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Phthalates, bisphenols, dioxins, and brominated flame retardants are among the persistent pollutants that have been brought into the environment by the rapid increase of xenobiotic chemicals. These pollutants represent serious threats to both the environment and human health. The need for sustainable alternatives is highlighted by the inefficiency and environmental harm of conventional disposal methods. In this study, we used computational methods to examine the biodegradation potential of dye-decolorizing peroxidase (DyP) from Amycolatopsis japonica. After obtaining the DyP protein sequence from NCBI and modeling it with AlphaFold, PROCHECK and ERRAT were used for structural validation. Complete catabolic modules for the breakdown of aromatic and halogenated chemicals were found by KEGG pathway analysis. Two possible active pockets were found using PrankWeb's binding site prediction; Pocket 1 had the highest confidence score. Strong binding affinities were shown by molecular docking with 28 plasticizers and phenolic-derived xenobiotic compounds; the most promising substrates were naftalofos (-8.8 kcal/mol), benzyl butyl phthalate (-8.4 kcal/mol), and 2,3,7,8-Tetrachlorodibenzo-p-dioxin-P-Dioxin (-8.4 kcal/mol). In the DyP active site, interaction analysis identified hydrophobic interactions and stable hydrogen bonds, especially involving Asp415, His323, and Arg348. These findings identify Amycolatopsis japonica DyP as a promising biocatalyst for xenobiotic degradation, giving structural and mechanistic insights for future enzyme engineering and scalable applications in biotechnology.

The widespread deployment of lithium iron phosphate (LiFePO₄, LFP) batteries has intensified the imperative to address the disposal challenges associated with retired LFP batteries, given their rapidly growing volumes. However, existing regeneration techniques remain constrained by their inherent complexity, high energy demands, and limited scalability, posing significant barriers to achieving efficient and economically viable solutions. Herein, inspired by medical injection therapy, a novel, non-invasive strategy for direct capacity rejuvenation is proposed by injecting recovery reagents into spent LFP batteries, circumventing the need for disassembly. This innovative approach leverages the I₃^-/I^- redox couple to activate residual/dead lithium on the graphite anode and selectively re-engineer the solid electrolyte interphase (SEI), preserving its functional components while optimizing interfacial dynamics. The restored lithium from the anode serves as an intrinsic source to replenish lithium deficits and rectify Li-Fe antisite defects within the degraded LFP cathode. The resulting regenerated pouch cells demonstrate remarkable recovery of electrochemical capacity, accompanied by superior kinetics performance and significantly extended cycle life. This pioneering strategy not only delivers an energy-efficient and cost-effective pathway for LFP battery regeneration but also holds transformative potential to redefine sustainable practices in lithium-ion battery reuse, thereby advancing their practical applications and prolonging their service life.

The rapid advancement of naturally microstructure-bioinspired flexible sensors has sparked interest in creating multifunctional systems for human-computer interaction (HCI). However, most existing biomimetic sensors struggle to integrate multiple sensing modes, limiting their practical applications. Herein, this study proposes a design concept for a fully biomimetic sensor. By employing hybrid manufacturing techniques to achieve layer-by-layer biomimicry of the natural layered structure of eggshells, a flexible sensor with multiple sensing modes is developed. The eggshell-inspired multifunctional hybrid flexible sensor (EMHFS) incorporates four functional layers: a triboelectric layer for noncontact sensing, a piezoresistive layer for pressure sensing, and hydrophilic-hydrophobic layers for directional moisture wicking, breathability, and antibacterial properties. The eggshell-inspired structure enables synergistic functionality, allowing seamless switching between contact and noncontact sensing modes. EMHFS demonstrates exceptional performance in multimodal HCI applications, including gesture-controlled robotic hands, wearable unmanned aerial vehicle control systems, and touchless screen password and gesture unlocking, while also exhibiting remarkable sensitivity to weak physiological signals such as breathing and pulse. This fully biomimetic approach offers a novel solution for advanced, flexible, and multifunctional HCI devices.

HCC predominantly develops in individuals with chronic hepatic conditions and liver cirrhosis, which is marked by high mortality. This study investigates the functional roles and molecular mechanisms by which FOXP2 modulates HCC progression through ferroptosis. After HCC and normal cells were cultured, the expression of FOXP2, RBM15B, and KDM4C was analyzed using western blot or RT-qPCR. After FOXP2 intervention, cellular metabolic activity was assessed via CCK-8 assay, while replicative capacity was quantified through EdU staining and colony formation assays; key regulators of ferroptosis were analyzed by western blot; iron content and oxidative stress levels were measured. The binding between FOXP2 and RBM15B was investigated through ChIP and dual-luciferase assays. Dual-luciferase reporter assay was used to verify the regulation of RBM15B on KDM4C via m6A modification. MeRIP was utilized to examine m6A enrichment on KDM4C mRNA. ChIP was employed to examine the enrichment of KDM4C and H3K9me3 on SLC7A11 promoters. Combined experiments investigated the role of the RBM15B/KDM4C axis in FOXP2-mediated ferroptosis and HCC cell proliferation. Xenograft models were developed in nude mice to validate the mechanism. FOXP2 expression was downregulated in HCC. FOXP2 overexpression significantly inhibited HCC cell proliferation and promoted ferroptosis. FOXP2 repressed RBM15B expression, suppressed the RBM15B-mediated m6A modification, inhibited KDM4C expression, upregulated H3K9me3 levels, and suppressed SLC7A11 expression, ultimately enhancing ferroptosis. Overexpression of RBM15B or KDM4C attenuated ferroptosis and reversed the suppression of HCC cell growth induced by FOXP2 overexpression. In conclusion, FOXP2 may promote ferroptosis and inhibit cell proliferation in HCC by decreasing SLC7A11 expression via the RBM15B/KDM4C axis in an m6A-dependent manner.

