The impact of recycling polyaluminium chloride and anionic polyacrylamide water treatment residuals on heavy metal adsorption in soils: implications for stormwater bioretention systems.

Despite the high adsorption capacity of polyaluminum chloride and anionic polyacrylamide water treatment residuals (PAC-APAM WTRs) for Pb2+, Cd2+, Cu2+, and Zn2+, their influence on the adsorption behavior of heavy metals in traditional bioretention soil media remains unclear. This study investigated the impact of PAC-APAM WTRs at a 20% weight ratio on the adsorption removal of Pb2+, Cd2+, Cu2+, and Zn2+ in three types of soils. The results demonstrated improved heavy metal adsorption in the presence of PAC-APAM WTRs, with enhanced removal observed at higher pH levels and temperatures. The addition of PAC-APAM WTRs augmented the maximum adsorption capacity for Pb2+ (from 0.98 to 3.98%), Cd2+ (from 0.52 to 10.99%), Cu2+ (from 3.69 to 36.79%), and Zn2+ (from 2.63 to 13.46%). The Langmuir model better described the data in soils with and without PAC-APAM WTRs. The pseudo-second-order model more accurately described the adsorption process, revealing an irreversible chemical process, although qe demonstrated improvement with the addition of PAC-APAM WTRs. This study affirms the potential of PAC-APAM WTRs as an amendment for mitigating heavy metal pollution in stormwater bioretention systems. Further exploration of the engineering application of PAC-APAM WTRs, particularly in field conditions for the removal of dissolved heavy metals, is recommended.

Elesclomol Loaded Copper Oxide Nanoplatform Triggers Cuproptosis to Enhance Antitumor Immunotherapy.

The induction of cuproptosis, a recently identified form of copper-dependent immunogenic cell death, is a promising approach for antitumor therapy. However, sufficient accumulation of intracellular copper ions (Cu2+) in tumor cells is essential for inducing cuproptosis. Herein, an intelligent cuproptosis-inducing nanosystem is constructed by encapsulating copper oxide (CuO) nanoparticles with the copper ionophore elesclomol (ES). After uptake by tumor cells, ES@CuO is degraded to release Cu2+ and ES to synergistically trigger cuproptosis, thereby significantly inhibiting the tumor growth of murine B16 melanoma cells. Moreover, ES@CuO further promoted cuproptosis-mediated immune responses and reprogrammed the immunosuppressive tumor microenvironment by increasing the number of tumor-infiltrating lymphocytes and secreted inflammatory cytokines. Additionally, combining ES@CuO with programmed cell death-1 (PD-1) immunotherapy substantially increased the antitumor efficacy in murine melanoma. Overall, the findings of this study can lead to the use of a novel strategy for cuproptosis-mediated antitumor therapy, which may enhance the efficacy of immune checkpoint inhibitor therapy.