A major efficiency limit for solution-processed perovskite optoelectronic devices (e.g. light-emitting diodes, LEDs) is trap-mediated non-radiative losses. Defect passivation using organic molecules has been identified as an attractive approach to tackle this issue. However, implementation of this approach has been hindered by a lack of deep understanding of how the molecular structures affect the passivation effectiveness. We show that the so far largely ignored hydrogen bonds play a critical role. By weakening the hydrogen bonding between the passivating functional moieties and the organic cation featuring the perovskite, we significantly enhance the interaction with defects sites and minimize non-radiative recombination losses. Consequently, we achieve exceptionally high-performance near infrared perovskite LEDs (PeLEDs) with a record external quantum efficiency (EQE) of 21.6%. In addition, our passivated PeLEDs maintain a high EQE of 20.1% and a wall-plug efficiency of 11.0% at a high current density of 200 mA cm-2 , making them more attractive than the most efficient organic and quantum-dot LEDs at high excitations.

Background/Aims: MicroRNAs (miRNAs) play important roles in tumorigenesis. We investigated the roles and mechanisms of miR-138 in human non-small cell lung cancer (NSCLC). Methods: The expression of miR-138 was first examined in NSCLC cell lines and tumourtissues by real-time PCR The in vitro and in vivo functional effect of miR-138 was examined further. A luciferase reporter assay was conducted to confirm target association between miR-138 and the enhancer of zeste homolog 2 (EZH2). Results: miR-138 was frequently downregulated in NSCLC cells and tissues. Overexpression of miR-138 inhibited proliferation of NSCLC cells in vitro and tumor growth in vivo. The EZH2 oncogene, which is often overexpressed in various human cancers and acts as an important regulator of cell growth and tumor invasion, was identified as a novel target of miR-138. miR-138 can bind to the 3′ untranslated region (3′ UTR) of EZH2 and suppress the expression of EZH2 at both mRNA and protein levels. Furthermore, knockdown of EZH2 phenocopied the tumor suppressive effects of miR-138 in cell models, whereas ectopic expression of EZH2 rescued the suppressive effects of miR-138. Conclusion: These findings define a tumor suppressor function for miR-138 in NSCLC and further suggest that miR-138 may represent a potential therapeutic target for NSCLC patients.

Interfacial reactions between the perovskite emitters and the interlayers are detrimental to the operational stability of the perovskite light-emitting diodes. Incorporating dicarboxylic acids into the precursor efficiently eliminates reactive organic ingredients in the perovskite emitters through an in situ amidation process, which is catalyzed by the alkaline zinc oxide substrate underneath. The formed amides improve the stability of the perovskite emitters and the charge injection contacts, ensuing notably improved operational stability of the resulting perovskite light-emitting diodes.

No abstract