Tin oxide (SnO 2 ) is widely used in perovskite solar cells (PSCs) as an electron transport layer (ETL) material. However, its high surface trap density has already become a strong factor limiting PSC development. In this work, phosphoric acid is adopted to eliminate the SnO 2 surface dangling bonds to increase electron collection efficiency. The phosphorus mainly exists at the boundaries in the form of chained phosphate groups, bonding with which more than 47.9% of Sn dangling bonds are eliminated. The reduction of surface trap states depresses the electron transport barriers, thus the electron mobility increases about 3 times when the concentration of phosphoric acid is optimized with 7.4 atom % in the SnO 2 precursor. Furthermore, the stability of the perovskite layer deposited on the phosphate-passivated SnO 2 (P-SnO 2 ) ETL is gradually improved with an increase of the concentration. Due to the higher electron collection efficiency, the P-SnO 2 ETLs can dramatically promote the power conversion efficiency (PCE) of the PSCs. As a result, the champion PSC has a PCE of 21.02%. Therefore, it has been proved that this simple method is efficient to improve the quality of ETL for high-performance PSCs.

Compared with traditional chemotherapeutics, vascular disruption agents (VDAs) have the advantages of rapidly blocking the supply of nutrients and starving tumors to death. Although the VDAs are effective under certain scenarios, this treatment triggers angiogenesis in the later stage of therapy that frequently leads to tumor recurrence and treatment failure. Additionally, the nonspecific tumor targeting and considerable side effects also impede the clinical applications of VDAs. Here we develop a customized strategy that combines a VDA with an anti-angiogenic drug (AAD) using mesoporous silica nanoparticles (MSNs) coated with platelet membrane for the self-assembled tumor targeting accumulation. The tailor-made nanoparticles accumulate in tumor tissues through the targeted adhesion of platelet membrane surface to damaged vessel sites, resulting in significant vascular disruption and efficient anti-angiogenesis in animal models. This study demonstrates the promising potential of combining VDA and AAD in a single nanoplatform for tumor eradication.

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