氟化苯并噻唑-苯并硫氮杂卓共轭聚合物提升钙钛矿太阳能电池性能

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在"Defects Passivation With Dithienobenzodithiophene-based π-conjugated Polymer for Enhanced Performance of Perovskite Solar Cell"这篇论文中,研究者们探索了一种新型策略来优化钙钛矿太阳能电池的性能。钙钛矿太阳能电池因其高效率和低成本而备受关注,但其稳定性问题,特别是缺陷导致的性能衰退是一个关键挑战。论文的核心在于介绍了一种基于二苯并硫氮杂卓(dithienobenzodithiophene, DBT)的π共轭聚合物,该聚合物由氟化苯并三唑和苯并噻二唑组成。 通过反溶剂法,这种含氟聚合物被成功地应用于钙钛矿晶体的表面,与未配位的铅离子(Pb2+)发生作用,形成稳定的Pb-F键。这个过程起到了有效的缺陷钝化作用,减少了陷阱态密度,从而改善了电子-空穴对的复合效率。缺陷的减少不仅提高了钙钛矿薄膜的内部电荷传输,也增强了其与 Spiro-OMeTAD(一种常用的有机电解质)之间的接触,有助于提高整体电流收集能力。 实验结果显示,经过这种聚合物钝化处理后,钙钛矿太阳能电池的功率转换效率(PCE)达到了18.03%,显示出显著的提升。令人印象深刻的是,在储存于湿度为60%的环境中长达1000小时后,设备仍能保持原始PCE的90%,证明了dithienobenzodithiophene基π共轭聚合物作为缺陷钝化材料的有效性和稳定性。 这项研究不仅推动了钙钛矿太阳能电池技术的发展,也为寻找新型材料和钝化策略提供了有价值的参考。它展示了π共轭聚合物在提高器件性能和耐久性方面的潜力,为未来的高效、稳定和大面积应用提供了新的可能。因此,这类基于DBT的聚合物在钙钛矿太阳能电池领域具有巨大的应用前景。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.请用nature杂志的风格润色成学术论文的形式。

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