The land reclaimed from the seaside may have a long-term subsidence trend, which poses a potential geohazard in the future land use. Xiamen Xiang’an New Airport (XXNA) is built on reclaimed land since 2016. Based on the spaceborne Sentinel-1 data between January 2018 to April 2019 and the time series interferometric synthetic aperture radar (InSAR) technique, this paper analyzed the reclaimed land subsidence evolution at XXNA in this period. InSAR measurements show that XXNA is suffering from severe subsidence, mainly in three regions because of the earth and sand compacting. By analyzing the spatial subsidence characterizations of the main subsiding areas combined with historical land reclamation and future land use planning, we find the potential threat of subsidence to future land use. Correlation between subsidence and the period of reclamation was found, indicating that the consolidation and compression in dredger fill is the main cause of subsidence. By combining subsidence monitoring results with different land use types and adopting the Expectation (Ex) and Entropy (En) methods, we analyzed the key area with potential subsidence geo-hazard. This work shows that with SAR interferometry, it is possible to find the large area ground subsidence in the airport reclaimed area. The areas with potential subsidence geo-hazards are consistent with the deep reclaimed earth, which means high subsidence risk in the future.
Potential landslides in the mountainous areas of southwest China pose a serious threat to the lives and property of local residents. Synthetic aperture radar interferometry (InSAR) technology has the advantages of wide coverage, all weather applicability, and low cost and can quickly and accurately identify large range of active landslides, making it a useful geodetic tool for the early identification and prevention of landslides. This paper employed small baseline subset InSAR (SBAS−InSAR) technology and ascending and descending Sentinel−1 data from January 2019 to December 2021 to early identify active landslides in the Maoxian County to Li County National Highway (G317 and G213). The InSAR deformation results were verified by geometric distortion analysis, optical remote sensing interpretation, and field investigation, and 115 active landslides were successfully determined, among which 23 active landslides were identified by ascending and descending Sentinel−1 data together. In addition, InSAR deformation results show that fault, stratigraphic lithology, and rainfall are the three main factors that accelerate the deformation of active landslides and can trigger new active landslides. This study can provide an important reference for the early identification and prevention of landslides in mountainous areas.
Objective Our previous study found that increased serum IL-27 could promote rheumatoid arthritis (RA) B cell dysfunction via activating mTOR signaling pathway. This study aimed to explore the effects of IL-27 on B cell metabolism and clarify the mechanisms via which IL-27 enhancing glycolysis to induce B cells hyperactivation.
Methods Peripheral CD19+ B cells were purified from healthy controls (HC) and RA patients and then cultured with or without anti-CD40/CpG and glycolysis inhibitor 2-deoxy-D-glucose (2-DG) or mTOR inhibitor rapamycin. Furthermore, the isolated CD19+ B cells were treated by HC serum or RA serum in the presence and absence of recombinant human IL-27 or anti-IL-27 neutralizing antibodies or 2-DG or rapamycin. The B cell glycolysis level, proliferation, differentiation, and inflammatory actions were detected by qPCR, flow cytometry or ELISA.
Results Compared to HC B cells, glycolysis was increased significantly in RA B cells and glycolysis inhibition downregulated the proliferation, differentiation, and inflammatory actions of RA B cells. RA serum and IL-27 promoted B cell glycolysis, which could be obviously rescued by anti-IL-27 antibodies or mTOR inhibitor rapamycin.
Conclusion Enhanced cellular glycolysis of RA B cells induced by IL-27 might contribute to B cells hyperactivation through activating the mTOR signaling pathway.
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