ABSTRACT
The No.4 tailings pond of the Dexing Copper Mine is the second largest in Asia. The tailing pond is a dangerous source of man-made debris flow with high potential energy. In view of the lack of effective and low-cost global safety monitoring means in this region, in this paper, the time-series InSAR technology is innovatively introduced to monitor the deformation of tailings dam and significant key findings are obtained. First, the surface deformation information of the tailings pond and its surrounding areas was extracted by using SBAS-InSAR technology and Sentinel-1A data. Second, the cause of deformation is explored by analyzing the deformation rate, deformation accumulation, and three typical deformation rate profiles of the representative observation points on the dam body. Finally, the power function model is used to predict the typical deformation observation points. The results of this paper indicated that: (1) the surface deformation of the tailings dam can be categorized into two directions: the upper portion of the dam moving away from the satellite along the Line of Sight (LOS) at a rate of -40 mm/yr, whereas the bottom portion approaching the satellite along the LOS at a rate of 8 mm/yr; (2) the deformation of the dam body is mainly affected by the inventory deposits and the construction materials of the dam body; (3) according to the current trend, deformation of two typical observation points in the LOS direction will reach the cumulative deformation of 80 mm and -360 mm respectively. The research results can provide data support for safety management of No.4 tailings dam in the Dexing Copper Mine, and provide a method reference for monitoring other similar tailings dams.
ABSTRACT
The immune response plays a crucial role in the functionality of oncolytic viruses. In this study, Albendazole, an antihelminthic drug known to modulate the immune checkpoint PD-L1, was combined with the oncolytic virus M1 (OVM1) to treat mice with either prostate cancer (RM-1) or glioma (GL261) tumors. This combination therapy enhanced anti-tumor effects in immunocompetent mice, but not in immunodeficient ones, without increasing OVM1 replication. Instead, it led to an increase in the number of CD8+ T cells within the tumor, downregulated the expression of PD1 on CD8+ T cells, and upregulated activation markers such as Ki67, CD44, and CD69 and the secretion of cytotoxic factors including interferon (IFN)-γ, granzyme B, and tumor necrosis factor (TNF)-α. Consistently, it enhanced the in vitro tumor-killing activity of lymphocytes from tumor-draining lymph nodes or spleens. The synergistic effect of Albendazole on OVM1 was abolished by depleting CD8+ T cells, suggesting a CD8+ T cell-dependent mechanism. In addition, Albendazole and OVM1 therapy increased CTLA4 expression in the spleen, and the addition of CTLA4 antibodies further enhanced the anti-tumor efficacy in vivo. In summary, Albendazole can act synergistically with oncolytic viruses via CD8+ T cell activation, and the Albendazole/OVM1 combination can overcome resistance to CTLA4-based immune checkpoint blockade therapy.