Bioplastics derived from renewable food crops or agricultural feedstocks are alternatives to petrochemical materials, but it is challenging to balance their mechanical properties, thermal stability, and shapeability. Here, we report a thermally stimulated supramolecular bioplastic that employs polyethylene glycol to optimize the assembly of cellulose and polyvinyl alcohol molecules. The resulting bioplastic showed a reinforced supramolecular architecture, with a mechanical elastic modulus of 3.23 GPa and an impact resistance higher than 8.15 kJ·m⁻¹. It also showed thermal stability from −40 to 135 °C while maintaining its structural integrity and toughness, giving it potential applications for various shaping processes, including weaving, pouring, and molding. The bioplastic could also undergo natural soil biodegradation within 55 d and exhibited promising recyclability and economic feasibility. This study provides a strategy for configuring supramolecular structures and enhancing the design and manufacture of bioplastics with optimal comprehensive properties.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the leading cause of chronic liver disease globally and constitutes an independent risk factor for cardiovascular disease and mortality. Paeoniflorin (PF), the primary active compound derived from the traditional Chinese herb Paeonia lactiflora Pall., demonstrates multiple pharmacological activities. However, its anti-MASLD mechanisms remain incompletely elucidated. This study revealed that PF markedly ameliorates MASLD pathology by reducing hepatic lipid accumulation, inflammation, and fibrosis; ameliorating insulin resistance and liver function parameters; modulating key lipid metabolism genes (acetyl-coA carboxylase [ACC], sterol regulatory element-binding protein 1 [SREBP1], peroxisome proliferator-activated receptor gamma [PPAR-γ], fatty acid synthase [FASN], carnitine palmitoyltransferase 1 [CPT1], peroxisome proliferator-activated receptor alpha [PPAR-α], adipose triglyceride lipase [ATGL], and cluster of differentiation 36 [CD36]); decreasing pro-inflammatory factors (interleukin-1β [IL-1β], IL-6, tumor growth factor-α [TGF-α], and monocyte chemoattractant protein-1 [MCP-1]); and suppressing hepatic fibrosis markers (alpha-smooth muscle actin [α-SMA], tissue inhibitor of metalloproteinases-1 [TIMP1], collagen type I alpha 1 chain [COL1α1], fibronectin 1 [FN1], platelet-derived growth factor receptor beta [PDGFRβ], and plasminogen activator inhibitor-1 [PAI-1]). Through integrated transcriptomics and pharmacological overexpression approaches, we identified the SYK/SH3BP2 signaling pathway as the crucial mechanism driving MASLD pathogenesis. PF effectively attenuated hepatic metabolic dysregulation, inflammation, and fibrotic activation through inhibition of this pathway. Our work provided the first evidence establishing the SYK/SH3BP2 signaling axis as a pivotal pathway in MASLD progression, unveiling novel therapeutic targets while furnishing a mechanistic foundation for PF’s potential application in MASLD treatment.

Irreversible electroporation (IRE) is a nonthermal ablation modality used clinically for treating unresectable tumors while preserving vital structures through controlled application of pulsed electric fields. Previous data suggest that patient outcomes are enhanced with the induction of an anti-tumor immune response, but current research focuses on using immune checkpoint inhibitors, which function through conventional immune pathways that may be down-regulated by cancer or dysregulated by chemo-induced lymphodepletion. Chimeric antigen receptor (CAR) T cells overcome this limitation, as they are engineered with synthetic receptors that redirect lymphocytes to recognize and target cells expressing tumor-specific structures. CARs are engineered to have an increased binding affinity compared to in situ T-cell binding, amplify internal stimulation cascades, and release pro-inflammatory cytokines that can modulate the endogenous immune system. However, there are still major limitations for adoptive cell therapies in solid tumors, including life-threatening on-target off-tumor cytotoxicity, antigen escape, and failure to infiltrate and persist in solid tumors. Given the substantial evidence that IRE overcomes many of the challenges associated with immune infiltration and persistence in solid tumors, there is a strong premise for using targeted cell therapies following IRE, which would then target residual cancer that could repopulate the lesion. Here, we present the first proof-of-concept combination of IRE with CAR T cells. We validated that the cell membrane CAR target is not affected in electroporated cells that survive IRE, allowing for subsequent binding and elimination of residual tumor. The research demonstrates the feasibility and synergy of a novel combination of 2 clinically used techniques.

