase training scheme. The proposed method shows better objective performance than AMR-WB and the state-of-the-art DNN-based speech codec with a similar network architecture. As an end-to-end model, it takes raw PCM signals as an input, but is also compatible with linear predictive coding (LPC), showing better subjective quality at high bitrates than AMR-WB and OPUS. The gain is achieved by using only 0.9 million trainable parameters, a significantly less complex architecture than the other DNN-based codecs in the literature.Comment: Accepted for publication in INTERSPEECH 201

GPER1 stimulation alters posttranslational modification of RGSz1 and induces desensitization of 5-HT1A receptor signaling in the rat hypothalamus

The final, published version of this article is available at http://www.karger.com/?doi=10.1159/000369467.Hyperactivity of the hypothalamic-pituitary-adrenal axis is a consistent biological characteristic of depression and response normalization coincides with clinical responsiveness to antidepressant medications. Desensitization of serotonin 1A receptor (5-HT1AR) signaling in the hypothalamic paraventricular nucleus (PVN) follows selective serotonin reuptake inhibitor (SSRI) antidepressant treatment and contributes to the antidepressant response. Estradiol alone produces a partial desensitization of 5-HT1AR signaling, and synergizes with SSRIs to result in a complete and more rapid desensitization than with SSRIs alone as measured by a decrease in the oxytocin and adrenocorticotrophic hormone(ACTH) responses to 5-HT1AR stimulation. G protein-coupled estrogen receptor1 (GPER1) is necessary for estradiol-induced desensitization of 5-HT1AR signaling, although the underlying mechanisms are still unclear. We now find that stimulation of GPER1 with the selective agonist G-1 and non-selective stimulation of estrogen receptors dramatically alter isoform expression of a key component of the 5-HT1AR signaling pathway, RGSz1, a GTPase activating protein selective for Gαz, the Gα subunit necessary for 5-HT1AR-mediated hormone release. RGSz1 isoforms are differentially glycosylated, SUMOylated, and phosphorylated, and differentially distributed in subcellular organelles. High molecular weight RGSz1 is SUMOylated and glycosylated, localized to the detergent-resistant microdomain (DRM) of the cell membrane, and increased by estradiol and G-1 treatment. Because activated Gαz also localizes to the DRM, increased DRM-localized RGSz1 by estradiol and G-1could reduce Gαz activity, functionally uncoupling 5-HT1AR signaling. Peripheral G-1 treatment produced partial reduction in oxytocin and ACTH responses to 5-HT1AR-stimulation similar to direct injections into the PVN. Together, these results identify GPER1 and RGSz1 as novel targets for the treatment of depression

Whole-genome transcription and DNA methylation analysis of peripheral blood mononuclear cells identified aberrant gene regulation pathways in systemic lupus erythematosus

Hypermethylated CpG sites in PBMC of SLE patients comparing normal controls by genome-wide DNA methylation analysis. Three group comparisons, SLE LN+ vs. NC (S3-1), SLE LN− vs. NC (S3-2), and SLE (LN− and LN+) vs. NC (S3-3), were performed to identify hypermethylated DNA CpG sites by fold change (FC) > 1.2 and q value < 5% within each group. The 1813 common hypermethylated sites identified in each of the three group comparisons were then selected and listed in S3-4. (XLSX 814 kb