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This paper describes the development of the fluxgate magnetometer on the Fengyun-4B satellite. The Fengyun-4 is the second generation of China’s geostationary orbit satellite with the function of monitoring the space environment in GEO orbit. A fluxgate magnetometer (FGM) is deployed on this satellite to observe the magnetic field as a necessary input to space weather forecasting. This payload adopts three 3-axis fluxgate sensors to obtain space magnetic field data by excluding the satellite’s interference. Each three-axis fluxgate sensor has an independent signal processing circuit. FGM uses digital signal processing technology to acquire magnetic field signals. First, the analog signal is oversampled using a high-speed ADC, then digital signal processing, such as phase-sensitive demodulation, integration, and filtering, is performed inside the FPGA, and the feedback signal is output to the feedback coil through the DAC. This signal processing loop constitutes an ADC system, and the quantization accuracy of the output digital quantity can reach 18 bits. the FGM performs in-orbit calibration during satellite rotation maneuver and Alfven wave events. Comparison with the GOES-16 satellite and Tsyganenko magnetic field model proves FGM to be effective in monitoring the magnetic field of the space environment. Through joint observations with GOES-16 satellite and geomagnetic stations, FY-4B describes the development of a typical magnetic storm on November 4, 2021. The Ground calibration and in-orbit preliminary results show the FY-4B satellite magnetometer outputs 20 bits of digital resolution data at a 30 Hz sampling rate, with the noise lower than 3×10-4nT2/Hz@1Hz in the ±600nT range.

Background: Cardiac fibrosis after myocardial infarction (MI) is a major cause of heart deterioration. Recently, the roles of microRNAs (miRNAs) in various cardiovascular diseases associated with cardiac fibrosis have been extensively investigated. The present study aimed to investigate the role and mechanism of miR-29b-3p in cardiac fibrosis after MI. Methods: miR-29b-3p expression in TGF-β1-activated cardiac fibroblasts (CFs) was detected by qRT-PCR. Cell Counting Kit-8 (CCK-8) and Trans-well assays were performed to evaluate CFs proliferation and migration ability, respectively. Protein expressions of α-SMA, collagen I, collagen III, MMP2, and MMP9 were examined by Western blot assay. Bioinformatics, luciferase, and RNA immunoprecipitation (RIP) assays were carried out to determine whether FOS was targeted by miR-29b-3p. Results: TGF-β1 treatment dose-dependently curbed miR-29b-3p expression in CFs. miR-29b-3p restrained the promotive impacts of TGF-β1 on CFs proliferation, migration, and differentiation. FOS was affirmed to be a target of miR-29b-3p, elevated expression of FOS reversed the inhibitory effects of miR-29b-3p on cell proliferation, migration, and differentiation in TGF-β1-activated CFs. Conclusion: miR-29b-3p degraded the pro-fibrosis effect induced by TGF-β1 via targeting FOS, providing a prospective therapeutic avenue for cardiac fibrosis after MI.

// Wei Teng 1, 2 , Chunguang Qiu 1 , Zhaohui He 2 , Guoliang Wang 2 , Yongliang Xue 2 and Xuezhi Hui 2 1 Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China 2 Department of Cardiology, The First Affiliated Hospital of Henan University, Kaifeng 475000, China Correspondence to: Chunguang Qiu, email: chunguangqiuedu@163.com Keywords: vascular endothelial cells, linc00152, cell apoptosis and migration, miR-4767, ceRNA Received: February 23, 2017 Accepted: May 22, 2017 Published: June 28, 2017 ABSTRACT Dysfunction of vascular endothelial cells (VECs), such as increased apoptosis and diminished migration, is closely connected with most cardiovascular diseases and angiogenesis-related events. LncRNAs have been involved in regulation of many pathological processes, but their roles in vascular endothelial function are hardly underreported. Here, we explore the role of a intergenic lncRNA named linc00152 in the apoptosis and migration of VECs. We found that linc00152 was downregulated in human umbilical vein VECs (HUVECs) in a dose- and time-dependent manner following treatment with oxLDL, which is a typical proinflammatory factor in the initiation and progression of vascular endothelial dysfunction. Gain- and loss-function experiments indicated that linc00152 distinctly inhibited apoptosis and improved migration in oxLDL-treated HUVECs. By sponging miR-4767, linc00152 positively regulated the expression of Bcl2L12 and EGFR proteins. Moreover, blocking miR-4767 rescued the decrease of Bcl2L12 and EGFR caused by linc00152 knockdown, as well as the changes in cell apoptosis and migration. Our findings propose a novel role of linc00152 in the improvement of vascular endothelial function and a potential target for the therapy of some cardiovascular diseases.