Search

Three polymer donors named Qx-8F, Qx-10F, and Qx-12F, with similar chemical structures, were synthesized. The energy level of these donors is manipulated by precisely controlling the fluorination sites. We demonstrate that the exciton dissociation efficiency is gradually enhanced from Qx-8F:Y6 to Qx-12F:Y6, leading to improved open circuit voltage VOC and short circuit current density JSC for donors with a higher degree of fluorination. Simultaneously, the trap-assisted recombination or bimolecular recombination intensity is reduced, while the extraction rate is enhanced because of increased charge carrier mobilities, leading to an increase in fill factor for donors with higher amount of fluorine atoms. The optimized device based on Qx-12F with the most fluorine atoms and the non-fullerene acceptor Y6 shows the highest power conversion efficiency of 15.21%, with a VOC of 0.85 V, JSC of 24.55 mA cm−2, and fill factor of 72.88%. It is further demonstrated that the optimized ternary device based on the Qx-12F:PM6:Y6 blend provides a power conversion efficiency of 16.32%. [ABSTRACT FROM AUTHOR]

Background: NADPH oxidase (NOX), a primary source of endothelial reactive oxygen species (ROS), is considered a key event in disrupting the integrity of the blood-retinal barrier. Abnormalities in neurovascular-coupled immune signaling herald the loss of ganglion cells in glaucoma. Persistent microglia-driven inflammation and cellular innate immune system dysregulation often lead to deteriorating retinal degeneration. However, the crosstalk between NOX and the retinal immune environment remains unresolved. Here, we investigate the interaction between oxidative stress and neuroinflammation in glaucoma by genetic defects of NOX2 or its regulation via gp91ds-tat., Methods: Ex vivo cultures of retinal explants from wildtype C57BL/6J and Nox2 -/- mice were subjected to normal and high hydrostatic pressure (Pressure 60 mmHg) for 24 h. In vivo, high intraocular pressure (H-IOP) was induced in C57BL/6J mice for two weeks. Both Pressure 60 mmHg retinas and H-IOP mice were treated with either gp91ds-tat (a NOX2-specific inhibitor). Proteomic analysis was performed on control, H-IOP, and treatment with gp91ds-tat retinas to identify differentially expressed proteins (DEPs). The study also evaluated various glaucoma phenotypes, including IOP, retinal ganglion cell (RGC) functionality, and optic nerve (ON) degeneration. The superoxide (O 2 - ) levels assay, blood-retinal barrier degradation, gliosis, neuroinflammation, enzyme-linked immunosorbent assay (ELISA), western blotting, and quantitative PCR were performed in this study., Results: We found that NOX2-specific deletion or activity inhibition effectively attenuated retinal oxidative stress, immune dysregulation, the internal blood-retinal barrier (iBRB) injury, neurovascular unit (NVU) dysfunction, RGC loss, and ON axonal degeneration following H-IOP. Mechanistically, we unveiled for the first time that NOX2-dependent ROS-driven pro-inflammatory signaling, where NOX2/ROS induces endothelium-derived endothelin-1 (ET-1) overexpression, which activates the ERK1/2 signaling pathway and mediates the shift of microglia activation to a pro-inflammatory M1 phenotype, thereby triggering a neuroinflammatory outburst., Conclusions: Collectively, we demonstrate for the first time that NOX2 deletion or gp91ds-tat inhibition attenuates iBRB injury and NVU dysfunction to rescue glaucomatous RGC loss and ON axon degeneration, which is associated with inhibition of the ET-1/ERK1/2-transduced shift of microglial cell activation toward a pro-inflammatory M1 phenotype, highlighting NOX2 as a potential target for novel neuroprotective therapies in glaucoma management., (© 2024. The Author(s).)