The poultry industry faces major challenges in preserving meat freshness and safety due to high water activity, rapid microbial growth, and oxidative spoilage. Traditional methods such as vacuum sealing and antioxidants are insufficient, as they cannot effectively suppress anaerobic pathogens and lack real-time freshness assessment. This review introduces a transformative strategy that applies coordination chemistry to design multifunctional nanomaterials for poultry preservation. Dynamic metal–ligand interactions—including redox-active centers, stimuli-responsive bonds, and host–guest adsorption—allow precise antibacterial control through 4 mechanisms: ligand-regulated ion release, reactive oxygen species (ROS) generation, coordination-triggered antimicrobial delivery, and electrostatic membrane disruption. In addition, freshness can be monitored by biomarker-specific coordination responses, such as nanoparticle aggregation for optical signals or MOF (metal–organic framework)-based volatile amine capture for colorimetric and electrochemical detection. Integration with oxygen scavengers, humidity regulators, and pH-responsive systems optimizes the packaging environment. Coupling with digital technologies further enables intelligent platforms for autonomous quality validation and supply chain transparency. This approach connects molecular-scale coordination principles with engineering practice while addressing biodegradability, environmental resilience, and scalability to reduce waste and achieve sustainable poultry preservation.

Boron neutron capture therapy (BNCT) is a targeted radiotherapy technique that enables dual targeting at the physico-biological level. Efficient neutron sources and specific boron carriers are essential for successful treatment. By exploiting the ¹⁰B(n,α)⁷Li nuclear reaction, the BNCT enables precise eradication of ¹⁰B-loaded tumor malignant cells while sparing adjacent healthy tissues, rendering it particularly advantageous for treating invasive or radioresistant recurrent tumors. Numerous clinical trials related to BNCT have focus on evaluating the safety and efficacy of treating glioblastoma, head and neck carcinoma, meningioma, malignant melanoma, and liver cancer. Preliminary studies have shown that BNCT treatment may extend the overall survival (OS) and improve the quality of life for patients with these cancers. Additionally, the scope of BNCT clinical trials has expanded to other tumor types, such as lung cancer, breast cancer, extramammary Paget’s disease, osteosarcoma, clear cell sarcoma, malignant peripheral nerve sheath tumor, angiosarcoma, thyroid cancer, recurrent chordoma, and gastrointestinal malignancies. This review provides a comprehensive overview of BNCT clinical trials, covering the therapeutic principles of BNCT and the current status and outcomes of clinical trials for various types of tumors. With advancements in neutron beam quality and the development of efficient, specific boron carriers, the therapeutic efficacy of BNCT is expected to be further enhanced, and its scope of application is anticipated to expand. Looking ahead, the BNCT is expected to be integrated with other tumor treatment modalities to augment local tumor control, thereby improving patients’ OS and quality of life.

Calculations of collisions involving excited electronic states play an important role in many high-energy environments, for example, in simulating thermal energy content and heat flux in flows around hypersonic reentry vehicles, and useful data are usually not available from either experiment or theory. We apply a deep learning framework—compatibilization by deep neural network—to automatically discover and fit a compatible potential energy matrix (CPEM) for singlet oxygen atom collisions with N₂ in the ¹A′ manifold of N₂O. The procedure yields not only a fit to the CPEM and its gradient but also analytic representations of the adiabatic potential energy surfaces and their gradients across a dense 13-state manifold; these potential energy surfaces are suitable for dynamics calculations of inelastic and reactive collisions across a broad range of collision energies extending above the dissociation threshold of N₂. We propose a new asymptotically extended formulation of the curvature-driven coherent switches with decay of mixing (κCSDM) semiclassical dynamics method that resolves the conflict between differing symmetries of the interacting atom–diatom system and the completely separated final states. We use the new dynamics method with the analytic representation of potential surface gradients to compute electronically nonadiabatic cross-sections for N₂(X ) + O(¹S) collisions, primarily producing N₂(X) + O(¹D), N₂(A) + O(³P), and NO(X) + N(²D). Our methods provide new capabilities for modeling electronic energy transfer under extreme conditions, with implications across chemistry, physics, and aerospace engineering.

