In Situ Dual-Interface Passivation Strategy Enables The Efficiency of Formamidinium Perovskite Solar Cells Over 25.

Perovskite solar cells (PSCs) are promising candidates for next-generation photovoltaics owing to their unparalleled power conversion efficiencies (PCEs). Currently, approaches to further improve device efficiencies tend to focus on the passivation of interfacial defects. Although various strategies have been developed to mitigate these defects, many involve complex and time-consuming post-treatment processes, thereby hindering their widespread adoption in commercial applications. In this work, a concise but efficient in situ dual-interface passivation strategy is developed wherein 1-butyl-3-methylimidazolium methanesulfonate (MS) is employed as a precursor additive. During perovskite crystallization, MS can either be enriched downward through precipitation with SnO2 , or can be aggregated upward through lattice extrusion. These self-assembled MS species play a significant role in passivating the defect interfaces, thereby reducing nonradiative recombination losses, and promoting more efficient charge extraction. As a result, a PCE >25% (certified PCE of 24.84%) is achieved with substantially improved long-term storage and photothermal stabilities. This strategy provides valuable insights into interfacial passivation and holds promise for the industrialization of PSCs.

A novel functional TagSNP Rs7560488 in the DNMT3A1 promoter is associated with susceptibility to gastric cancer by modulating promoter activity.

DNA-methyltransferase (DNMT)-3A which contains DNMT3A1 and DNMT3A2 isoforms have been suggested to play a crucial role in carcinogenesis and showed aberrant expression in most cancers. Accumulated evidences also indicated that single nucleotide polymorphisms (SNP) in DNMT genes were associated with susceptibility to different tumors. We hypothesized that genetic variants in DNMT3A1 promoter region are associated with gastric cancer risk. We selected the tagSNPs from the HapMap database for the Chinese and genotyped in a case-control study to evaluate the association with gastric cancer (GC) in a Chinese population. We identified that the functional tagSNP rs7560488 T>C associated with a significantly increased risk of GC. In vitro functional analysis by luciferase reporter assay and EMSA indicated that the tagSNP rs7560488 T>C substantially altered transcriptional activity of DNMT3A1 gene via influencing the binding of some transcriptional factors, although a definite transcriptional factor remains to be established. Compared with TT homozygotes, subjects who were TC heterozygotes and CC homozygotes exhibited a reduced expression of DNMT3A1. Furthermore, stratified analysis showed that individuals who harbor TC or CC genotypes less than 60 years old were more susceptible to GC. Our results suggest that the genetic variations in the DNMT3A1 promoter contribute to the susceptibility to GC and also provide an insight that tagSNP rs7560488 T>C may be a promising biomarker for predicting GC genetic susceptibility and a valuable information in GC pathogenesis.