Channel Estimation for Frequency Division Duplexing Multi-user Massive MIMO Systems via Tensor Compressive Sensing

To make full use of space multiplexing gains for the multi-user massive multiple-input multiple-output, accurate channel state information at the transmitter (CSIT) is required. However, the large number of users and antennas make CSIT a higher-order data representation. Tensor-based compressive sensing (TCS) is a promising method that is suitable for high-dimensional data processing; it can reduce training pilot and feedback overhead during channel estimation. In this paper, we consider the channel estimation in frequency division duplexing (FDD) multi-user massive MIMO system. A novel estimation framework for three dimensional CSIT is presented, in which the modes include the number of transmitting antennas, receiving antennas, and users. The TCS technique is employed to complete the reconstruction of three dimensional CSIT. The simulation results are given to demonstrate that the proposed estimation approach outperforms existing algorithms

Reliability Modeling and Optimization Strategy for Manufacturing System Based on RQR Chain

Accurate and dynamic reliability modeling for the running manufacturing system is the prerequisite to implement preventive maintenance. However, existing studies could not output the reliability value in real time because their abandonment of the quality inspection data originated in the operation process of manufacturing system. Therefore, this paper presents an approach to model the manufacturing system reliability dynamically based on their operation data of process quality and output data of product reliability. Firstly, on the basis of importance explanation of the quality variations in manufacturing process as the linkage for the manufacturing system reliability and product inherent reliability, the RQR chain which could represent the relationships between them is put forward, and the product qualified probability is proposed to quantify the impacts of quality variation in manufacturing process on the reliability of manufacturing system further. Secondly, the impact of qualified probability on the product inherent reliability is expounded, and the modeling approach of manufacturing system reliability based on the qualified probability is presented. Thirdly, the preventive maintenance optimization strategy for manufacturing system driven by the loss of manufacturing quality variation is proposed. Finally, the validity of the proposed approach is verified by the reliability analysis and optimization example of engine cover manufacturing system

Pathway Switching Explains the Sharp Response Characteristic of Hypoxia Response Network

Hypoxia induces the expression of genes that alter metabolism through the hypoxia-inducible factor (HIF). A theoretical model based on differential equations of the hypoxia response network has been previously proposed in which a sharp response to changes in oxygen concentration was observed but not quantitatively explained. That model consisted of reactions involving 23 molecular species among which the concentrations of HIF and oxygen were linked through a complex set of reactions. In this paper, we analyze this previous model using a combination of mathematical tools to draw out the key components of the network and explain quantitatively how they contribute to the sharp oxygen response. We find that the switch-like behavior is due to pathway-switching wherein HIF degrades rapidly under normoxia in one pathway, while the other pathway accumulates HIF to trigger downstream genes under hypoxia. The analytic technique is potentially useful in studying larger biomedical networks

Present-day activity and seismic potential of the north Qinling fault, southern ordos block, central China, as revealed from GPS data and seismicity

The North Qinling Fault, located at the boundary of the North China Block and the South China Block, represents an important tectonic structure between the Weihe Basin and the Qinling Mountains, and controls the subsidence and expansion of the Weihe Basin. This fault has been highly active and has caused strong earthquakes since the Holocene and in a pre-seismic stage currently, as indicated by the many paleoearthquake traces found along it. To determine the present-day activity and seismic potential of the North Qinling Fault, by inverting GPS data, we produced fault locking depth, slip rate, and regional strain fields maps; moreover, based on seismicity, we produced a seismic b-value map. Combining this information with modern seismicity, we were able to comprehensively analyze the seismic potential of different fault segments. Our inversion of GPS data showed that the slip rate of the western segment of the fault (Qingjiangkou–Xitangyu) and the correspondent locking depth are 1.33 mm/a and 13.54 km, respectively, while the slip rate of the middle segment (Xitangyu–Fengyukou) and the correspondent locking depth are 0.45 mm/a and 8.58 km, respectively; finally, the slip rate of the eastern segment (Xitangyu–Daiyu) and the correspondent locking depth are 0.36 mm/a and 21.46 km, respectively. The locking depths of the western and middle segments of the fault are shallower than 90% of the seismic cutoff depth, while the locking depth of the eastern segment of the fault is similar to 90% of the seismic cutoff depth, indicating that “deep creep” occurs in the western and middle segments, while the eastern segment is locked. Modern small earthquakes have involved the western and middle segments of the fault, while the eastern segment has acted as a seismic gap with weak seismicity, characterized by a higher shear strain value and a lower b-value. These characteristics reflect the relationship between the locking depth and seismicity distribution. The results of our comprehensive analysis, combined with field geological surveys, show that the eastern segment of the North Qinling Fault has a strong seismic potential and is presently locked

RNA-seq reveals role of cell-cycle regulating genes in the pathogenicity of a field very virulent infectious bursal disease virus