Primary breast cancer (PBC) with axillary lymph node metastasis (ALNM+) is associated with distinct clinical outcomes, including reduced survival (The Cancer Genome Atlas/Foshan cohorts, P < 0.05) and an attenuated response to anti-programmed cell death protein 1 antibody/anti-programmed death-ligand 1 antibody (anti-PD-1/anti-PD-L1) therapy. Through ALNM-stratified single-cell RNA sequencing profiling, we identified 3 hallmark immune subsets in ALNM+ PBC: (a) proliferative MKI67+ T cells, (b) exhausted GZMA+ CD8+ T cells, and (c) CCL13/CXCL10/TOP2A+ macrophages. Cross-modal integration of metastasis–epithelial–mesenchymal transition (EMT) signatures with Mendelian colocalization analysis prioritized TFF3 as a central mechanistic regulator. We validated malignant-cell-specific TFF3 expression across pan-cancer single-cell profiles and in PBC lineages. Integration of Mendelian colocalization signatures with pan-cancer spatial atlases established the TFF3 oncogene as a regulator of spatial EMT programs. Radiogenomic modeling that incorporated machine-learning-derived computed tomography features identified a TFF3-based radiomics risk score. Spatial multi-omics analyses—including bulk RNA sequencing, proteomics, and spatial transcriptomics—established a correlation between TFF3 expression and both MAPK signaling activation and EMT markers. Functional validation demonstrated that TFF3 plays a dual role as an amplifier of the MAPK–EMT axis and a modulator of immune checkpoints. Critically, the prometastatic phenotype driven by TFF3 was rescued upon pharmacological inhibition of MAPK signaling, providing direct evidence of this mechanistic link. In vivo xenograft models confirmed that TFF3 knockdown suppressed metastasis. Pharmacogenomic screening identified 6-mercaptopurine as a novel TFF3 antagonist, which exhibited dose-dependent inhibition of the MAPK–EMT axis. Furthermore, the antimigratory effect of 6-mercaptopurine was reversed by TFF3 overexpression, confirming the functional specificity of this drug–target interaction. Notably, tumors with high TFF3 expression (TFF3hi) exhibited elevated resistance to PD-1 inhibitors but heightened sensitivity to MAPK inhibitors, suggesting a potential theranostic framework for ALNM stratification.

Drug-associated reward memory underlies both the development and relapse of addiction, yet its molecular basis remains poorly understood. Here, transcriptomic profiling and functional validation identified a novel long non-coding RNA (lncRNA), Gm44763, as a critical regulator of morphine-induced reward memory specifically in neurons of the medial prefrontal cortex (mPFC). Behavioral and molecular analyses demonstrated that Gm44763 functions as a sponge for miR-298-5p, thereby relieving the repression of the downstream target gene, eukaryotic translation initiation factor 4E (eIF4E), and modulating both the acquisition and retrieval of reward memory. Golgi staining and fiber photometry further revealed that Gm44763 normalized morphine-induced alterations in synaptic structure and neuronal excitability. miR-298-5p bidirectionally regulated morphine-induced reward memory and reversed both behavioral and neuronal effects mediated by Gm44763. Mechanistically, the downstream effector eIF4E modulates translation via its interaction with eIF4G, thereby contributing to morphine-induced memory regulation. This process can be effectively modulated by 4EGI-1, a selective inhibitor of the eIF4E/eIF4G interaction. In summary, this study characterized lncRNA expression profiles in the mPFC of mice with morphine-induced conditioned place preference. We identified and validated Gm44763 as a novel lncRNA regulator of morphine-induced reward memory and synaptic plasticity. We further delineate a previously uncharacterized Gm44763/miR-298-5p/eIF4E axis that may represent a novel regulatory pathway linking transcriptional and translational control to drug-associated memory formation.

