Organic cation and halide anion defects are omnipresent in the perovskite films, which will destroy perovskite electronic structure and downgrade the properties of devices. Defect passivation in halide perovskites is crucial to the application of solar cells. Herein, tiny amounts of trivalent rhodium ion incorporation can help the nucleation of perovskite grain and passivate the defects in the grain boundaries, which can improve efficiency and stability of perovskite solar cells. Through first-principle calculations, rhodium ion incorporation into the perovskite structure can induce ordered arrangement and tune bandgap. In experiment, rhodium ion incorporation with perovskite can contribute to preparing larger crystalline and uniform film, reducing trap-state density and enlarging charge carrier lifetime. After optimizing the content of 1% rhodium, the devices achieved an efficiency up to 20.71% without obvious hysteresis, from 19.09% of that pristine perovskite. In addition, the unencapsulated solar cells maintain 92% of its initial efficiency after 500 h in dry air. This work highlights the advantages of trivalent rhodium ion incorporation in the characteristics of perovskite solar cells, which will promote the future industrial application.

Efficient perovskite solar cells fabricated by manganese cations incorporated in hybrid perovskites.

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Background The role of HOX transcript antisense RNA (HOTAIR) has been proven to be important in tumorigenesis. However, how this molecule promotes metastasis and invasion in PCa is still unclear. Methods The relationship between HOTAIR and hepatocellular adhesion molecule (hepaCAM) in PCa was identified by immunohistochemistry, immunofluorescence, plasmid transfection, quantitative real-time PCR and immunoblotting. The regulatory effects of HOTAIR on hepaCAM and MAPK signalling and their key roles in PCa metastasis were investigated in vitro. Results The expression of HOTAIR was inversely correlated with hepaCAM in the blood and tissue of PCa patients. Here, hepaCAM was identified as a novel target gene of HOTAIR and was critical for the invasiveness of PCa. HOTAIR recruited PRC2 to the hepaCAM promoter, resulting in high levels of H3K27me3 and the absence of hepaCAM with an abnormally activated MAPK pathway. Both HOTAIR depletion and EZH2 inhibition could induce hepaCAM re-expression with inhibitory MAPK signalling and decrease the invasive and metastatic capabilities of PCa cells. Conclusions This study demonstrates that HOTAIR promotes invasion and metastasis of PCa by decreasing the inhibitory effect of hepaCAM on MAPK signalling. Therefore, the HOTAIR/hepaCAM/MAPK axis may provide a new avenue towards therapeutic strategies and prognostic indicators for advanced prostate cancer.