Notable Performance Enhancement of CsPbI2Br Solar Cells by a Dual-Function Strategy with CsPbBr3 Nanocrystals.

Herein, a dual-function strategy, in which CsPbI2Br is treated by CsPbBr3 nanocrystals (NCs) via addition and surface modification to construct the "electron bridge" and gradient heterojunction, respectively, to notably improve the performance of the CsPbI2Br solar cells, is proposed. The "electron bridge" formed by the CsPbBr3 NCs provides an extra transport channel for the photogenerated electrons in the CsPbI2Br layer, thus facilitating electron transport. Meanwhile, surface modification of CsPbI2Br by the CsPbBr3 NCs forms a gradient heterojunction between the CsPbI2Br layer and the P3HT layer, enhancing hole extraction accordingly. In addition, the CsPbBr3 NC treatment passivates the defects at the bulk and surface of the CsPbI2Br layers, thus suppressing carrier recombination. Thanks to these positive effects of the CsPbBr3 NCs, the demonstration device with a simple configuration of ITO/SnO2/CsPbI2Br/P3HT/Ag achieves a notable power conversion efficiency of 17.03%, which is among the highest efficiencies reported for CsPbI2Br-based solar cells.

Improved Comprehensive Photovoltaic Performance and Mechanisms by Additive Engineering of Ti3C2Tx MXene into CsPbI2Br.

CsPbI2Br is promising in the application of perovskite solar cells (PSCs) owing to its reasonable bandgap and good thermal stability. However, the reported power conversion efficiency (PCE) of the CsPbI2Br solar cells is still much lower than that of the organic-inorganic hybrid PSCs, mainly due to relatively poor CsPbI2Br crystal quality. Herein, additive engineering to the photoactive layer of CsPbI2Br using the Ti3C2Tx MXene nanosheets is reported. Thanks to the improved crystallinity/reduced defect density, together with the formation of the Schottky junction between the MXene nanosheets and CsPbI2Br, enhanced separation and transfer of the photogenerated electron-hole pairs can be achieved for optimal MXene addition. A simple device configuration of ITO/SnO2/Ti3C2Tx-added CsPbI2Br/P3HT/Ag can thus deliver a significantly boosted PCE of 15.10%, i.e., a ∼16.69% relative increment compared with that (12.94%) of the control device without adding MXene. In addition, the enhanced humidity resistance is achieved for the MXene-added CsPbI2Br layers.

Evaluation of vitrectomy combined preoperative intravitreal ranibizumab and postoperative intravitreal triamcinolone acetonide for proliferative diabetic retinopathy.

BACKGROUND: To explore the treatment efficacy of the combination of preoperative intravitreal ranibizumab (IVR) and postoperative intravitreal triamcinolone acetonide (IVTA) in patients undergoing pars plana vitrectomy (PPV) for proliferative diabetic retinopathy (PDR). METHODS: A retrospective comparative study was performed on 128 eyes of 128 patients who had PDR and underwent PPV. Patients who received a single PPV were assigned to Group A. Those who received PPV with preoperative IVR were assigned to Group B. Patients in Group C underwent PPV combined preoperative IVR and postoperative IVTA. Intraoperative findings, changes in mean best-corrected visual acuity (BCVA) and postoperative adverse events, were retrospectively evaluated at 6-month follow-up. RESULTS: The incidences of iatrogenic breaks, severe intraoperative bleeding, using long-term internal tamponade agents, recurrent vitreous hemorrhage (VH), and duration of surgery were statistically significantly less in Group B and Group C than in Group A. The postoperative BCVA was statistically significantly better in Groups B and Group C than in Group A, respectively, at 1 month after surgery. The mean 3-month postoperative visual acuity was better in Group C. The incidence of high intraocular pressure (IOP) was significantly higher in Group C at the first postoperative week. There were no statistically significant differences in the incidence of exudative retinal detachment and choroidal detachment among the three groups. CONCLUSION: In patients undergoing PPV for PDR, preoperative IVR significantly reduced the occurrence of intraoperative and postoperative complications, and the combination of preoperative IVR and postoperative IVTA can better improve the postoperative visual outcome.

Baicalein suppresses the androgen receptor (AR)-mediated prostate cancer progression via inhibiting the AR N-C dimerization and AR-coactivators interaction.

BACKGROUND: Androgen receptor (AR) plays a critical role in prostate cancer (PCa) development and progression. Androgen deprivation therapy with antiandrogens to reduce androgen biosynthesis or prevent androgens from binding to AR are widely used to suppress AR-mediated PCa growth. However, most of ADT may eventually fail with development of the castration resistance after 12-24 months. Here we found that a natural product baicalein can effectively suppress the PCa progression via targeting the androgen-induced AR transactivation with little effect to AR protein expression. METHODS: PCa cells including LNCaP, CWR22Rv1, C4-2, PC-3, and DU145, were treated with baicalein and luciferase assay was used to evaluate their effect on the AR transactivation. Cell growth and IC50 were determined by MTT assay after 48 hrs treatment. RT-PCR was used to evaluate the mRNA levels of AR target genes including PSA, TMPRSS2, and TMEPA1. Western blot was used to determine AR and PSA protein expression. RESULTS: The natural product of baicalein can selectively inhibit AR transactivation with little effect on the other nuclear receptors, including ERα, and GR. At a low concentration, 2.5 µM of baicalein effectively suppresses the growth of AR-positive PCa cells, and has little effect on AR-negative PCa cells. Mechanism dissection suggest that baicalein can suppress AR target genes (PSA, TMPRSS2, and TMEPA1) expression in both androgen responsive LNCaP cells and castration resistant CWR22Rv1 cells, that may involve the inhibiting the AR N/C dimerization and AR-coactivators interaction. CONCLUSIONS: Baicalein may be developed as an effective anti-AR therapy via its ability to inhibit AR transactivation and AR-mediated PCa cell growth.