Eavesdropping on wastewater pollution: Detecting discharge events from river outfalls via fiber-optic distributed acoustic sensing.

Wastewater discharge from outfall pipes can significantly impact river water quality and aquatic ecosystems. Effective outfall monitoring is critical for controlling pollution and protecting public health. This study demonstrates a novel distributed acoustic sensing (DAS) approach for detecting wastewater discharge events from outfall pipes located along rivers. Controlled field experiments were conducted in an industrial park river to systematically evaluate DAS performance. DAS detects vibrational signals imparted to suspended fiber-optic cables by turbulent wastewater flows, predominantly within 10-30 Hz, enabling continuous monitoring along entire river lengths. Vibrational power analysis locates outfalls with meter-level accuracy, while time-frequency techniques discern discharge timing and characteristics. Cable type and outfall-fiber separation influence on detection capability was assessed. Thermoplastic-jacketed tight buffer cables optimized detection through enhanced vibrational coupling. Vibrational energy decreased exponentially with separation, highlighting benefits of proximal deployment for sensitivity. However, detection range scales with discharge flow rate. Frequency centroid proved a robust feature with potential for automated discharge identification. Overall, DAS enables high spatiotemporal resolution monitoring to pinpoint concealed outfalls minimally invasively. This positions DAS as a promising tool supporting improved water governance through early pollution warnings and rapid source localization via outfall vibrational signatures emanating across river networks.

Microanchored borehole fiber optics allows strain profiling of the shallow subsurface.

Vertical deformation profiles of subterranean geological formations are conventionally measured by borehole extensometry. Distributed strain sensing (DSS) paired with fiber-optic cables installed in the ground opens up possibilities for acquiring high-resolution static and quasistatic strain profiles of deforming strata, but it is currently limited by reduced data quality due to complicated patterns of interaction between the buried cables and their surroundings, especially in upper soil layers under low confining pressures. Extending recent DSS studies, we present an improved approach using microanchored fiber-optic cables-designed to optimize ground-to-cable coupling at the near surface-for strain determination along entire lengths of vertical boreholes. We proposed a novel criterion for soil-cable coupling evaluation based on the geotechnical bearing capacity theory. We applied this enhanced methodology to monitor groundwater-related vertical motions in both laboratory and field experiments. Corroborating extensometer recordings, acquired simultaneously, validated fiber optically determined displacements, suggesting microanchored DSS as an improved means for detecting and monitoring shallow subsurface strain profiles.

Knockdown of long noncoding RNA TP73-AS1 suppresses the malignant progression of breast cancer cells in vitro through targeting miRNA-125a-3p/metadherin axis.

BACKGROUND: TP73 antisense RNA 1 (TP73-AS1) is a long noncoding RNA which has been shown to be involved in the progression of multiple malignant tumors. Previous studies have demonstrated the oncogenic role of TP73-AS1 in breast cancer. However, its molecular mechanism remains largely unknown in breast tumorigenesis. METHODS: Expression of TP63-AS1, miRNA-125a-3p (miR-125a) and metadherin (MTDH) was detected by real-time quantitative PCR and western blotting. The malignancy was evaluated by cell counting kit 8 (CCK-8), transwell assays, flow cytometry and western blotting. The target binding was confirmed by dual luciferase reporter assay. Xenograft tumor model was performed to detect tumor growth in vivo. RESULTS: Expression of TP73-AS1 was higher in breast cancer tissues and cell lines. Biologically, its knockdown could promote cell apoptosis rate, and inhibit proliferative capacity, migration and invasion ability in HCC-70 and MB231 cells, accompanied with higher cleaved caspase 3 level and lower Ki67, N-cadherin and Vimentin level. Moreover, TP73-AS1 downregulation restrained the tumor growth of HCC-70 cells in vivo. Mechanically, TP73-AS1 functioned as a molecular "sponge" for miR-125a to modulate MTDH, a downstream target of miR-125a. Intriguingly, both miR-125a overexpression and MTDH silencing exerted a tumor-suppressive effect in the malignant progression of HCC-70 and MB231 cells, which was counteracted by TP73-AS1 upregulation and miR-125a downregulation, respectively. CONCLUSION: Knockdown of TP73-AS1 inhibited cell proliferation, migration and invasion, but facilitated apoptosis in breast cancer cells in vitro through targeting miR-125a and upregulating MTDH, suggesting a novel TP73-AS1/miR-125a/MTDH pathway in the malignant progression of breast cancer.