Both bismuth and copper are non-toxic and earth-abundant elements suitable for lead-free halide perovskite-like photovoltaic devices. Here, we report a highly facile route for in-situ producing copper-bismuth-iodide (CuBiI 4) thin films directly on ITO substrate at room temperature, by utilizing a Bi-Cu alloy layer as precursor. X-ray diffraction and transmission electron microscopy (TEM) results verified the formation of well crystallized CuBiI 4 thin films with [222] orientation. The transient photovoltage (TPV) analysis revealed that the CuBiI 4 is an n-type semiconductor with a suitable band gap of~1.81 eV, preferable to photoelectric conversion compared with CH 3 NH 3 PbI 3. It is very interesting that the subsequent spin-coating process of the classical Spiro-MeOTAD organic solution with TBP and acetonitrile resulted in a dense and smooth CuBiI 4 :Spiro-MeOTAD bulk-heterojunction film. The preliminarily fabricated simple sandwich structures of ITO/CuBiI 4 :Spiro-MeO-TAD/Au hybrid solar cell devices displayed efficient photovoltaic performance with the PCE up to 1.119% of the best sample. The room temperature direct metal surface elemental reaction (DMSER) method may provide a new insight for all-inorganic lead free perovskite-like A a B b X x compounds and high performance photovoltaic devices.

BackgroundMicroRNAs (miRNAs) regulate a lot of physiological and pathological processes, including myocardial ischemia/reperfusion. Recent studies reported that knockdown of miR-92a could attenuate ischemia/reperfusion-induced myocardial injury. In the present study, we examined the potential anti-apoptotic effects of miR-92a in a rat myocardiocyte cell line, and the possible role of Smad7 in such actions.Methodology and ResultsIn a preliminary bioinformatic analysis, we identified SMAD family member 7 (Smad7) as a potential target for miR-92a. A luciferase reporter assay indeed demonstrated that miR-92a could inhibit Smad7 expression. Myocardial ischemia/reperfusion was simulated in rat H9c2 cells with 24-h hypoxia followed by 12-h reoxygenation. Prior to hypoxia/reoxygenation, cells were transfected by miR-92a inhibitor. In some experiments, cells were co-transfected with siRNA-Smad7. The miR-92a inhibitor dramatically reduced the release of lactate dehydrogenase and malonaldehyde, and attenuated cardiomyocyte apoptosis. The miR-92a inhibitor increased SMAD7 protein level and decreased nuclear NF-κB p65 protein. Effects of the miR-92a inhibitor were attenuated by co-transfection with siRNA-Smad7.ConclusionInhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by targeting Smad7.

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The formation of a Bi gradient with a Bi/Cu bilayer as the precursor can improve the photoinduced charge carrier transportation in CuBiI4 films.