Porous Bi Nanosheets Derived from ß-Bi2O3 for Efficient Electrocatalytic CO2 Reduction to Formate.

The electrochemical CO2 reduction reaction (ECO2RR) is a promising strategy for converting CO2 into high-value chemical products. However, the synthesis of effective and stable electrocatalysts capable of transforming CO2 into a specified product remains a huge challenge. Herein, we report a template-regulated strategy for the preparation of a Bi2O3-derived nanosheet catalyst with abundant porosity to achieve the expectantly efficient CO2-to-formate conversion. The resultant porous bismuth nanosheet (p-Bi) not only exhibited marked Faradaic efficiency of formate (FEformate), beyond 91% in a broad potential range from -0.75 to -1.1 V in the H-type cell, but also demonstrated an appreciable FEformate of 94% at a high current density of 262 mA cm-2 in the commercially important gas diffusion cell. State-of-the-art X-ray absorption near edge structure spectroscopy (XANES) and theoretical calculation unraveled the distinct formate production performance of the p-Bi catalyst, which was cocontributed by its smaller size, plentiful porous structure, and stronger Bi-O bond, thus accelerating the absorption of CO2 and promoting the subsequent formation of intermediates. This work provides an avenue to fabricate bismuth-based catalysts with high planar and porous morphologies for a broad portfolio of applications.

Nanoparticulates reduce tumor cell migration through affinity interactions with extracellular migrasomes and retraction fibers.

Nano-tumor interactions are fundamental for cancer nanotherapy, and the cross-talk of nanomedicines with the extracellular matrix (ECM) is increasingly considered essential. Here, we specifically investigate the nano-ECM interactivity using drug-free nanoparticulates (NPs) and highly metastatic cancer cells as models. We discover with surprise that NPs closely bind to specific types of ECM components, namely, retraction fibers (RFs) and migrasomes, which are located at the rear of tumor cells during their migration. This interaction is observed to alter cell morphology, limit cell motion range and change cell adhesion. Importantly, NPs are demonstrated to inhibit tumor cell removal in vitro, and their anti-metastasis potential is preliminarily confirmed in vivo. Mechanically, the NPs are found to coat and form a rigid shell on the surface of migrasomes and retraction fibers via interaction with lipid raft/caveolae substructures. In this way, NPs block the recognition, endocytosis and elimination of migrasomes by their surrounding tumor cells. Thereby, NPs interfere with the cell-ECM interaction and reduce the promotion effect of migrasomes on cell movement. Additionally, NPs trigger alteration of the expression of proteins related to cell-cell adhesion and cytoskeleton organization, which also restricts cell migration. In summary, all the findings here provide a potential target for anti-tumor metastasis nanomedicines.