ABSTRACT
Measuring the isotopic composition of Hg in natural waters is challenging due to the ultratrace level of aqueous Hg (ng L-1). At least 5 ng of Hg mass is required for Hg isotopic analysis. Given the low Hg concentration in natural waters, a large volume of water (>10 L) is typically needed. The conventional grab sampling method is time-consuming, laborious, and prone to contamination during transportation and preconcentration steps. In this study, a DGT (diffusive gradients in thin films) method based on aminopropyl and mercaptopropyl bi-functionalized SBA-15 nanoparticles was developed and extended to determine the concentration and isotopic composition of aqueous Hg for the first time. The results of laboratory analysis showed that Hg adsorption by DGT induces â¼ -0.2 mass-dependent fractionation (MDF) and little mass-independent fractionation (MIF). The magnitude of MDF exhibits a dependence on the diffusion-layer thickness of DGT. Since Hg-MDF can occur in a broad range of environmental processes, monitoring the δ202Hg of aqueous Hg using the DGT method should be performed with caution. Field results show consistent MIF signatures (Δ199Hg) between the DGT and conventional grab sampling method. The developed DGT method serves as a passive sampling method that effectively characterizes the MIF of Hg in waters to understand the biogeochemical cycle of Hg at contaminated sites.
ABSTRACT
Background: Temozolomide (TMZ) resistance is a serious hindrance in clinical chemotherapy for glioma. Circular RNA homeodomain interacting protein kinase 3 (circHIPK3) can be involved in regulating the progression of glioma, but the molecular mechanism of circHIPK3 in TMZ-resistant-glioma is completely unclear. Materials and Methods: The levels of circRNA, miRNA, and mRNA were examined using quantitative real-time polymerase chain reaction. 3-(4,5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide assay was used for assessing the half inhibitory concentration (IC50) of TMZ and cell proliferation. Cell apoptosis and metastasis (migration and invasion) were detected by flow cytometry and transwell assay, respectively. Western blot and dual-luciferase reporter assay were performed several times to analyze the expression levels of associated proteins and the targeted relation. Results: The upregulation of circHIPK3 was found in TMZ-resistant glioma tissues and cells. Both circHIPK3 knockdown and kinesin family member 2A (KIF2A) inhibition could facilitate TMZ sensitivity and apoptosis but repress proliferation and metastasis in TMZ-resistant glioma cells. CircHIPK3 targeted microRNA-524-5p (miR-524-5p) and KIF2A functioned as a downstream target of miR-524-5p. Decrease of miR-524-5p relieved the effects of si-circHIPK3 on TMZ-resistant glioma cells by upregulating KIF2A. Downregulation of circHIPK3 refrained the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signal pathway partly through miR-524-5p/KIF2A axis. Conclusions: Knockdown of circHIPK3 promoted TMZ sensitivity in glioma by modulating proliferation, metastasis, and apoptosis through miR-524-5p/KIF2A-mediated PI3K/AKT pathway. CircHIPK3 may be the potential target for the diagnosis and therapy of TMZ-resistant glioma.