Infectious bursal disease virus (IBDV) infection causes highly contagious and immunosuppressive disease in poultry. The thymus, serving as the primary organ for T cell maturation and differentiation, plays an important role in the pathogenicity of IBDV in the infected chickens. However, there are no reports on the molecular pathogenesis of IBDV in the thymus currently. The aim of the study was to elucidate the molecular mechanisms underlying the pathogenicity of a field very virulent (vv) IBDV strain NN1172 in the thymus of SPF chickens using integrative transcriptomic and proteomic analyses. Our results showed that a total of 4,972 Differentially expressed genes (DEGs) in the thymus of NN1172-infected chickens by transcriptomic analysis, with 2,796 up-regulated and 2,176 down-regulated. Meanwhile, the proteomic analysis identified 726 differentially expressed proteins (DEPs) in the infected thymus, with 289 up-regulated and 437 down-regulated. Overall, a total of 359 genes exhibited differentially expression at both mRNA and protein levels, with 134 consistently up-regulated and 198 genes consistently down-regulated, as confirmed through a comparison of the RNA-seq and the proteomic datasets. The gene ontology (GO) analysis unveiled the involvement of both DEGs and DEPs in diverse categories encompassing cellular components, biological processes, and molecular functions in the pathological changes in IBDV-infected thymus. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the host mainly displayed severely disruption of cell survival/repair, proliferation and metabolism pathway, meanwhile, the infection triggers antiviral immune activation with a potential emphasis on the MDA5 pathway. Network inference analysis identified seven core hub genes, which include CDK1, TYMS, MCM5, KIF11, CCNB2, MAD2L1, and MCM4. These genes are all associated with cell-cycle regulating pathway and are likely key mediators in the pathogenesis induced by NN1172 infection in the thymus. This study discovered dominant pathways and genes which enhanced our understanding of the molecular mechanisms underlying IBDV pathogenesis in the thymus

Polyhydroxy Fullerenes (Fullerols or Fullerenols): Beneficial Effects on Growth and Lifespan in Diverse Biological Models

Recent toxicological studies on carbon nanomaterials, including fullerenes, have led to concerns about their safety. Functionalized fullerenes, such as polyhydroxy fullerenes (PHF, fullerols, or fullerenols), have attracted particular attention due to their water solubility and toxicity. Here, we report surprisingly beneficial and/or specific effects of PHF on model organisms representing four kingdoms, including the green algae Pseudokirchneriella subcapitata, the plant Arabidopsis thaliana, the fungus Aspergillus niger, and the invertebrate Ceriodaphnia dubia. The results showed that PHF had no acute or chronic negative effects on the freshwater organisms. Conversely, PHF could surprisingly increase the algal culture density over controls at higher concentrations (i.e., 72% increase by 1 and 5 mg/L of PHF) and extend the lifespan and stimulate the reproduction of Daphnia (e.g. about 38% by 20 mg/L of PHF). We also show that at certain PHF concentrations fungal growth can be enhanced and Arabidopsis thaliana seedlings exhibit longer hypocotyls, while other complex physiological processes remain unaffected. These findings may open new research fields in the potential applications of PHF, e.g., in biofuel production and aquaculture. These results will form the basis of further research into the mechanisms of growth stimulation and life extension by PHF

A miR-327–FGF10–FGFR2-mediated autocrine signaling mechanism controls white fat browning

Understanding the molecular mechanisms regulating beige adipocyte formation may lead to the development of new therapies to combat obesity. Here, we report a miRNA-based autocrine regulatory pathway that controls differentiation of preadipocytes into beige adipocytes. We identify miR-327 as one of the most downregulated miRNAs targeting growth factors in the stromal-vascular fraction (SVF) under conditions that promote white adipose tissue (WAT) browning in mice. Gain- and loss-of-function experiments reveal that miR-327 targets FGF10 to prevent beige adipocyte differentiation. Pharmacological and physiological β-adrenergic stimulation upregulates FGF10 levels and promotes preadipocyte differentiation into beige adipocytes. In vivo local delivery of miR-327 to WATs significantly compromises the beige phenotype and thermogenesis. Contrarily, systemic inhibition of miR-327 in mice induces browning and increases whole-body metabolic rate under thermoneutral conditions. Our data provide mechanistic insight into an autocrine regulatory signaling loop that regulates beige adipocyte formation and suggests that the miR-327–FGF10–FGFR2 signaling axis may be a therapeutic targets for treatment of obesity and metabolic diseases

Survival effect of PDGF-CC rescues neurons from apoptosis in both brain and retina by regulating GSK3β phosphorylation

Platelet-derived growth factor CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase 3β (GSK3β) activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-hydroxydopamine–induced Parkinson’s dopaminergic neuronal death, and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody, or short hairpin RNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3β phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC–PDGF receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions

Induction of Epithelial Mesenchimal Transition and Vasculogenesis in the Lenses of Dbl Oncogene Transgenic Mice

BACKGROUND: The Dbl family of proteins represents a large group of proto-oncogenes involved in cell growth regulation. The numerous domains that are present in many Dbl family proteins suggest that they act to integrate multiple inputs in complicated signaling networks involving the Rho GTPases. Alterations of the normal function of these proteins lead to pathological processes such as developmental disorders and neoplastic transformation. We generated transgenic mice introducing the cDNA of Dbl oncogene linked to the metallothionein promoter into the germ line of FVB mice and found that onco-Dbl expression in mouse lenses affected proliferation, migration and differentiation of lens epithelial cells. RESULTS: We used high density oligonucleotide microarray to define the transcriptional profile induced by Dbl in the lenses of 2 days, 2 weeks, and 6 weeks old transgenic mice. We observed modulation of genes encoding proteins promoting epithelial-mesenchymal transition (EMT), such as down-regulation of epithelial cell markers and up-regulation of fibroblast markers. Genes encoding proteins involved in the positive regulation of apoptosis were markedly down regulated while anti-apoptotic genes were strongly up-regulated. Finally, several genes encoding proteins involved in the process of angiogenesis were up-regulated. These observations were validated by histological and immunohistochemical examination of the transgenic lenses where vascularization can be readily observed. CONCLUSION: Onco-Dbl expression in mouse lens correlated with modulation of genes involved in the regulation of EMT, apoptosis and vasculogenesis leading to disruption of the lens architecture, epithelial cell proliferation, and aberrant angiogenesis. We conclude that onco-Dbl has a potentially important, previously unreported, capacity to dramatically alter epithelial cell migration, replication, polarization and differentiation and to induce vascularization of an epithelial tissue