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This study aimed to explore the underlying role and mechanism of LINC00313 in osteoarthritis (OA) progression. CHON-001 chondrocytes were treated with interleukin (IL)-1β to induce OA in vitro, and then transfected with LINC00313 overexpression plasmids (pcDNA-LINC00313) or small interfering RNA against tumor necrosis factor (TNF) receptor-associated factor 1 (si-TRAF1). Cell viability, apoptosis, levels of inflammatory cytokines tumor necrosis factor-α (TNF-α), IL-6 and IL-8, and expression of extracellular matrix (ECM) degradation related proteins in CHON-001 cells were determined. TRAF1 promoter methylation were was detected with methylation‐specific polymerase chain reaction (MSP) assay. Furthermore, a c-Jun N-terminal kinase (JNK) signaling activator was used to confirm whether the apoptosis signal-regulating kinase 1 (ASK1)/JNK signaling pathway was involved in the function of LINC00313/TRAF1 axis in chondrocytes. In addition, an OA mouse model was established and lentivirus LINC00313 overexpression vector (Lv-LINC00313) was injected, and then inflammatory cytokine levels, ECM protein expression, and pathological changes in cartilage tissues were detected. LINC00313 was downregulated and TRAF1 was upregulated in OA cartilage tissues. LINC00313 overexpression or TRAF1 silencing attenuated IL-1β-induced viability inhibition, apoptosis, inflammation and ECM degradation in CHON-001 cells. Moreover, LINC00313 inhibited TRAF1 expression through promoting DNA methyltransferase 1 (DNMT1) mediated promoter methylation. TRAF1 overexpression reversed the effects of LINC00313 on IL-1β-induced chondrocyte injury. LINC00313 overexpression inhibited the ASK1/JNK signaling pathway, and JNK activator reversed the effect. In addition, Lv-LINC00313 treatment alleviated cartilage tissue damage and cartilage matrix degradation in OA mice. LINC00313 alleviated OA progression through inhibiting TRAF1 expression and the ASK1/JNK signaling pathway.

The saturation characteristics is an important index of high power broadband traveling wave tubes. In this paper, an adaptive variable power stepping method is proposed to measure the saturation characteristics of broadband TWTs. In this method, we perform fast sweeping in the linear region and accurate sweeping in the saturation region respectively. Furthermore, the multi-level protection mechanism used in the measurement system can fully guarantee the safety and reliability of the measurement process. And this is of great significance in real measurement systems.

This paper introduces an automatic magnetic field distribution measurement system for traveling wave tube magnetic ring based on virtual instrument, which is mainly used to measure the axial magnetic field strength of TWT magnetic bunching system. The hardware system consists of optical table, non-magnetic chuck, motor controller, electronically controlled translation platform, high-precision Gauss meter, etc. In the LabWindows/CVI virtual instrument programming environment, modular development and debugging of measurement software are carried out, and finally the distributed measurement of the axial magnetic field of the traveling wave tube is achieved.

Aiming at catching up with the leading countries, this paper gives the right development direction of large aperture optical remote sensor in China. Firstly, we introduced the current situation of large aperture remote sensors using traditional and new imaging systems. Then we summarized the monolithic and deployable remote sensors with full range spectra and high spectrum resolution are the future main development trends. Furthermore, we discussed the key technologies include large aperture lightweight monolithic reflective mirror, active support, precise deployment, co-phasing in orbit, fabrication of large aperture membrane diffractive optics element (DOE) and high performance imaging processing technology of interferometric imaging system. Finally, we conclude China should give more attention to the large aperture monolithic and deployable optical remote sensors, and tackle the key technology in 1.5m~3m aperture monolithic remote sensors at first step and 4m aperture monolithic and the deployable remote sensors next.

In this paper, we combine the second generation of Non-dominated Sorting Genetic Algorithm (NSGA-II) [1] and the Electronic Optics Simulator (EOS) [2-3] in Microwave Tube Simulator Suite (MTSS) [4] to quickly optimize the design of the multistage depressed collectors, which greatly enhances the software's design capabilities. In addition to, the method can be extended to the simulation design of other modules, and lays a solid foundation for the subsequent development of intelligent regulating system of traveling wave tube based on the automatic test system of electrical parameters.

This paper proposes a method for the measurement of output port hot-VSWR in TWT. This method is aimed at solving the following problems in the traditional test method: 1) test equipment is not common; 2) test process may damage the traveling wave tube; 3) test process is complicated. In addition, this method not only improves the test convenience and security, but also greatly improves the test accuracy and test speed.

This paper introduces the design and realization of the electric parameters' automatic test system for traveling wave tube. Firstly, the overall design architecture and the relationship between the modules are described. Secondly, the functions of the system are described in detail, including the development environment, bus interface, user interface, measurement tasks, database and so on. Finally, the development status of the system is summarized, and the subsequent work arrangements are planned.

Focusing on the uncertainty of the environment, a grid map building method based on the multi ultrasonic sensors is provided. Firstly, the single ultrasonic sensor grid model is constructed by dividing the detected area into three regions. Then the evidences which are needed to fuse are self-adaptively approximate in order to remove the counter-intuitive behaviors. Finally, the unknown environment map is built by using the D-S evidence theory to fuse the approximate evidence. Aiming at proving the method is right, the simulation is carried out in Matlab. The simulation result shows that the method is valid in unknown environment map building.

Abr deactivates Ras-related C3 botulinum toxin substrate (Rac), a master molecular switch that positively regulates many immune cell functions, by converting it to its GDP-bound conformation. In this article, we report that, in the absence of Abr function, cockroach allergen (CRA)-immunized mice experienced a fatal asthma attack when challenged with CRA. The asthma in abr(-/-) mice was characterized by increased pulmonary mucus production, elevated serum IgE, and leukocyte airway infiltration. Decreased pulmonary compliance was further documented by increased airway resistance upon methacholine challenge. Peribronchial and bronchoalveolar lavage eosinophils, key cells associated with allergic asthma, were increased in abr(-/-) mice, but adoptive transfer of this cell type from immunized mice to naive controls, followed by CRA challenge, showed that eosinophils are not primarily responsible for differences in airway resistance between controls and abr-null mutants. CD4(+) T cell numbers in the airways of CRA-challenged abr(-/-) mice also were significantly increased compared with controls, as were the Th2 T cell-secreted cytokines IL-4 and IL-5 in total lung. Interestingly, when control and abr(-/-) CD4(+) T cells from CRA-immunized mice were transferred to wild-type animals, airway resistance upon challenge with CRA was significantly higher in mice transplanted with T cells lacking Abr function. CD4(+) T cells from CRA-immunized and challenged abr(-/-) mice contained elevated levels of activated GTP-bound Rac compared with wild-type controls. Functionally, abr(-/-) CD4(+) T cells from CRA-exposed mice showed significantly enhanced chemotaxis toward CCL21. These results identify Abr-regulated CD4(+) T cell migration as an important component of severe CRA-evoked allergic asthma in mice.