Neurodegenerative diseases (NDDs) are characterized by the progressive degeneration of specific neuronal populations, remain incurable, and impose an escalating global health burden due to aging populations. While therapeutic options had expanded in recent years, their overall efficacy remained limited. Neuroinflammation emerged as a central factor in the pathogenesis of NDDs. Hydrogen sulfide (H₂S), an endogenous gasotransmitter known for its potent anti-inflammatory properties, gained attention as a potential therapeutic agent. This review provided a comprehensive overview of the role of neuroinflammation in NDDs, elucidated the molecular mechanisms through which H₂S exerted its anti-inflammatory effects, and discussed recent advancements and potential clinical applications. Special emphasis was placed on the modulation of glial activity, disruption of the blood–brain barrier, regulation of the gut–brain axis, and the interplay between mitochondria and inflammasomes. Furthermore, the review integrated preclinical data on dose–exposure–response relationships to define the therapeutic window of various H₂S donors. It also explored the potential of spatial multiomics and microbiota-targeted approaches to facilitate more precise H₂S-based interventions. These insights provide important scientific merit for elucidating the mechanisms of NDDs and hold urgent practical relevance for developing novel therapeutics to mitigate disease progression.

Gastric cancer (GC) remains a leading cause of global cancer mortality. Analysis of clinical tissues and multiple cohorts (TCGA, ACRG, Singapore, KUGH) associated high RBM15 expression with favorable prognosis. Functional assays in vitro and in vivo demonstrated that RBM15 suppresses GC cell proliferation, migration, and invasion. Integrated RNA-seq and bioinformatics analyses identified the oncogene ECT2 and the epithelial–mesenchymal transition (EMT) pathway as key downstream effectors of RBM15. Mechanistically, RBM15 regulates the m6A methylation of ECT2 mRNA at the 2,909-base pair site, which modulates its binding to the reader protein IGF2BP3, as confirmed by MeRIP, RIP-qPCR, and RNA pull-down assays. A luciferase reporter assay further validated that this m6A modification regulates ECT2 expression. Furthermore, animal and patient-derived organoid models revealed that RBM15 enhances the sensitivity of GC to 5-fluorouracil (5-FU) chemotherapy in an ECT2-dependent manner. In conclusion, this study defines a novel RBM15/IGF2BP3–ECT2 signaling axis that regulates EMT and chemosensitivity in GC via m6A methylation, providing both mechanistic insights and a potential therapeutic strategy.

Achieving both selective pollutant degradation and real-time detection within a single micromotor system remains challenging for environmental monitoring. To address this limitation, we engineered gold-nanostar-decorated, molecularly imprinted BiVO₄ micromotors that combine simultaneous capture, photocatalytic degradation, and in situ detection of pollutants via surface-enhanced Raman spectroscopy (SERS). Plasmonic gold nanostars provide strong SERS enhancement for real-time tracking of pollutant degradation, while micromotors maintain autonomous propulsion under visible light irradiation. Surface molecular imprinting ensures selective recognition of rhodamine 6G and synergistically improves both photocatalytic and sensing performance. This multifunctional design establishes an all-in-one micromotor platform that bridges environmental remediation and on-board monitoring, opening opportunities for advanced water treatment technologies.

Lightweight multifunctional aerogels hold great promise in applications, e.g., electromagnetic microwave absorption, thermal insulation, and acoustic damping. However, conventional aerogels often suffer from limited functionalities, complicated manufacturing, and poor sustainability. Metal-organic frameworks (MOFs), with tunable porosity and abundant active sites, offer a compelling route to high-performance multifunctional aerogels, but it has remained a grand challenge to develop sustainable multifunctional MOF-based aerogels. Here, we report a sustainable multifunctional bio-aerogel (Ni-CCA) by integrating hierarchical scale-like topological Ni-MOF-NH₂ with cellulose through simple pretreatment using deep eutectic solvent followed by stepwise assembly–carbonization. The resulting aerogel features an ultralow density and a 3-dimensional layered porous structure. With 5 wt.% filler loading, Ni-CCA achieves a minimum reflection loss (RL_min) of −53.47 dB and an effective absorption bandwidth of 4.42 GHz, along with a radar cross-section suppression of 27.90 dB·m². Additionally, Ni-CCA shows enhanced flame retardancy (64.3% reduction in peak heat release), low thermal conductivity [33.3 mW/(m·K)] and improved acoustic damping (NRC of 0.31, 15 to 23 dB attenuation). The multifunctionalities of this bio-aerogel stem from its hierarchical architecture and synergistic loss mechanisms, offering a promising strategy for creating the next generation of lightweight multifunctional protective materials.

