Fe3O4 nanoparticles encapsulated in boron nitride support via N-doped carbon layer as a peroxymonosulfate activator for pollutant degradation: Important role of metal boosted C-N sites.

Developing highly efficient and stable catalysts for peroxymonosulfate (PMS) based advanced oxidation processes (AOPs) are crucial in the field of environmental remediation. In this work, a facile encapsulated-precursor pyrolysis strategy was reported to prepare a competent PMS-activation catalyst, in which uniformly distributed Fe3O4 nanoparticles were firmly anchored on porous boron nitride (BN) nanosheets by N-doped carbon shell (NC layer). Taking advantage of strong metal-support interaction, the as-synthesized catalyst (BFA-500) could efficiently activate PMS to achieve 100% removal of 4-chlorophenol (4-CP) in 6 min, and the corresponding turnover frequency (TOF) value was 1-2 orders of magnitude higher than that of the benchmark homogeneous (Fe2+) and nanoparticle (Fe0 and Fe3O4) catalysts. Moreover, the well protected encapsulated structure of BFA-500 ensured the remarkable stability that could effectively resist the interference of complex water environment, including initial pH value, various inorganic ions and actual water, and its catalytic activity remained almost unchanged in 5 use-regeneration cycles. More importantly, the generation of O2•- and 1O2 radicals for the 4-CP removal in BFA-500/PMS system was ascribed to Fe3O4 boosted C-N sites containing pyridinic N, where electrons transferred from the embedded Fe3O4 nanoparticles to C-N sites to secure the PMS dissociation into reactive radicals. Overall, this work provided a promising way to design desired PMS-activation catalyst toward wastewater purification.

Selenocystine-Derived Label-Free Fluorescent Schiff Base Nanocomplex for siRNA Delivery Synergistically Kills Cancer Cells.

Chemo and siRNA synergic treatments for tumors is a promising new therapeutic trend. Selenocystine, a selenium analog of cysteine, has been considered a potential antitumor agent due to its redox perturbing role. In this study, we developed a nanocarrier for siRNA based on a selenocystine analog engineered polyetherimide and achieved traceable siRNA delivery and the synergic killing of tumor cells. Notably, we applied the label-free Schiff base fluorescence mechanism, which enabled us to trace the siRNA delivery and to monitor the selenocystine analogs' local performance. A novel selenocystine-derived fluorescent Schiff base linker was used to crosslink the polyetherimide, thereby generating a traceable siRNA delivery vehicle with green fluorescence. Moreover, we found that this compound induced tumor cells to undergo senescence. Together with the delivery of a siRNA targeting the anti-apoptotic BCL-xl/w genes in senescent cells, it achieved a synergistic inhibition function by inducing both senescence and apoptosis of tumor cells. Therefore, this study provides insights into the development of label-free probes, prodrugs, and materials towards the synergic strategies for cancer therapy.

Impact of air pollution on human activities: Evidence from nine million mobile phone users.

To measure the effects of air pollution on human activities, this study applies statistical/econometric modeling to hourly data of 9 million mobile phone users from six cities in China's Zhejiang Province from December 18 to 21, 2013. Under a change in air quality from "Good" (Air Quality Index, or AQI, between 51 and 100) to "Heavily Polluted" (AQI between 201 to 300), the following effects are demonstrated. (i) Consistent with the literature, for every one million people, 1, 482 fewer individuals are observed at parks, 95% confidence interval or CI (-2, 229, -735), which represents a 15% decrease. (ii) The number of individuals at shopping malls has no statistically significant change. (iii) Home is the most important location under worsening air quality, and for every one million people, 63, 088 more individuals are observed at home, 95% CI (47, 815, 78, 361), which represents a 19% increase. (iv) Individuals are on average 633 meters closer to their home, 95% CI (529, 737); as a benchmark, the median distance from home ranges from 300 to 1900 meters across the cities in our sample. These effects are not due to weather or government regulations. We also provided provisional evidence that individuals engage in inter-temporal activity substitutions within a day, which leads to mitigated (but not nullified) effects of air pollution on daily activities.

MicroRNA-155-5p Contributes to 5-Fluorouracil Resistance Through Down-Regulating TP53INP1 in Oral Squamous Cell Carcinoma.

The anticancer drug 5-fluorouracil (5-FU) resistance is a major obstacle to reducing the effectiveness of cancer treatment, and its detailed mechanism has not been fully elucidated. Here, in 5-FU-resistant human oral squamous cell carcinoma (OSCC) HSC3 cells (HSC3/5-FU), the levels of 21 miRNA candidates were detected using RT-PCR and miR-155-5p level increased strikingly in HSC3/5-FU cells compared to HSC3 cells. Compared with HSC3 cells, the CCK-8 assay showed that the HSC3/5-FU cells transfected with miR-155-5p inhibitors decreased 5-FU IC50. Ectopic expression of miR-155-5p in HSC3 and HSC4 cells increased 5-FU IC50 (CCK-8 assay), migration (wound-healing and transwell assays) and invasion (transwell assay) abilities. Seven miR-155-5p target candidates were discovered by miRNA prediction algorithms (miRDB, Targetscan, and miRWalk), and the RT-PCR results showed that in HSC3/5-FU cells TP53INP1 was of the lowest mRNA expression level compared with HSC3 cells. The RT-PCR and Western blotting assays showed that ectopic expression of miR-155-5p in HSC3 and HSC4 cells decreased TP53INP1 expression level. Furthermore, the luciferase reporter and RNA pull-down assays determined the interference effect of miR-155-5p on TP53INP1 expression. The enhancement of cell viability (CCK-8 assay), migration (wound-healing and transwell assays) and invasion (transwell assay) by miR-155-5p after 5-FU treatment was reversed by TP53INP1 overexpression. After treatment with 5-FU, HSC3-miR-155-5p tumor-bearing nude mice presented growing tumors, while HSC3-TP53INP1 group possessed shrinking tumors. In conclusion, these results lead to the proposal that miR-155-5p enhances 5-FU resistance by decreasing TP53INP1 expression in OSCC.