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In this letter, a dilating and embedding scheme for constructing sparse multiple-input and multiple-output radar arrays is addressed, which seeks to increase the uniform degrees of freedom (uDOFs) and reduce the mutual coupling effects for a given number of transmitters and receivers (Tx/Rx). According to this scheme, a dilated maximum interelement spacing constraint (MISC) array with an embedded thinned coprime array in the collocated MIMO radar for DOA estimation is proposed. Theoretical analysis shows that the proposed array can provide higher uDOFs and is robust in a scenario with heavy levels of mutual coupling. Numerical simulations are conducted to validate its aforementioned advantages in line with the design scheme. [ABSTRACT FROM AUTHOR]

Cisplatin (CP) is used as an antineoplastic drug in the clinic, but its nephrotoxicity limits its use. Grape seed proanthocyanidin extract (GSPE) is a powerful antioxidant. In this study, we investigated whether GSPE can prevent CP-induced nephrotoxicity and explored the underlying mechanism. Male C57/BL6 mice were randomly divided into four groups: control group (N), CP group (C), receiving an intraperitoneal (ip) injection of 20 mg/kg CP, GSPE group (G), receiving an intragastric (ig) dose of 500 mg/kg GSPE, and CP+GSPE group (C+G), where ig administration of GSPE was performed 30 min prior to ip injection of CP, followed by an additional ig administration of GSPE 72 h later. Blood and kidney samples were collected 120 h after treatment. The pathological changes in the kidney were examined by periodic acid-Schiff (PAS) staining, while the protein levels of glucose-regulated protein 78 (GRP78), phosphorylated-extracellular signal-regulated kinase (p-ERK) and caspase-12 were examined by western blotting and immunohistochemical staining. Apoptosis was examined by a terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Compared to the CP group, the CP+GSPE group had a significant decrease in the level of blood urea nitrogen (BUN), serum creatinine (Scr) and reduced renal index (RI) (P<0.05), and showed limited histopathological damage. The number of TUNEL-positive cells was significantly reduced in the CP+GSPE group compared to the CP group (P<0.05), and the protein expression of GRP78, p-ERK and caspase-12 was significantly reduced in the CP+GSPE group (P<0.05). We conclude that GSPE can protect the renal function from CP-induced nephrotoxicity and can attenuate the endoplasmic reticulum (ER) stress-induced apoptosis via regulation of the caspase-12 pathway. [ABSTRACT FROM AUTHOR]

Bone morphogenetic protein 7 (BMP7) is a member of the transforming growth factor-β (TGF-β) superfamily and was initially identified as a protein that may induce bone and cartilage growth in the bone matrix. The present study was conducted in order to investigate the effect of BMP7 on the expression of nestin and glial fibrillary acidic protein (GFAP) in the brain tissue of rats after cerebral ischemia-reperfusion injury. A total of 40 adult healthy male Sprague-Dawley rats were used in this study, of which 10 randomly received a sham operation and the remaining 30 were subjected to a 2-h ischemia and 24-h reperfusion by ligation of the left external and internal carotid arteries. Twenty successfully modeled rats were equally randomized into the treatment and control groups. The rats in the treatment group were intervened with 250 μl BMP7 (0.1 mg/kg) via tail vein injection, whereas the rats in the control and sham operation groups were injected with an equal volume of sterile water for injection. Neurological deficits were evaluated by the Bederson's method at 24 h after ischemia-reperfusion and the brain infarct volume was assessed by 2,3,5-triphenyl tetrazolium chloride coloring. The neuronal apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end-labelling (TUNEL) staining and the expression of nestin and GFAP in the three groups was analyzed by immunohistochemistry. Bederson's score (t=4.66, P<0.01) and focus infarction (t=6.98, P<0.01) were lower in the BMP7 treatment group compared to those in the control group. In addition, the number of TUNEL-positive cells in the treatment group was lower compared to that in the control group (P<0.01). Compared to the control group, the expression of nestin and GFAP was enhanced in the BMP7 treatment group (P<0.01). Therefore, BMP7 may upregulate the expression of nestin and GFAP and promote neural regeneration to protect animals against ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

