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Pd modified electrodes possess problems such as easy agglomeration and low electrolytic ability, and the use of manganese dioxide (MnO2) to facilitate Pd reduction of organic pollutants is just started. However, there is still a limited understanding of how to match the Pd load and MnO2 to realize optimal dechlorination efficiency at minimum cost. Here, a Pd/MnO2/Ni foam cathode was successfully fabricated and applied for the efficient electrochemical dechlorination of 2,4,6-trichlorophenol (2,4,6-TCP). The optimal electrocatalytic hydrodechlorination (ECH) performance with 2,4,6-TCP dechlorination efficiency (92.58% in 180 min) was obtained when the concentration of PdCl2 precipitation was 1 mmol/L, the deposition time of MnO2 was 300 s and cathode potential was −0.8 V. Performance influenced by the exogenous factors (e.g., initial pH and coexisted ions) were further investigated. It was found that the neutral pH was the most favorable for ECH and a reduction in dechlorination efficiency (6% ∼ 47.6%) was observed in presence of 5 mmol/L of NO 2 − , NO 3 − , S2− or SO 3 2 − . Cyclic voltammetry (CV) and quenching experiments verified the existence of three hydrogen species on Pd surface, including adsorbed atomic hydrogen (H*ads), absorbed atomic hydrogen (H*abs), and molecular hydrogen (H2). And the introduction of MnO2 promoted the generation of atomic H*. Only adsorbed atomic hydrogen (H*ads) was confirmed that it truly facilitated the ECH process. Besides H*ads induced reduction, the direct reduction by cathode electrons also participated in the 2,4,6-TCP dechlorination process. Pd/MnO2/Ni foam cathode shows excellent dechlorination performance, fine stability and recyclable potential, which provides strategies for the effective degradation of persistent halogenated organic pollutants in groundwater.

Top and side views of the Y2CT2 (T = O, F and OH).

Background Explore how exosomes released by X-ray irradiated tumor cells promote the formation of pulmonary metastatic nodules by inducing the recruitment of MDSCs to the lung. Methods BALB/c mice were injected with 4T1 tumor cells into the mammary adipose pad and allowed to grow for 28 days. On the 10th day of tumor inoculating, the primary tumor was irradiated by X-ray with a single dose of 20Gy. The mice were monitored for tumor growth, the number of pulmonary metastasis nodules and frequency of MDSCs. Antibody microarray and ELISA methods were used to analyze the altered cytokines (G-CSF, GM-CSF and CXCL1) in exosomes released by 4T1 cells after X-ray irradiation. The effects of the exosomes on the recruitment of MDSCs in the lung and facilitating the colonization of 4T1 in the lung were observed in normal BALB/c mice. Transwell method was used to observe the promotion of MDSCs migration by exosomes, lung tissue extracts from 4T1 tumor-bearing mice and GM-CSF via CCR2/CXCR2 signals, meanwhile, the effect of MDSCs on T lymphocytes function and migration of 4T1 cells were observed by the co-culture system. Results Even though radiotherapy reduced the burden of primary tumors and larger lung metastatic nodules (≥ 0.5 mm2), the number of smaller metastases (2) significantly increased. In addition, radiotherapy markedly potentiated M-MDSCs and reduced PMN-MDSCs recruitment in lung of 4T1 tumor-bearing mice. Moreover, the frequency of M-MDSCs in lung was positively correlated with the number of smaller metastatic nodules. Using co-culture experiments, we provided evidence that M-MDSCs of the lung in 4T1 tumor-bearing mice markedly inhibited T cell proliferation and killing activity, while M-MDSCs and PMN-MDSCs had a similar role in facilitating tumor cell dissemination. The G-CSF, GM-CSF and CXCL1 rich exosomes derived from irradiated 4T1 (ir/4T1-exo) could facilitate both M-MDSCs and PMN-MDSCs migration by CXCL1/CXCR2 signal. While the lung tissue extracts of irradiated mice or culture medium of macrophage treated with ir/4T1-exo showed an obvious tendency to chemotaxis on M-MDSCs. Mechanistically, ir/4T1-exo could induce macrophage to produce GM-CSF, which in turn further promoted CCL2 release in an autocrine manner to recruit M-MDSCs via CCL2/CCR2 axis. Conclusions Our work has identified an undesired effect of radiotherapy promoting immunosuppressive premetastatic niches by recruiting M-MDSCs to lung. Further studies on RT combined inhibition of CXCR2 or CCR2 signals were necessary.

Mass concentration, seasonal variation and sources of organic carbon (OC), element carbon (EC), methanol-soluble organic carbon (MSOC), and seven carbon components (OC1-4, EC1-3) were detected by thermal-optical analysis of 353 PM

Nasopharyngeal carcinoma (NPC) is a common malignancy in Southern China and Southeast Asia. In this study, we investigated the functional and molecular mechanisms by which CDC42-interacting protein 4 (CIP4) influences NPC. The expression levels of CIP4 were examined by Western blot, qRT-PCR or IHC. MTT assay was used to detect the proliferative rate of NPC cells. The invasive abilities were examined by matrigel and transwell assay. The metastatic abilities of NPC cells were revealed in BALB/c nude mice. We report that CIP4 is required for NPC cell motility and invasion. CIP4 promotes the activation of N-WASP that controls invadopodia formation and activates EGFR signaling, which induces downstream MMP2 (matrix metalloproteinase 2) upregulation. In addition, CIP4 could promote NPC metastasis by activating the EGFR pathway. In nude mouse models, distant metastasis was significantly inhibited in CIP4-silenced groups. High CIP4 expression is an independent adverse prognostic factor of overall survival (OS) and distant metastasis-free survival (DMFS). We identify the critical role of CIP4 in metastasis of NPC which suggest that CIP4 may be a potential therapeutic target of NPC patients.