Massive MIMO Channel Models: A Survey

The exponential traffic growth of wireless communication networks gives rise to both the insufficient network capacity and excessive carbon emissions. Massive multiple-input multiple-output (MIMO) can improve the spectrum efficiency (SE) together with the energy efficiency (EE) and has been regarded as a promising technique for the next generation wireless communication networks. Channel model reflects the propagation characteristics of signals in radio environments and is very essential for evaluating the performances of wireless communication systems. The purpose of this paper is to investigate the state of the art in channel models of massive MIMO. First, the antenna array configurations are presented and classified, which directly affect the channel models and system performance. Then, measurement results are given in order to reflect the main properties of massive MIMO channels. Based on these properties, the channel models of massive MIMO are studied with different antenna array configurations, which can be used for both theoretical analysis and practical evaluation

Challenges of massive access in highly dense LTE-advanced networks with machine-to-machine communications

The Main purpose of the present study was to evaluate whether REM sleep deprivation (RSD) influences the development of anhedonia in rats in a peripheral neuropathy model induced by sciatic nerve constriction injury (CCI). Anhedonia was measured by assessing daily water/sucrose intake. Four groups were assessed: control (CTRL), CCI, RSD, and CCI + RSD (n = 8/group). Intake data were collected at baseline (mean of 3 days), on the 1st and 2nd days after a CCI or SHAM procedure, during 4 days of RSD, and during an additional 10 days (rebound period or equivalent in home-cage rats). Control rats spontaneously and progressively increased Sucrose intake, reaching final daily volumes significantly greater than respective initial baseline amounts. RSD promoted an additional and immediate significant increase in sucrose intake during sleep deprivation days. The CCI group did not display a spontaneous, progressive increase in sucrose intake. When CO was combined with RSD, the increase in sucrose intake induced by RSD was significantly lower than in animals submitted to RSD alone; the (CCI + RSD) group also failed to show a spontaneous and progressive increase in sucrose intake. The present findings indicate that animal model of chronic neuropathy exhibits reduced sucrose ingestion. Accordingly, this anhedonic condition that constitutes to the core manifestation of depressive states did not occur in response to a single episode of total RSD. (C) 2009 Elsevier B.V. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Breast Cancer Stem Cells Are Regulated by Mesenchymal Stem Cells through Cytokine Networks

International audienceWe have used in vitro and mouse xenograft models to examine the interaction between breast cancer stem cells (CSC) and bone marrow-derived mesenchymal stem cells (MSC). We show that both of these cell populations are organized in a cellular hierarchy in which primitive aldehyde dehydrogenase expressing mesenchymal cells regulate breast CSCs through cytokine loops involving IL6 and CXCL7. In NOD/SCID mice, labeled MSCs introduced into the tibia traffic to sites of growing breast tumor xenografts where they accelerated tumor growth by increasing the breast CSC population. With immunochemistry, we identified MSC-CSC niches in these tumor xenografts as well as in frozen sections from primary human breast cancers. Bone marrow-derived MSCs may accelerate human breast tumor growth by generating cytokine networks that regulate the CSC population. Cancer Res; 71(2); 614-24. (C) 2011 AACR

mir-93 regulates the cell cycle in SUM159 cells.

<p>A. SUM159 cells were stained with Aldefluor and Hoechst33342 and dead cells excluded by 7-AAD staining. Cells from G0/G1 and S/G2/M were sorted from ALDH⁺ or ALDH⁻ populations and mir-93 expression was measured with qRT-PCR. B. Cell cycle analysis of pTRIPZ-SUM159-mir-93 cells in the presence or absence of DOX for 7 days. Propidium iodide staining followed by flow cytometry was used to analyze cell cycle distribution. mir-93 induction with DOX resulted in a decreased proportion of cells in G0/G1 and an increased proportion of cells in S/G2/M. *p<0.05; Error bars represent mean ± STDEV.</p

mir-93 inhibits tumor growth and metastasis by decreasing CSCs in SUM159 cells.

<p>A. SUM159 cells were transduced with the pTRIPZ-mir-93 lentivirus and selected with Puromycin for 7 days. Tetracycline (DOX) induces mir-93 expression in suspension-cultured SUM159 cells by 10 hours; B. 1×10⁶ SUM159 cells or pTRIPZ-SUM159 -mir-93 cells were plated in T75 flasks and, after overnight, the cells were treated with Vehicle control, with (DOX) or without (CTRL) DOX (1 ug/ml), docetaxel (10 nM) or the combination for 7 days. Cells were utilized for Aldefluor assay and stained for Annexin V-APC and DAPI for apoptosis assay. C. 100 k pTRIPZ-SUM159-mir-93 cells were injected into the 4^th fatpads of NOD/SCID mice. The treatment started as indicated by the red arrow. DOX alone (1 mg/ml in drinking water), or docetaxel (10 mg/kg i.p. once weekly) alone, or the combination inhibits SUM159 tumor growth in vivo (note: The Y-axis is on a logarithmic scale). D. Tumors from each group were collected. ALDH was accessed by the Aldefluor assay on viable dissociated cells and by ALDH1 immunohistochemistry on fixed sections. E. Serial dilutions of cells obtained from these xenografts were implanted in the 4^th fatpads of secondary mice, which received no further treatment. F. 10k pTRIPZ-SUM159-mir-93 cells were injected into the 4^th fatpads of NOD/SCID mice. The treatment started immediately after injection as indicated by the red arrow and stopped as indicated by the green arrow. G. 200k pTRIPZ-SUM159-mir-93-Luc cells in 100 ul of PBS were injected into the left ventricle of NOD/SCID mice. The treatment started immediately after injection as indicated by the red arrow and stopped as indicated by the green arrow. Metastasis formation was monitored using bioluminescence imaging. Quantification of the normalized photon flux, measured at weekly intervals following inoculation. *p<0.05; Error bars represent mean ± STDEV. The colored “*” on the side of the tumor growth curve indicates that the tumor growth or metastasis is significantly different between the control group and the group with the same colored curve.</p

mir-93 targets stem cell regulatory genes.

