RESUMEN
Improving thermal stability is of great importance for the industrialization of polymer solar cells (PSC). In this paper, we systematically investigated the high-temperature thermal annealing effect on the device performance of the state-of-the-art polymer:non-fullerene (PM6:Y6) solar cells with an inverted structure. Results revealed that the overall performance decay (19% decrease) was mainly due to the fast open-circuit voltage (VOC, 10% decrease) and fill factor (FF, 10% decrease) decays whereas short circuit current (JSC) was relatively stable upon annealing at 150 °C (0.5% decrease). Pre-annealing on the ZnO/PM6:Y6 at 150 °C before the completion of cell fabrication resulted in a 1.7% performance decrease, while annealing on the ZnO/PM6:Y6/MoO3 films led to a 10.5% performance decay, indicating that the degradation at the PM6:Y6/MoO3 interface is the main reason for the overall performance decay. The increased ideality factor and reduced built-in potential confirmed by dark J - V curve analysis further confirmed the increased interfacial charge recombination after thermal annealing. The interaction of PM6:Y6 and MoO3 was proved by UV-Vis absorption and XPS measurements. Such deep chemical doping of PM6:Y6 led to unfavorable band alignment at the interface, which led to increased surface charge recombination and reduced built-in potential of the cells after thermal annealing. Inserting a thin C60 layer between the PM6:Y6 and MoO3 significantly improved the cells' thermal stability, and less than 2% decay was measured for the optimized cell with 3 nm C60.
RESUMEN
OBJECTIVE: The purpose of this study was to investigate the relationships between TP53 Pro72Arg (rs1042522) polymorphism and susceptibility to type 2 diabetes (T2DM) and its related complications. METHODS: The TP53 Pro72Arg polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 206 T2DM patients and 446 healthy controls. Mitochondrial DNA (mtDNA) content, mtDNA transcriptional level and large-scale mtDNA deletion were evaluated in leukocytes of T2DM patients using fluorescence-based quantitative PCR (FQ-PCR), reverse transcriptase-quantitative PCR (RT-qPCR) and long-range PCR approaches, respectively. The data of our study were processed by GraphPad Prism software (version 7.00). RESULTS: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164). T2DM patients with Arg/Arg genotype had significantly decreased prevalences of diabetic neuropathy and retinopathy compared to those without (6.5% vs 19.4%, p=0.018 and 14.8% vs 30.7%, p=0.018, respectively). T2DM patients with Arg/Arg genotype had higher mtDNA content and mtRNA expression level than those who were not Arg/Arg genotype (p<0.05 for all), and we did not observe mtDNA 4977-base pair (bp) deletion mutations in the leukocytes of T2DM patients. CONCLUSION: There was a significant association of the TP53 Pro72Arg polymorphism with susceptibility to T2DM, and the homozygous Arg/Arg genotype of this gene locus might be a protective factor for diabetic complications. Those results suggested that the TP53 Arg72 variant had a different association with type 2 diabetes and its complications, and it might be related to mtDNA maintenance of the TP53 Arg72 variant under hyperglycemia-induced stress.