Sepsis-induced cardiac dysfunction (SICD) is a major contributor to mortality in sepsis. Kinesin family member 13B (KIF13B) has been identified as a critical protective factor for metabolic disorder and cardiovascular disease; however, the role of KIF13B in SICD remains unknown. After introducing lipopolysaccharide or cecal ligation and puncture surgery to wild-type (WT) and global Kif13b knockout (Kif13b^−/−) mice combined with lipopolysaccharide-treated neonatal rat cardiomyocytes, we found that KIF13B expression levels were markedly down-regulated in septic hearts and cardiomyocytes. Kif13b deletion exacerbated SICD progress with reduced cardiac contractile function and resulted in increased mortality, accompanied by promoted lipid accumulation, fibrosis, and mitochondrial impairment. Mechanistically, the loss of KIF13B enhanced the lysosomal degradation of the lipid-droplet-associated protein perilipin 5 (PLIN5), thus disrupting the mitochondrial localization of PLIN5 and then impairing cardiac lipid homeostasis and proper mitochondrial function. Nevertheless, cardiac-directed AAV9-PLIN5 gene therapy sufficiently corrected cardiac dysfunction, inhibited lipid accumulation, and reduced oxidative stress in Kif13b^−/− mice with SICD. In summary, these findings provide a new insight into the molecular mechanism underlying the pathogenesis of SICD, highlighting the KIF13B/PLIN5 axis as a potential therapeutic target for the treatment of SICD.

Small inspection robots are highly desirable for inspecting complex machinery and detecting damage in confined spaces. However, common climbing robots that rely on vacuum suction or bioinspired dry adhesion often suffer from bulky sizes or slow locomotion speeds. Developing compact yet intelligent wall-climbing robots that mimic the agility and payload capacity of geckos remains an important challenge. In this work, we design a 20-g, 10-cm artificial intelligence (AI)-integrated robot capable of carrying a 70-g payload while climbing on vertical and inverted surfaces at a speed of 70 mm/s. Acoustic adhesion is generated by vibrating a flexible annular disk on smooth surfaces, where air is periodically absorbed and expelled, resulting in negative pressure. The thin air layer with negative pressure indicates anisotropic performance, characterized by strong normal adhesion and negligible tangential resistance, making it highly suitable for designing small, yet strong, climbing robots. The theoretical model and laser surface morphology measurements reveal the thickness-dependent adhesion of a thin air layer beneath the disk. A servo-spring system is designed to meet the stringent requirements of a thin air layer thickness, yielding robust normal adhesion. Resonance analysis and the use of proper spring material stiffness further enhance adhesion performance. Therefore, combining this innovative acoustic adhesion with optimized structural design, our robot achieves gecko-like mobility and payload capacity. Additionally, integrated AI techniques simplify robot control, allowing voice-commanded operation and autonomous task execution. We demonstrate the functions of these climbing robots through agile inspections in a 3-dimensional maze and retired aircraft engines. This work presents the design of small, strong, and agile climbing robots that utilize anisotropic acoustic adhesions, demonstrating agile mobility across gaps, right corners, and discontinuous curved surfaces. It offers potential solutions for in situ damage detection in aero-engines and other complex equipment cavities.

The performance of hard carbon anodes in sodium-ion batteries is restricted by competing mechanisms: excessive surfaces cause irreversible reactions lowering the initial coulombic efficiency, while insufficient active sites limit capacity. To mitigate this trade-off effect, a synergistic strategy of ultramicropore confinement and electronic-state modulation in lignin-derived hard carbon was created. Using sodium lignosulfonate, a common sulfonated polymer in paper-making waste, we developed N/S-codoped hard carbon microspheres (N-S@HDM) via preoxidation-induced cross-linking and optimized pyrolysis. Preoxidation inhibits graphitic alignment, creating an expanded interlayer spacing and a closed-pore-dominated structure (94.27% at 1,300 °C). This interconnected network (f_a = 0.85) enables ultramicropore confinement, thus shortening diffusion paths, boosting kinetics, and providing ample Na⁺ storage sites to reduce interfacial decomposition. Concurrent N/S doping optimizes electronic states by enhancing electron delocalization, lowers charge-transfer resistance, and generates high-density adsorption sites. The optimized N-S@HDM-1300 achieves an ultrahigh initial coulombic efficiency of 90.6% and a reversible capacity of 401.5 mAh g⁻¹ (0.03 A g⁻¹), with exceptional cyclability (95.0% retention after 500 cycles). This study pioneers a dual-regulation paradigm for biomass-derived carbon materials, coupling pore engineering and electronic optimization to advance sodium-ion battery anode design.