The development of efficacious pain management strategies remains a pivotal challenge, requiring the creation of sustainable, biomass-derived interfaces for real-time techniques. Existing assessment approaches are either invasive, rendering them inappropriate for extended home-based monitoring, or dependent on patient-reported subjective evaluations. In this study, we fabricated a multifunctional biomass-inspired polydopamine-based hydrogel (polyvinyl alcohol [PVA]/polyacrylamide [PAM]/lithium chloride [LiCl]/polydopamine [PDA]/lidocaine hydrochloride [LiH]) wearable patch. Encapsulating lidocaine, a local anesthetic, this biomass-composite patch integrated pain-sensing-assisted assessment and treatment functionalities. It exhibited remarkable properties, including good stretchability (534.22%), low modulus (0.044 kPa), fine tissue adhesion (1.82 kPa), high conductivity (3.90 S m⁻¹), rapid self-healing ability, and antibacterial properties. The patch enabled accurate sensing of diverse motion-related signals. Combined with deep learning algorithms, patients diagnosed with scapulohumeral periarthritis and lumbar diseases were recruited as volunteers for pain signal monitoring and evaluation (accuracy rate ~100%). Moreover, the hydrogel patch prolonged local photothermal analgesia in paw withdrawal threshold (>31% vs. Ctrl) and cumulative pain score (<10) by using a mouse plantar incision pain model. PVA/PAM/LiCl/PDA-based hydrogels elicited no detectable skin irritation or sensitization under the tested conditions. Therefore, this work not only pioneers the construction of a wearable integrated patch for pain management featuring “AI-assisted sensing evaluation” and “on-demand therapy”, but also provides a highly promising intelligent solution based on biomass-derived patches for the objective and prospective assessment and treatment of various types of pain.

The worldwide decline in male fertility represents a growing public health challenge, with fluoride exposure recognized as a key environmental factor exacerbating this decline. Fluoride hurts male reproduction, yet the specific mechanism remains unclear. Here, we demonstrate that fluoride reduced mouse sperm quality, destroyed the structure of testicular tissue, and caused severe damage to testicular somatic cells (Leydig and Sertoli cells). Meanwhile, the number of autophagosomes increased in Leydig cells and decreased in Sertoli cells. Network toxicology and functional analysis identified miR-34a-5p as the pivotal miRNA orchestrating fluoride-induced autophagic imbalance in testicular somatic cells. REST was identified as a novel miR-34a-5p target gene exhibiting pro-autophagic activity. Fluoride down-regulates miR-34a-5p and up-regulates REST in Leydig cells, whereas it exerts the opposite effects in Sertoli cells. The rescue experiment elucidated specific mechanisms: Fluoride down-regulates miR-34a-5p in Leydig cells, thereby derepressing REST to activate autophagy. Conversely, in Sertoli cells, fluoride up-regulates miR-34a-5p to suppress REST expression and inhibit autophagy. Collectively, the present study reveals an important mechanism underlying fluoride-induced male reproductive toxicity and provides a potential therapeutic target.

Radiotherapy (RT) and photodynamic therapy (PDT) for breast cancer are limited by tumor hypoxia and suboptimal photosensitizer performance. We developed folate-modified copper-doped carbon dots and loaded them with 5-aminolevulinic acid (ALA) to yield FCA, a nanoplatform that executes cascade nanozyme activities to remodel the tumor microenvironment: decomposing H₂O₂ to relieve hypoxia, generating hydroxyl radicals and singlet oxygen (¹O₂), and depleting glutathione (GSH). This priming enabled efficient ALA-to-protoporphyrin IX conversion, which subsequently amplified reactive oxygen species generation. The elevated oxidative stress then synergized with RT to accumulate DNA double-strand breaks and trigger cell cycle arrest. Consequently, FCA-PDT-RT reduced 4T1 cell viability to 20.09% and induced 83.82% apoptosis outcomes mechanistically linked to nuclear factor erythroid 2-related factor 2 (NRF2)–Kelch-like ECH-associated protein 1 (KEAP1)–heme oxygenase 1 (HMOX1) pathway activation. Despite compensatory upregulation of antioxidant genes (HMOX1 and glutamate–cysteine ligase modifier subunit [GCLM]), intracellular GSH and adenosine triphosphate were severely depleted, establishing a metabolic crisis wherein synthesis could not match consumption. This redox/energy collapse drove the pronounced cytotoxicity observed. In an orthotopic 4T1 model, FCA-PDT-RT achieved superior tumor control at only 12 Gy, which correlated with increased CD3⁺/CD8⁺ T cell infiltration and suppressed angiogenesis, while maintaining favorable safety. FCA thus enables synergistic PDT-RT through sequential microenvironment remodeling, oxidative amplification, and metabolic exhaustion, offering a dose-sparing strategy with translational promise for breast cancer therapy.