Exosomes released by epithelial keratinocytes and dermal fibroblasts significantly accelerate wound healing. Moreover, endogenous electric fields (EFs) were demonstrated to promote wound healing by directing the migration of epidermal cells toward the wound center, it is currently unclear whether EFs may facilitate wound healing by regulating the secretion of exosomes in these cells. In this study, we demonstrated that physiological-intensity EFs significantly enhanced exosome secretion from HaCaT cells, with the total protein content of the exosomes increased by approximately 1.5 times higher than that of the control group. Additionally, the exosomes derived from EF-stimulated HaCaT cells accelerated the wound healing rate of HaCaT and HSF cells, and the wound closure rate increased by approximately 20%. Mechanistically, we identified that EFs regulated exosome secretion by influencing the expression of exosome-related proteins-including ALIX and TSG101. Overall, our research results indicate that the electric field is an effective regulatory factor for enhancing exosome secretion and establish a novel high-exosome-producing strategy based on bioelectrics. This may lay the foundation for the translational application of exosomes in wound healing and other fields.

Recently, self-assembled monolayers (SAMs) have been confirmed as a promising hole-selective contact and interfacial modifier for inverted perovskite solar cells (IPSCs), contributing to an inspiring record power conversion efficiency close to 27%, along with excellent stability. This review demonstrates the critical role of SAMs in enhancing the performance of IPSCs. First, the structure-property and structure-stability relationship of SAMs is systematically expounded by examining their electronic structure, spatial configuration, and the resulting intermolecular forces. Second, it concludes the underlying mechanisms how their unique properties promote the performance of IPSCs, including energy-level alignment, defect passivation, improved interface carrier extraction/transport, and the suppression of ion migration. Third, the applications of SAMs in IPSCs are systematically summarized, covering their roles as hole-selective contacts, interface modifiers, and as components in Co-SAMs strategies. Large-scalable fabrication methods are also summarized to promote industrial processing of IPSCs. Finally, the prevailing challenges and future research directions are outlined, proposing a roadmap for designing SAM-based IPSCs with superior longevity. By critically evaluating the pivotal role of SAMs, this review provides a strategic framework to guide future research and accelerate the development of self-assembled molecules in high-performance and stable photovoltaic devices.

Conductive hydrogels are revolutionizing the fields of wearable sensors, implantable bioelectronics, and soft robotics. However, achieving both mechanical robustness and high conductivity within a single system remains challenging. Here, inspired by the cooperative vascular-neural networks in biological tissues, we develop a nanofiber-reinforced conductive hydrogel composed of poly(vinyl alcohol) (PVA), aramid nanofibers (ANFs), and in situ polymerized PEDOT:PSS. Through solvent- and thermally induced structural reorganization, the hydrogel evolves into a bi-continuous architecture in which the mechanical and conductive networks are intimately coupled. The tough, ANF-reinforced porous PVA mimics the vascular system, providing mechanical support and maintaining toughness, while the poly(3,4-ethylenedioxythiophene) (PEDOT) network resembles neural pathways, enabling efficient electron transport. This structural evolution enables a rare synergy of high tensile strength (10.72 MPa) and ultrahigh conductivity (452.75 S m^-1) with excellent biocompatibility. The hydrogel maintains stable conduction under impact and complex deformation, supporting multimodal sensing from large-amplitude joint motion to low-amplitude electrophysiological signals: electrocardiographic and electromyographic. When integrated with a convolutional neural network, it achieves 99.54% accuracy in recognizing five complex hand gestures. This bioinspired strategy paves the way for developing robust and conductive hydrogels toward next-generation intelligent wearable electronics.

This study probed the mechanism of MARCH6 in endoplasmic reticulum autophagy (ER-phagy) during glioma development by regulating FAM134B stability. MARCH6 and FAM134B expression levels were measured in glioma tissues. A comparative analysis was conducted on the correlation between clinical parameters and FAM134B expression in 46 glioma patients. FAM134B and MARCH6 were knocked down in glioma cells, followed by detection of cell viability and apoptosis, typical ER stress (ERS) markers (PERK, IRE1α, eIF2α, and CHOP), autophagy-related proteins (P62 and LC3B), and autophagosome cytoplasmic accumulation. A mouse glioma model was established for in vivo validation. MARCH6-FAM134B interaction, FAM134B ubiquitination levels, and protein stability were examined. FAM134B expression was high and MARCH6 expression was low in glioma tissues. MARCH6 induced FAM134B protein ubiquitination and degradation, reducing its stability in glioma cells. Knockdown of FAM134B reduced glioma cell survival, inhibited PERK, IRE1α, eIF2α, and CHOP expression, decreased LC3I to LC3II conversion, lowered LC3B fluorescence expression, and reduced the accumulation of autophagosomes with continuous ER structures in the cytoplasm, while enhancing apoptosis and P62 expression. This effect can be reversed by knocking down MARCH6. In vivo, FAM134B knockdown suppressed tumorigenesis in mice. MARCH6 exerts a repressive effect on ERS responses and ER-phagy in glioma cells by destabilizing FAM134B.