Two dimensional (2-D) Ti3C2Tx nanosheets are obtained by etching bulk Ti3C2Tx powders in HF solution and delaminating ultrasonically, which exhibit excellent removal capacity for toxic Cr(VI) from water, due to their high surface area, well dispersibility, and reductivity. The Ti3C2Tx nanosheets delaminated by 10% HF solution present more efficient Cr(VI) removal performance with capacity of 250 mg g(-1), and the residual concentration of Cr(VI) in treated water is less than 5 ppb, far below the concentration (0.05 ppm) of Cr(VI) in the drinking water standard recommended by the World Health Organization. This kind of 2-D Ti3C2Tx nanosheet can not only remove Cr(VI) rapidly and effectively in one step from aqueous solution by reducing Cr(VI) to Cr(III) but also adsorb the reduced Cr(III) simultaneously. Furthermore, these reductive 2-D Ti3C2Tx nanosheets are generally explored to remove other oxidant agents, such as K3[Fe(CN)6], KMnO4, and NaAuCl4 solutions, by converting them to low oxidation states. These significantly expand the potential applications of 2-D Ti3C2Tx nanosheets in water treatment.

A range of hydroxypyridinone-L-phenylalanine conjugates were synthesized starting from kojic acid. Their tyrosinase activity was determined, and it was found that one of the compounds ((S)-(5-(benzyloxy)-1-octyl-4-oxo-1,4-dihydropyridin-2-yl)methyl 2-amino-3-phenylpropanoate, 5e) showed potent inhibitory effect against mushroom tyrosinase, the IC50 values for monophenolase and diphenolase activities being 12.6 and 4.0 μM, respectively. It was also demonstrated that these conjugates are mixed-type inhibitors, suggesting they could bind to both the free enzyme and the enzyme-substrate complexes. MTT assay indicated that 5e was nontoxic to three cell lines. This compound may find applications in food preservation and cosmetics.

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Purpose: Immunotherapies targeting immune checkpoint molecules have shown promising treatment for a subset of cancers; however, many “cold” tumors, such as prostate cancer, remain unresponsive. We aimed to identify a potential targetable marker relevant to prostate cancer and develop novel immunotherapy. Experimental Design: Analysis of transcriptomic profiles at single-cell resolution was performed in clinical patients' samples, along with integrated analysis of multiple RNA-sequencing datasets. The antitumor activity of YY001, a novel EP4 antagonist, combined with anti–programmed cell death protein 1 (PD-1) antibody was evaluated both in vitro and in vivo. Results: We identified EP4 (PTGER4) as expressed in epithelial cells and various immune cells and involved in modulating the prostate cancer immune microenvironment. YY001, a novel EP4 antagonist, inhibited the differentiation, maturation, and immunosuppressive function of myeloid-derived suppressor cells (MDSC) while enhancing the proliferation and anticancer functions of T cells. Furthermore, it reversed the infiltration levels of MDSCs and T cells in the tumor microenvironment by overturning the chemokine profile of tumor cells in vitro and in vivo. The combined immunotherapy demonstrated a robust antitumor immune response as indicated by the robust accumulation and activation of CD8+ cytotoxic T cells, with a significantly decreased MDSC ratio and reduced MDSC immunosuppression function. Conclusions: Our study identified EP4 as a specific target for prostate cancer immunotherapy and demonstrated that YY001 inhibited the growth of prostate tumors by regulating the immune microenvironment and strongly synergized with anti–PD-1 antibodies to convert completely unresponsive prostate cancers into responsive cancers, resulting in marked tumor regression, long-term survival, and lasting immunologic memory.

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