Impaired mitophagy and the accumulation of damaged mitochondria are key drivers of endothelial cell (EC) dysfunction in diabetic wounds. While mitochondrial transplantation (MT) has demonstrated therapeutic potential in such mitochondrial damage-related diseases, its application is still thwarted by elusive mechanisms and practical hurdles such as poor targeting specificity and low delivery efficiency. Here, we reveal that MT acts by reactivating mitophagy to selectively eliminate dysfunctional mitochondria, thereby restoring mitochondrial homeostasis and rescuing EC functionality. To exploit this discovery, we engineer a biomimetic MT strategy through coating EC-derived apoptotic vesicle membrane (AVM) onto the surface of isolated mitochondria. The resulting mitochondria–AVM complex (Mito-AVM) leverages homologous targeting and phosphatidylserine-mediated “eat-me” signaling, achieving a remarkable 150% increase in delivery efficiency to ECs in diabetic wounds. Furthermore, we construct a 3-aminophenylboric acid-modified hyaluronic acid/polyvinyl alcohol hydrogel for the diabetic wound microenvironment, enabling reactive oxygen species/glucose-triggered sustained release of encapsulated Mito-AVM at the wound site. In summary, our work elucidates a fundamental mechanism of MT and provides an efficient and targeted strategy for MT therapy, offering fresh perspectives for diabetic wound treatment.

Follicle-stimulating hormone (FSH) coordinates ovarian follicle development by aligning mitochondrial biogenesis with increased metabolic demand. Although FSH is known to stimulate glycolysis in granulosa cells (GCs), the mechanism by which glycolytic flux coupled to mitochondrial biogenesis remains unclear. Here, we demonstrate that histone lactylation functions as a lactate-sensitive epigenetic mediator linking FSH-driven metabolic alterations to mitochondrial biogenesis in GCs. Mechanistically, FSH increases intracellular lactate levels through glycolytic activation, thereby promoting P300/CBP-dependent lactylation of histone H4 at lysine 5 (H4K5la). H4K5la directly enhances HDAC4 expression, and HDAC4 subsequently deacetylates PGC-1α at lysine residues 329/330. Deacetylated PGC-1α cooperates with nuclear respiratory factors NRF1/2 to drive transcription of key mitochondrial regulators (TFAM, TFB1M, TFB2M), ultimately promoting mitochondrial biogenesis. Disruption of the H4K5la/HDAC4/PGC-1α axis markedly impaired mitochondrial biogenesis and follicular development, evidenced by reduced ovarian weight, smaller follicle size, decreased antral follicle number, and impaired GC proliferation and estradiol (E2) production in FSH-treated mice. These findings identify a metabolic–epigenetic regulatory pathway in which histone lactylation links glycolysis to mitochondrial adaptation, providing mechanistic insight into FSH-dependent reproductive physiology.