Background: Astragalus is a widely used traditional Chinese medicine and has been proven beneficial for many aspects of human health. It is important to explore the neuroprotective effect and mechanism of astragalus injection in cerebral ischemia reperfusion injury. Methods: The focal cerebral ischemic model with middle cerebral artery occlusion (MCAO) reperfusion was established by Longa's method in healthy adult male Wistar rats, and treated by injecting intraperitoneally astragalus injection (3 ml/kg). The neurobehavioral function of rats was evaluated by Longa's test. The cerebral blood flow (CBF) was measured by laser Doppler flowmetry and the cerebral infarct volume was calculated by tetrazolium chloride (TTC) stain. The shape and structure of neurons in parahippocampal area was observed by HE stain and the neuronal apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and flow cytometry. The expressions of c-jun N-terminal kinase 3 (JNK3) mRNA and protein were determined by RT-PCR and immunohistochemical assay and Western blotting respectively. Results: After treatment with astragalus injection, the expressions of JNK3 mRNA and protein reduced significantly, the number of neuronal apoptosis minus, the cerebral infarct volume shrink, the neuronal shape-structure and animal neurobehavioral function improved significantly than those in model rats. Conclusions: It is suggested that astragalus injection could inhibit neuronal apoptosis, reduce infarct volume and improve neurobehavioral function by down-regulating the expression of JNK3 gene after cerebral ischemia reperfusion injury in rats. [ABSTRACT FROM AUTHOR]

The rapid growth of mobile applications in recent years has created a need for wideband wireless communication. The only predictable trend is that data-rate and QoS requirements will increase rapidly. This demand is pushing Time- division-synchronous code-division multiple access (TD-SCDMA) to evolve in order to provide higher and higher data rates. This article presents the evolution map from TD-SCDMA to Future Terrestrial Universal Radio Environment (FuTURE) TDD in China. The evolution includes four phases: low chip rate (LCR), high-speed downlink/uplink packet access (HSxPA)/TD- SCDMA EV 1x, long-term evolution (LTE) TDD, and FuTURE Beyond 3G TDD. The main features of each phase are described in detail. By introducing the new technologies into the system step by step, for example, multiple input and multiple output (MIMO), orthogonal frequency-division multiplexing (OFDM), TD-SCDMA system can evolve to FuTURE B3G TDD smoothly, and provide high-data-rate services with low cost, low latency, and improved coverage and capacity. [ABSTRACT FROM AUTHOR]

As the main equipment for earthquake disaster rescue and reconnaissance battlefield, the robustness of UAV swarm communication system is an important index of destruction resistance. In this paper, we model the UAV swarm communication system with the help of complex dependency network theory, introduce the relative network effectiveness ratio as an index of the overall robustness of the communication system network, which accurately reflects the interdependence between nodes, and provides a new perspective for evaluating the robustness of the communication system under the target attack. A new perspective is provided for assessing the robustness of communication systems under target attack. Based on the classical M-L model and the load redistribution strategy with dynamic information, we establish the dependent homogeneous ER-ER and heterogeneous ER-BA network models, consider the characteristics of the degree of dependent nodes in the two-layer network for target attack, and analyze the dynamic process of their cascading failure under the attack, as well as the influence of the characteristic parameters, such as the probability of connecting edges of any two nodes, the average degree and the capacity coefficient, on the overall robustness of the communication network. It is shown that network robustness and network dependency strength are negatively correlated, and a reduction of 52.09% to 72.9% dependency strength can be considered in the cascade failure process to resist more serious communication network collapse. For isomorphic networks, the difference in dependency patterns has a greater impact by reducing the overall robustness of RL and AL compared to DL by 9.25% and 15.95%, respectively.

MicroRNA-155 (miR-155) was previously found involved in the development of systemic lupus erythematosus (SLE) and other autoimmune diseases and the inflammatory response; however, the detailed mechanism of miR-155 in SLE is not fully understood. To explore the in vivo role of miR-155 in the pathogenesis of SLE, miR-155-deficient Fas1pr/1pr (miR-155-/- Fas1pr/1pr) mice were obtained by crossing miR-155-/- and Fas1pr/1pr mice. Clinical SLE features such as glomerulonephritis, autoantibody levels, and immune system cell populations were compared between miR-155-/-Fas1pr/1pr and Fas1pr/1pr mice. Microarray analysis, RT-PCR, Western blot, and luciferase reporter gene assay were used to identify the target gene of miR-155. miR-155-/-Fas1pr/1pr mice showed milder SLE clinical features than did Fas1pr/1pr mice. As compared with Fas1pr/1pr mice, miR-155-/-Fas1pr/1pr mice showed less deposition of total IgA, IgM, and IgG and less infiltration of inflammatory cells in the kidney. Moreover, the serum levels of IL-4 and IL-17a, secreted by Th2 and Thl7 cells, were lower in miR-155-/-Fas1pr/1pr than Fas1pr/1pr mice; the CD4+/CD8+ T cell ratio was restored in miR-155-/- Fas1pr/1pr mice as well. Sphingosine-1-phosphate receptor 1 (S1PR1) was found as a new target gene of miR-155 by in vitro and in vivo studies; its expression was decreased in SLE patients and Fas1pr/1pr mice. miR-155-/-Fas1pr/1pr mice are resistant to the development of SLE by the regulation of the target gene S1pr1. miR-155 might be a new target for therapeutic intervention in SLE. [ABSTRACT FROM AUTHOR]