Phosphorus Co-Existing in Water: A New Mechanism to Boost Boron Removal by Calcined Oyster Shell Powder

The removal of boron (B) from water by co-precipitation with hydroxyapatite (HAP) has been extensively studied due to its low cost, ease of use and high efficiency. However, there is no explicit mechanism to express how resolved B was trapped by HAP. Thus, in this work, the process of removing B from water was studied using a low-cost calcium (Ca) precipitation agent derived from used waste oyster shells. The results showed that the removal rate of B in the simulated wastewater by calcined oyster shell (COS) in the presence of phosphorus (P) is up to more than 90%, as opposed to virtually no removal without phosphate. For B removal, the treated water needs to be an alkaline solution with a high pH above 12, where B is removed as [CaB(OH)4]+ but is not molecular. Finally, the synergistic mechanism of co-precipitation between HAP and dissolved B, occlusion co-precipitation, was explained in detail. The proposed method discovered the relationship between Ca, P and B, and was aimed at removing B without secondary pollution through co-precipitation.

Gadolinium-Based Nanoparticles Combined With Checkpoint Blockade Amplify Radiation-Induced Abscopal Effect And Cancer Immunotherapy

Both immunotherapy checkpoint blocking and radiotherapy used alone in solid tumors show limited anticancer effect, due to the insufficient T cells infiltration and rarely elicited systemic immune responses. Methods: AGuIX has recently been developed for magnetic resonance imaging-guided radiotherapy and proven to act as an efficient radiosensitizer. In order to further improve the efficiency of tumor treatment, a unique synergistic strategy based on Gadolinium-based nanoparticles-AGuIX mediated radiotherapy and immunotherapy checkpoint blocking was developed for B16 tumor therapy in the present study. Clone formation, cell apoptosis and immunofluorescence were performed to detect the radiosensitization effect of AGuIX nanoparticles. The therapeutic effect was validated in both abscopal and metastasis tumor models, and analyzed the synergistic mechanism in vivo. Results: AGuIX as a radiosensitizer exacerbated radiation-induced DNA damage, cell cycle arrest and apoptosis on B16 cells. More importantly, it could efficiently induce the immunogenic cell death (ICD) of irradiated B16 tumor cells, and consequently triggered the maturation of dendritic cells (DCs) and activated systemic T-cell responses. Combining AGuIX-mediated radiotherapy with programmed cell death protein 1 (PD1) blocking demonstrated excellent synergistic therapeutic effects in both abscopal and metastasis tumor models by a significant increase in the infiltration of effector CD8+ T cells and effectively alleviating the immunosuppressive microenvironment, including regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in tumors.Conclusion: Our findings indicate that this combination therapy provided a new and powerful immunotherapy model to achieve durable anti-tumor responses, which is likely to be a promising comprehensive treatment strategy for cancer treatment.

Synergistic Inhibitory Effects of 5-Aza-2'-Deoxycytidine and Cisplatin on Urothelial Carcinoma Growth via Suppressing TGFBI-MAPK Signaling Pathways

This study is to reveal the gene transcriptional alteration, possible molecular mechanism, and pathways involved in the synergy of 5-aza-2'-deoxycytidine (DAC) and CDDP in UC. Two UC cell lines, 5637 and T24, were used in the study. A cDNA microarray was carried out to identify critical genes in the synergistic mechanism of both agents against UC cells. The results showed that several key regulatory genes, such as interleukin 24(IL24), fibroblast growth factor 1(FGF1), and transforming growth factor beta-induced (TGFBI), were identified and may play critical roles in the synergy of DAC and CDDP in UC. Pathway enrichment suggested that many carcinogenesis-related pathways, such as ECM-receptor interaction and MAPK signaling pathways, may participate in the synergy of both agents. Our results suggested that TGF-β1 stimulates the phosphorylation levels of ERK1/2 and p38 via increasing TGFBI expression, TGFBI-MAPK signaling pathway plays an important role in the synergy of DAC and CDDP against UC. Therefore, we revealed the synergistic mechanism of DAC and CDDP in UC, several key regulatory genes play critical roles in the synergy of combined treatment, and TGFBI-MAPK signaling pathway may be an important potential target of these two agents.