Evaluating chemical toxicity and its potential hazards to human health and the environment is essential in diverse fields, including medicine, industry, and agriculture. Multi-species acute toxicity prediction (MSATP) is critical in toxicity assessment. Traditional methods rely on exposing animals to a single high dose of a compound and observing its toxicity. However, with growing ethical concerns regarding animal testing, advancements in computational technology have positioned the artificial intelligence-based MSATP as an efficient alternative. Current research on MSATP commonly employs multi-task deep neural networks for modeling. However, the small size, high dimensionality, and sparsity of MSATP tabular data render them unsuitable for neural network approaches. To address this, we proposed a multi-task cascade forest framework for MSATP. This framework integrated feature enhancement through knowledge transfer, sample enhancement using a greedy search strategy with the covariance distance measure. The framework accommodated tasks of varying sizes in multi-task learning and was specifically designed for tabular data, achieving a 12% improvement in performance compared to current state-of-the-art methods (R² equals to 0.64, root mean square error equals to 0.57). In a single-view context, we conducted ablation experiments to validate the effectiveness of the data enhancement strategy and introduced external dataset experiments to assess the generalization capability of the proposed method for cross-species prediction. In a multi-view context, the feature fusion method and consensus ensemble were demonstrated to further enhance the model performance. Additionally, we analyzed feature importance vectors to provide interpretable insights into species toxicity correlations. Overall, this framework effectively addressed MSATP tasks and exhibited substantial potential for application in various toxicity prediction domains.

Developing sustainable energy technologies is among the foremost challenges of this century and spawns the emergence of materials for ambient energy harvesting, such as photovoltaics, triboelectrics, and pyroelectrics. The conversion of ambient thermal energy (temperature fluctuations) into electricity through pyroelectric materials offers a promising route toward sustainable energy technologies. However, there is a critical limitation: The conventional pyroelectric effect is inherently restricted to noncentrosymmetric crystals, but excludes the centrosymmetric materials, even though they exhibit otherwise favorable properties. This symmetry dependence severely constrains the development of pyroelectric energy technology. Here, we demonstrate that the pyroelectric effect, typically observed only in noncentrosymmetric materials, can be induced in centrosymmetric materials via the flexoelectric effect. By introducing strain gradients using an atomic force microscope, we generated a giant pyroelectric coefficient of up to 1.25 × 10⁶ μC·m⁻²·K⁻¹ in SrTiO₃. This strain gradient-induced pyroelectric effect, termed as the flexo-pyroelectric effect, decouples pyroelectric functionality from intrinsic material polarity. Our findings exceed the long-standing symmetry limitation in pyroelectric energy technology by proving that centrosymmetric materials can also exhibit robust pyroelectricity through strain engineering. The flexo-pyroelectric effect redefines the understanding of pyroelectricity and unlocks the vast library of centrosymmetric materials for designing next-generation energy harvesters, advancing sustainable technology development.

Addressing the critical demand for next-generation lightweight, high-efficiency microwave absorbers, this paper proposes a “micro-meso-macro” multi-scale synergistic regulation strategy. Specifically, core@shell mesoporous carbon hollow nanospheres (HNSs)@carbon bean-shaped nanofibers (BNFs) are designed and fabricated efficiently using SiO₂/carbon solid nanospheres as precursor through a continuous electrostatic spinning, heat treatment, carbonization, and hydrofluoric (HF) etching. The acquired results suggest that the regulation of carbonization temperature greatly improves the graphitized degree of mesoporous carbon HNSs@carbon BNFs, which significantly enhances the values of complex permittivity. Furthermore, the introduction of a controllable number of mesoporous carbon HNSs at the mesoscale significantly increases the specific surface area and promotes the interfacial polarization effects. The macroscopic 3-dimensional continuous conductive network constructed via electrospinning further enhances electron transport capability and conductive loss efficiency. Benefiting from the excellent collaborative design between multi-scale structure and composition, the optimized mesoporous carbon HNSs@carbon BNFs display excellent microwave absorption properties with a minimum reflection loss (RL_min) of −61.03 dB at 2.42 mm and an effective absorption bandwidth (EAB) of 6.2 GHz at 2.18 mm. Meanwhile, the acquired mesoporous carbon HNSs@carbon BNFs also present excellent corrosion resistance, hydrophobicity, flexibility, and lightweightness. Generally, the finding proposes a simple route for the production of novel core@shell C@C nanocomposites, which makes the best of multi-scale construction strategy to develop lightweight multifunctional microwave absorbers.

