Cupric chloride

Structural reconstruction of electrocatalysts plays a pivotal role in catalytic performances for CO2 reduction reaction (CO2RR), whereas the behavior is by far superficially understood. Here, we report that CO2 accessibility results in a universal self-adaptive structural reconstruction from Cu2O to Cu@CuxO composites, ending with feeding gas-dependent microstructures and catalytic performances. The CO2-rich atmosphere favors reconstruction for CO2RR, whereas the CO2-deficient one prefers that for hydrogen evolution reaction. With the assistance of spectroscopic analysis and theoretical calculations, we uncover a CO2-induced passivation behavior by identifying a reduction-resistant but catalytic active Cu(I)-rich amorphous layer stabilized by *CO intermediates. Additionally, we find extra CO production is indispensable for the robust production of C2H4. An inverse correlation between durability and FECO/FEC2H4 is disclosed, suggesting that the self-stabilization process involving the absorption of *CO intermediates on Cu(I) sites is essential for durable electrolysis. Guided by this insight, we design hollow Cu2O nanospheres for durable and selective CO2RR electrolysis in producing C2H4. Our work recognizes the previously overlooked passivation reconstruction and self-stabilizing behavior and highlights the critical role of the local atmosphere in modulating reconstruction and catalytic processes.

Cell death-based therapies combined with immunotherapy have great potential in cancer therapy. To further explore and apply the combined therapies, the immunogenicity of different cell death modes in colorectal cancer (CRC) was evaluated by a cause-and-effect framework encompassing 12 cell death modes. Results show robust correlations among cuproptosis, immunogenic cell death (ICD) and immunity in CRC, as observed in our in-house and other independent cohorts, which are substantiated by in vitro and in vivo experiments. Subsequent investigations demonstrate that cuproptosis induces endoplasmic reticulum stress, leading to the release of damage-associated molecular patterns from CRC cells and triggering the maturation of antigen-presenting cells. Moreover, for in vivo therapeutic approaches, an in situ cuproptosis-inducing system was devised, which can further strengthen the effects of immune cells. Through the combined analysis including single-cell RNA sequencing, cuproptosis is shown to mobilize cytotoxic T lymphocytes and M1 macrophages within the tumor microenvironment (TME). Additionally, co-treatment with Imiquimod, the TLR7 agonist, augments the anti-tumor immune responses induced by cuproptosis. Overall, we provide compelling evidence that cuproptosis induces ICD thus fostering an inflammatory TME, and the cuproptosis-based delivery system further promotes this inflammatory environment, demonstrating considerable potential for enhancing tumor therapy efficacy.