Check dam storage capacity calculation based on high-resolution topogrammetry: Case study of the Cutou Gully, Wenchuan County, China.

Debris flows are a common natural trigger of disasters in mountainous areas, and check dams are standard structural measures for controlling debris flows. Despite their prevalence in debris flow-prone areas worldwide, the capacity of check dams is still calculated using empirical formulas, which lead to large calculation errors. This paper proposes a new method that uses GIS to calculating the design storage capacity of a check dam in the debris flow-prone Cutou Gully in Wenchuan County, China. Large-scale digital surface models derived from unmanned aerial vehicle imagery and ground surveys identify local topographic changes in the debris flow path and develop appropriate maintenance plans for check dams. The measured storage capacity of the check dam is determined by analyzing the DEM differences. This study uses the newly proposed method to calculate the design storage capacity of the check dam. The accuracy of the calculation results was evaluated using the checkpoint method, and the results showed that the design and measured siltation surface errors ranged from -1.16-2.96 m, with a root mean square error of 0.93 m. The design capacity of the check dam is 33.6× 104 m3, and the actual capacity is 36.7× 104 m3, with an absolute error of 3.1× 104 m3 and relative error of 8.6%. The results prove the validity of the proposed calculation method; moreover, this study shows that the new method is accurate, easy to operate, and highly efficient for visualizing the spatial distribution of the siltation depth behind the check dam. This work will help improve future engineering decisions, design strategies, and find optimal design solutions to minimize the risk of debris flow hazards.

Wnt7a activates canonical Wnt signaling, promotes bladder cancer cell invasion, and is suppressed by miR-370-3p.

Once urinary bladder cancer (UBC) develops into muscle-invasive bladder cancer, its mortality rate increases dramatically. However, the molecular mechanisms of UBC invasion and metastasis remain largely unknown. Herein, using 5637 UBC cells, we generated two sublines with low (5637 NMI) and high (5637 HMI) invasive capabilities. Mass spectrum analyses revealed that the Wnt family protein Wnt7a is more highly expressed in 5637 HMI cells than in 5637 NMI cells. We also found that increased Wnt7a expression is associated with UBC metastasis and predicted worse clinical outcome in UBC patients. Wnt7a depletion in 5637 HMI and T24 cells reduced UBC cell invasion and decreased levels of active ß-catenin and its downstream target genes involved in the epithelial-to-mesenchymal transition (EMT) and extracellular matrix (ECM) degradation. Consistently, treating 5637 NMI and J82 cells with recombinant Wnt7a induced cell invasion, EMT, and expression of ECM degradation-associated genes. Moreover, TOP/FOPflash luciferase assays indicated that Wnt7a activated canonical ß-catenin signaling in UBC cells, and increased Wnt7a expression was associated with nuclear ß-catenin in UBC samples. Wnt7a ablation suppressed matrix metalloproteinase 10 (MMP10) expression, and Wnt7a overexpression increased MMP10 promoter activity through two TCF/LEF promoter sites, confirming that Wnt7a-mediated MMP10 activation is mediated by the canonical Wnt/ß-catenin pathway. Of note, the microRNA miR-370-3p directly repressed Wnt7a expression and thereby suppressed UBC cell invasion, which was partially restored by Wnt7a overexpression. Our results have identified an miR-370-3p/Wnt7a axis that controls UBC invasion through canonical Wnt/ß-catenin signaling, which may offer prognostic and therapeutic opportunities.

A pH-sensitive binary drug delivery system based on poly(caprolactone)-heparin conjugates.

PCL-heparin conjugates were synthesized by coupling mono-hydroxyl terminated PCL (Mn = 2000-10000 g/mol) with heparin via EDC/NHS chemistry. The conjugates enabled to self-assemble into the core-shell nanoparticles in around 100 nm diameter to load binary anti-cancer drugs. Lipophilic and neutral paclitaxel (PTX) was first encapsulated in the core, and then hydrophilic and positive charged doxorubicin (DOX) was incorporated into the negative charged shell of PTX loaded nanoparticles via the electrostatic interaction. The in vitro release profiles of the binary-drug loaded nanoparticles revealed that both PTX and DOX were sustainably released from the particles but behaved differently. The release of DOX was pH dependent, ensuring more drug to be released in the tumor cells than in the normal ones. Hence these particles were featured by a sequential controlled drug delivery behavior with a significant cytotoxicity to cervical cancer (Hela cell) and breast cancer (MDA-MB-321) cells. The CLSM observations clearly indicated that both loaded PTX and DOX aggregated in the nucleus of tumor cells to exert their anti-tumor pharmacodynamic effect on the cells.