No abstract

Minimization of defects and ion migration in organic–inorganic lead halide perovskite films is desirable for obtaining photovoltaic devices with high power conversion efficiency (PCE) and long‐term stability. However, achieving this target is still a challenge due to the lack of efficient multifunctional passivators. Herein, to address this issue, n‐type goethite (FeOOH) quantum dots (QDs) are introduced into the perovskite light‐absorption layer for achieving efficient and stable perovskite solar cells (PSCs). It is found that the iron, oxygen, and hydroxyl of FeOOH QDs can interact with iodine, lead, and methylamine, respectively. As a result, the crystallization kinetics process can be retarded, thereby resulting in high quality perovskite films with large grain size. Meanwhile, the trap states of perovskite can be effectively passivated via interaction with the under‐coordinated metal (Pb) cations, halide (I) anions on the perovskite crystal surface. Consequently, the PSCs with FeOOH QDs achieve a high efficiency close to 20% with negligible hysteresis. Most strikingly, the long‐term stability of PSCs is significantly enhanced. Furthermore, compared with the CH3NH3PbI3‐based device, a higher PCE of 21.0% is achieved for the device assembled with a Cs0.05FA0.81MA0.14PbBr0.45I2.55 perovskite layer.

Multiple amino acid (glutamine and lysine)-modified gold nanoparticles a with pH-switchable zwitterionic surface were fabricated through coordination bonds using ferrous iron (Fe2+) as bridge ions, which are able to spontaneously and selectively assemble in tumor cells for accurate tumor therapy combining enzyme-triggered photothermal therapy and H2O2-dependent catalytic medicine. These gold nanoparticles showed electric neutrality at pH 7.4 (hematological system) to prevent endocytosis of normal cells, which could be positively charged at pH 6.8 (tumor microenvironment) to promote the endocytosis of tumor cells to these nanoparticles, performing great tumor selectivity. After cell uptake, the specific enzyme (transglutaminase) in tumor cells would catalyze the polymerization of glutamine and lysine to cause the intracellular assembly of these gold nanoparticles, resulting in an excellent photothermal property for accurate tumor therapy. Moreover, the Fe2+ ion could decompose excess hydrogen peroxide (H2O2) in tumor cells via the Fenton reaction, resulting in a large amount of hydroxyl radicals (·OH). These radicals would also cause tumor cell damage. This synergetic therapy associating with high tumor selectivity generated an 8-fold in vitro cytotoxicity against tumor cells compared with normal cells under 48 h incubation with 10 min NIR irradiation. Moreover, in vivo data from tumor-bearing nude mice models showed that tumors can be completely inhibited and gradually eliminated after multimode treatment combining catalytic medicine and photothermal therapy for 3 weeks. This system takes advantage of three tumor microenvironment conditions (low pH, enzyme, and H2O2) to trigger the therapeutic actions, which is a promising platform for cancer therapy that achieved prolonged circulation time in the blood system, selective cellular uptake, and accurate tumor therapy in multiple models.

Multiresponsive adjuvant nanoparticles (RMmAGL) are fabricated to perform tumor‐specific photothermal therapy while regulating the behavior of tumor‐associated immune cells for primary tumor eradication and metastasis inhibition. Core–satellite‐like RMmAGL have a core of mannose‐functionalized mesoporous silica nanoparticles loaded with the TLR7 agonist imiquimod (R837@MSN‐mannose) connected via hydrazone bonds to satellites of glutamine (Glu)‐ and lysine (Lys)‐comodified gold nanoparticles (AuNPs‐Glu/Lys). During therapy, the acidic environment in tumor tissue cleaves the hydrazone bonds to release AuNPs‐Glu/Lys, which further accumulate in tumor cells. After internalization, photothermal agents (aggregated AuNPs‐Glu/Lys) are generated in situ through the intratumoral enzyme‐catalyzed reaction between Glu and Lys, resulting in tumor‐specific photothermal therapy. The detachment of AuNPs‐Glu/Lys also triggers the release of R837, which matured dendritic cells (DCs) via a vaccine‐like mechanism along with the tumor‐associated antigens generated by photothermal therapy. These matured DCs further activates surrounding T cells for immunotherapy. Moreover, the resulting free MSN‐mannose serves as an artificial glycocalyx to continuously induce the polarization of tumor‐associated macrophages from an immunosuppressive phenotype to an inflammatory phenotype, thus further enhancing immunotherapy. Both in vivo and in vitro experiments demonstrate significant inhibition of malignant tumors after therapy.