RESUMEN
B-γ-CsSnI3 perovskite solar cells (PSCs) are simulated employing diverse electron-transporting layers (ETLs, including TiO2, ZnO, SnO2, GaN, C60, and PCBM), and a comparative study has been made. Both regular and inverted planar structures are simulated. Effects of the thickness of absorbers and ETLs, doping of ETLs, and interface trap states on the photovoltaic performance are studied to optimize the device structures. The regular structures have larger short-circuit current density (J sc) than the inverted structures, but the inverted structures have larger fill factor (FF). All of the simulated optimal PSCs have similar open-circuit voltages (V oc) of â¼0.96 V. The PSCs with TiO2 ETLs have the best photovoltaic performance, and the optimum structure exhibits the highest efficiency of 20.2% with a V oc of 0.97 V, J sc of 29.67 mA/cm2, and FF of 0.70. The optimal PSCs with ZnO, GaN, C60, and PCBM ETLs exhibit efficiencies of 17.88, 18.09, 16.71, and 16.59%, respectively. The optimal PSC with SnO2 ETL exhibits the lowest efficiency of 15.5% in all of the simulated PSCs due to its cliff-like band offset at the SnO2/CsSnI3 interface. Furthermore, the increase of interface trap density and capture cross section is found to reduce the photovoltaic performance of PSCs. This work contributes to designing and fabricating CsSnI3 PSCs.
RESUMEN
A major reason for the failure of advanced colorectal cancer (CRC) treatment is the occurrence of chemoresistance to oxaliplatin-based chemotherapy. Recently, studies have shown that long non-coding RNAs (lncRNAs) play an important role in drug resistance. Using HiSeq sequencing methods, we identified that lncRNAs show differential expression levels in oxaliplatin-resistant (OxR) and non-resistant CRC patients. RT-qPCR was then performed in tissues and serum samples, and lncRNA MEG3 was verified to be downregulated in non-responding patients and to have considerable discriminating potential to identify responding patients from non-responding patients. Moreover, decreased serum MEG3 expression was associated with poor chemoresponse and low survival rate in CRC patients receiving oxaliplatin treatment. Subsequently, OxR cell lines were established, and MEG3 was significantly downregulated in HT29 OxR and SW480 OxR cells. In addition, overexpression of MEG3 with pMEG3 reversed oxaliplatin resistance in both CRC cell lines. Flow cytometric apoptosis analysis indicated that MEG3 promoted CRC cell apoptosis. More importantly, MEG3 enhanced oxaliplatininduced cell cytotoxicity in CRC. In conclusion, our integrated approach demonstrated that decreased expression of lncRNA MEG3 in CRC confers potent poor therapeutic efficacy, and that MEG3 promotes chemosensitivity by enhancing oxaliplatin-induced cell apoptosis. Thus, overexpression of MEG3 may be a future direction by which to develop a novel therapeutic strategy to overcome oxaliplatin resistance of CRC patients.