<p>A. Schematic representation of the experimental design to identify the direct targets of mir-93 in SUM159 cells. B. Activity of the luciferase gene linked to the 3′UTR of AKT3, SOX4, or STAT3. The pMIR-REPORT firefly luciferase reporter plasmids with the wild-type 3′UTR sequences of AKT3, SOX4, or STAT3 were transiently transfected into pTRIPZ-mir-93-SUM159 cells and an internal control ACTB luciferase reporter was co-transfected for normalization. The cells were treated with or without DOX. Luciferase activities were measured after 48 hr. The relative luciferase activity was calculated as the ratio of (the results from the cells transfected by individual reporter)/(the results from the cells transfected by the internal control in the same cell group). The data are mean and standard deviation (SD) of separate transfections (n = 4). *p<0.05; Error bars represent mean ± STDEV.</p

mir-93 promotes tumor growth by increasing CSCs in MCF7 cells.

<p>A. Mir-93 is expressed equally in CD24⁻CD44⁺ and bulk (non-CD24⁻CD44⁺) populations of MCF7 cells. B. 1×10⁶ pTRIPZ-MCF7-mir-93 cells were plated in T75 flasks and, after overnight, the cells were treated with Vehicle control, DOX (1 ug/ml), docetaxel (10 nM) or the combination for 7 days. DOX alone, docetaxel alone or the combination increased the CD24⁻CD44⁺ population <i>in vitro</i>. C. 1000k pTRIPZ-MCF7-mir-93 cells were injected into the 4^th fatpads of NOD/SCID mice. Treatment was initiated as indicated by the red arrow. DOX alone (1 mg/ml in drinking water) promoted MCF7 tumor growth in vivo; docetaxel (10 mg/kg i.p. once weekly) alone or the combination inhibits MCF7 tumor growth in vivo. D. Tumors from each group were collected. Analysis for CD24 and CD44 was performed on dissociated cells. DOX alone, docetaxel alone, or the combination increased the CD24⁻CD44⁺ populations in MCF7. E. Serial dilutions of cells obtained from these xenografts were implanted in the 4^th fatpads of secondary mice, which received no further treatment. Cells from DOX-, docetaxel-, or combination-treated tumors formed secondary tumors at all dilutions (50000, 5000, 500), whereas only higher numbers of cells (50000, 5000) obtained from control xenografts were able to generate tumors. *p<0.05; Error bars represent mean ± STDEV. The colored “*” on the side of the tumor growth curve indicates that tumor growth is significantly different between the control group and the group with the same colored curve.</p

mir-93-negative SUM159 cells have increased tumor-initiating capacity.

<p>A. ALDH⁺ cells from SUM159 cells shows lower mir-93 expression level in comparison to ALDH⁻ cells as accessed by qRT-PCR. P<0.05; Error bars represent mean ± STDEV. B. A schematic of mir-93-Sensor-GFP lentiviral construct; C. SUM159 cells were transduced with the mir-93-sensor-GFP lentivirus and selected with hygromycin B, and cells were sorted based on the GFP expression. A serial dilution of mir-93-negative (sensor/GFP-positive) SUM159 cells and mir-93-positive (sensor/GFP-negative) SUM159 cells were injected into the 4^th fatpads of NOD/SCID mouse. *p<0.05. D. mir-93-negative cells gave rise to tumors containing both mir-93-negative and mir-93-positive cell populations, but mir-93-positive cells only gave rise to tumors containing mir-93-positive cell populations.</p

mir-93 initiates MET in SUM159 cells.

<p>A. pTRIPZ-SUM159-mir-93 cells were plated in 2-well chamber slides with (DOX) or without (CTRL) Doxycycline for 7 days. E-Cadherin and Vimentin were deleted by immunofluorescence staining. Expression of mir-93 in SUM159 cells causes them to assume a more epithelial appearance associated with a decrease in Vimentin and an increase in membrane localized E-Cadherin expression. The phase micrographs for CTRL and DOX are also shown. E-Cadherin, Green; Vimentin, Red; DAPI, Blue. A representative sample from 3 independent samples is shown. B. The effect of mir-93 expression on a panel of epithelial and mesenchymal markers at the mRNA level as accessed by qPCR. pTRIPZ-SUM159-mir-93 cells were plated with or without DOX, and ALDH⁺ and ALDH⁻ cells were sorted at different times (12 hours, 1 day, 3 days, 8 days, 15 days) by Aldefluor assay. qRT-PCR was utilized to access the effects of mir-93 on mRNA expression of mesenchymal markers (Vimentin, N-Cadherin and Twist), epithelial markers (E-Cadherin and Claudin), and TGFβR2. *p<0.05; Error bars represent mean ± STDEV.</p