Kai Xiang

A green solvent additive, isopropanol (IPA), is employed to regulate the morphology of the active layer and yields an outstanding efficiency of 20.0% with chloroform as the main solvent and 19.4% wit...

An innovative molecular design strategy of incorporating “highly luminescent” and “3D-architectured” substituents into NFAs is proposed to improve its photoluminescence quantum yield and reduce nonra...

An innovative molecular design strategy of incorporating “highly luminescent” and “3D-architectured” substituents into NFAs is proposed to improve its photoluminescence quantum yield and reduce nonradiative energy loss. A triptycene derivative-modified NFA TQX-IC is synthesized, showing a high PLQY of 12.80%. Binary D18:TQX-IC OSCs achieve high

Younger-onset type 2 diabetes (T2D, onset <40 years) represents a growing global health challenge, characterized by heterogenous pathophysiology and accelerated complications. Current ‘one-size-fits-all” treatment approaches may be inadequate for this population. To address this heterogeneity, we performed clinical variable-based clustering using BMI, onset age, HbA

Background The hepatocellular carcinoma (HCC) immune microenvironment is heavily influenced by immunosuppressive neutrophils, yet the mechanisms driving their senescence-associated reprogramming remain elusive. Objectives To elucidate the role of Selenoprotein P (Sepp1)-mediated selenium metabolism in driving the accumulation and immunosuppressive function of senescent-like neutrophils in HCC, and its impact on tumour immune evasion. Design We performed integrative single-cell RNA sequencing analyses in HCC mouse models, coupled with functional, metabolic and epigenetic assays to characterise neutrophil subpopulations and dissect the regulatory pathways linking Sepp1 and selenium metabolism to neutrophil senescence-associated reprogramming and tumour progression. Results We identified a distinct subpopulation of senescent-like tumour-infiltrating neutrophils marked by hepatic depletion of Sepp1, elevated Cdkn1a, S100a8/9 and Vegfa. Loss of tumour-derived Sepp1 impaired selenium uptake via Lrp8-mediated transport, suppressing intracellular selenium metabolism and hydrogen selenide production. This led to S-adenosylmethionine accumulation and increased histone H3 protein of trimethylation of lysine 4 histone modification, driving a prosenescence chromatin landscape. Selenium supplementation reversed these effects, restoring Sepp1 expression, reducing neutrophil senescence-associated reprogramming and reinvigorating anti-tumour immunity. Moreover, selenium synergised with anti-programmed cell death 1 therapy to suppress tumour growth. Conclusions Sepp1 is a key regulator of neutrophil senescence-associated reprogramming and immune suppression in HCC through selenium-dependent epigenetic remodelling. Targeting senescent-like neutrophils via selenium supplementation holds therapeutic promise to enhance immunotherapy efficacy in liver cancer. Data are available in a public, open access repository. Data are available upon reasonable request. The raw CUT&RUN sequencing data generated in this study have been deposited in the Genome Sequence Archive (GSA) under accession number CRA032287. The single-cell RNA sequencing data generated in this study have been deposited in the Gene Expression Omnibus (GEO) database under accession number GSE317333. Processed data, analysis scripts and additional sequencing datasets generated and/or analysed during the current study are available from the corresponding author upon reasonable request.

Four isomeric dimeric acceptors were developed to study the effects different conjugated-sites of end-groups on molecular optoelectronic properties. Among these acceptors, Dimer-2, with two inside methoxy-substituted end-groups and two outside methoxy-free end-groups, achieved an efficiency of 20.32%, ranking the highest value among ternary devices with non-fully conjugated dimeric acceptors.