SCIENCE CHINA Materials•2026•DOI: 10.1007/s40843-025-3793-9
Organic solar cells (OSCs) require both a high donor/acceptor (D/A) interfacial area for efficient exciton dissociation and a vertically phase-separated morphology for efficient charge transport. Traditional bulk heterojunctions (BHJs) provide large interfacial areas but lack vertical phase separation, while quasi-planar heterojunctions (QPHJs) achieve vertical separation at the cost of reduced interfacial contact. Here, we introduce an in situ pore-forming strategy for polymer thin films. By incorporating an excess of additives as pore-forming agents into the donor layer, a nanoporous film with a fibrous nano-network is generated. Subsequent deposition of acceptor molecules fills these nanopores, creating a hybrid planar/bulk heterojunction (HP/BHJ) that synergizes the strengths of both architectures. This design enhances performance by: (1) increasing the D/A interfacial area via nanopores, forming a three-dimensional network that accelerates exciton dissociation; (2) promoting close molecular packing that minimizes carrier recombination and establishes low-defect charge transport channels; and (3) fostering vertical phase separation through layer-by-layer deposition. Binary OSCs fabricated with this strategy achieve a power conversion efficiency (PCE) of 20.0%, surpassing conventional BHJ and QPHJ devices by a significant margin. The approach demonstrates general applicability, with analogous improvements observed in D18/BTP-eC9-4F and PM6/L8-BO systems, underscoring its potential for advancing OSC performance.
SCIENCE CHINA Materials•2026•DOI: 10.1007/s40843-025-3642-4
High-density glass scintillators are promising alternatives to crystals for next-generation radiation detection due to their low cost, excellent physical and chemical stability, and processability. In this study, a series of Ce3+-activated gadolinium gallium borosilicate (GGBS x) glasses were synthesized via vacuum melt-quenching. With increasing Gd2O3 content, glass density increased from 5.86 to 6.05 g/cm3, and molar volume from 36.43 to 39.79 cm3/mol. Extended X-ray absorption fine structure (EXAFS) analysis revealed that in GGBS 1 glass, Ce3+ exclusively adopts a hexahedral [CeO6] configuration, while Gd3+ exhibits both hexahedral and octahedral coordination with a bond length of 2.35±0.1 Å and Debye-Waller factor σ2 of 0.0122±0.0015 Å2. As Gd2O3 content increased, shallow trap depth rose from 0.804 to 0.858 eV, while deep trap depth first increased from 0.948 to 1.434 eV then decreased to 1.010 eV. GGBS 1 glass exhibited high transmittance (~80%) in the visible range and a photoluminescence quantum yield of 78.4%. Under X-ray irradiation, its X-ray excited luminescence intensity reached 128.5% of that of Bi4Ge3O12 (BGO) crystal, with a spatial resolution of 29.1 lp/mm, approaching the highest reported for glass scintillators. Under γ-ray excitation, it achieved a light yield of 1058 photons/MeV and an energy resolution of 23.7% at 662 keV. These results indicate that GGBS 1 glass scintillator warrants further development for applications in X-ray imaging and γ-ray spectroscopy.
Environmental Chemistry•2026•DOI: 10.7524/j.issn.0254-6108.2026030601
Bisphenol A (BPA), a high-volume industrial chemical, is implicated in neurotoxicity and chronic neurodegenerative diseases. This study integrates network toxicology, molecular docking, and molecular dynamics simulations to systematically delineate the common mechanisms linking BPA to Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Using the human astrocyte cell line SVGP12 as an in vitro model, we identified six key toxic functional proteins—TP53, HSP90AA1, HSP90AB1, INS, BCL2, and AKT1—that mediate BPA's effects across these diseases, with BCL2 emerging as the most central node. Experimental validation demonstrated that BPA induces oxidative stress and cell cycle arrest, suppresses the INS-AKT1-BCL2 anti-apoptotic pathway, and activates the TP53-HSP90 pro-apoptotic pathway, culminating in mitochondrial apoptosis of astrocytes and disruption of neural microenvironment homeostasis. These findings reveal a convergent mechanism by which BPA accelerates neurodegeneration, filling a critical gap in understanding BPA's role in AD, PD, and HD. The study provides a novel theoretical framework and experimental evidence for BPA neurotoxicity risk assessment and informs preventive and therapeutic strategies for BPA-related neurodegenerative disorders.