Steric hindrance induced low exciton binding energy enables low-driving-force organic solar cells

Exciton binding energy(E_(b))has been regarded as a critical parameter in charge separation during photovoltaic conversion.Minimizing the E_(b) of the photovoltaic materials can facilitate the exciton dissociation in low-driving force organic solar cells(OSCs)and thus improve the power conversion efficiency(PCE);nevertheless,diminishing the E_(b) with deliberate design principles remains a significant challenge.Herein,bulky side chain as steric hindrance structure was inserted into Y-series acceptors to minimize the E_(b) by modulating the intra-and intermolecular interaction.Theoretical and experimental results indicate that steric hindrance-induced optimal intra-and intermolecular interaction can enhance molecular polarizability,promote electronic orbital overlap between molecules,and facilitate delocalized charge trans-fer pathways,thereby resulting in a low E_(b).The conspicuously reduced E_(b) obtained in Y-ChC5 with pinpoint steric hindrance modulation can minimize the detrimental effects on exciton dissociation in low-driving-force OSCs,achieving a remarkable PCE of 19.1%with over 95%internal quantum efficiency.Our study provides a new molecular design rationale to reduce the E_(b).

GSDME maintains hematopoietic stem cells by balancing pyroptosis and apoptosis

GSDME contains a pore-forming domain at its N-terminal region to execute pyroptosis.Our previous study has reported that forced expression of Gsdme impairs the reconstitution capacity of hematopoietic stem cells(HSCs).While,how GSDME-mediated pyroptosis regulates HSCs remains unknown.Here,we show that hematopoietic stem and progenitor cells are capable to undergo pyroptosis in response to cisplatin treatment and GSDME is one of the genes mediating such process.Gsdme^(-/-)mice revealed no difference in the steady state of blood system while Gsdme^(-/-)HSCs exhibited compromised reconstitution capacity due to increased apoptosis.Briefly,this study reveals that GSDME modulates HSC function by coordinating pyroptosis and apoptosis.