Engineering protein thermostability is a key aspect of rational protein design, aiming to broaden the applicability of enzymes and enhance their industrial utility. In this study, we introduce a strategy for identifying and reinforcing dynamic stability centers of local structure (DSCLSs) to improve protein thermostability. A DSCLS comprises key structural residues and their interactions, representing the structural basis of protein stability. Molecular dynamics, cross-correlation amino acid networks, and other analytical techniques were integrated into the method. This approach was initially inspired by thermostability engineering of exodiol dioxygenases (EDOs). The method was validated through mutational analyses of mesophilic EDO MT-2, CpKR (ketoreductase from Candida parapsilosis), and CaPETase (polyethylene terephthalate hydrolase from Cryptosporangium aurantiacum). Subsequently, we applied the approach to engineer thermostability in xp-EctC (ectoine synthase) from Rhodococcus and mesophilic EDO L1 from Bacillus, with the best-performing mutants showing T_m increases of ~15 °C. Notably, the catalytic efficiency of the optimal mesophilic EDO L1 mutant (T70Y) was 1.6-fold higher than that of the wild type at 60 °C, while the xp-EctC mutant (I2R) exhibited a 2.1-fold increase over the wild type. By characterizing and enhancing DSCLSs, this work presents a practical and generalizable strategy for thermostability engineering that also reduces mutational screening efforts, offering important potential for industrial applications.

The detection of gravitational waves from extreme-mass-ratio inspirals (EMRIs) in space-based antennas like Taiji and Laser Interferometer Space Antenna promises deep insights into strong-field gravity and black hole physics. However, the complex, highly degenerate, and nonconvex likelihood landscapes characteristic of EMRI parameter spaces pose severe challenges for conventional Markov chain Monte Carlo (MCMC) methods. Under realistic instrumental noise and broad priors, these methods demand impractical computational costs but are prone to becoming trapped in local maxima, leading to biased and unreliable parameter estimates. To address these challenges, we introduce flow-matching MCMC (FM-MCMC), a novel Bayesian framework that integrates continuous normalizing flows (CNFs) with parallel tempering MCMC (PTMCMC). By generating high-likelihood regions via CNFs and refining them through PTMCMC, FM-MCMC enables robust exploration of the nontrivial parameter spaces, achieves orders-of-magnitude improvement in computational efficiency, and, more importantly, ensures statistically unbiased inference. By enabling real-time, unbiased parameter inference, FM-MCMC could unlock the full scientific potential of EMRI observations, and would serve as a scalable pipeline for precision gravitational-wave astronomy.

Meniscal injuries are common in the knee joint. Minor meniscal injuries usually respond well to conservative treatment, while severe cases often require complete meniscal replacement. Meniscal injuries cause inflammatory responses that importantly hinder meniscal tissue regeneration. Despite ongoing advances in research, considerable breakthroughs in meniscal regeneration remain out of reach. This study introduces programmable macrophage mimics (PMMs), which enable sequential regulation from anti-inflammatory responses to meniscal fibrocartilage regeneration. PMMs were prepared by encapsulating the transforming growth factor-β3 and insulin-like growth factor-1 growth factors within mesoporous silica nanoparticles modified with branched polyethyleneimine via disulfide bonding. This design allows the initial adsorption of proinflammatory cytokines followed by the controlled release of growth factors that promote adipose-derived stem cell (ADSC) differentiation into fibrochondrocytes. The PMMs were integrated into meniscus-specific acellular matrix hydrogels (mGC), which provided suitable mechanical properties critical for effective regeneration. In rabbit osteoarthritis models, ADSC-loaded PMMs@mGC hydrogels showed marked fibrocartilage regeneration. Additionally, the team developed an advanced biofabrication approach that combines a 3-dimensionally printed polycaprolactone framework designed for total meniscus replacement. This research suggests that PMMs act as a bifunctional “core–shell” nano-delivery system, offering a promising therapeutic strategy for managing inflammatory meniscal conditions.

Aerosol viral transmission monitoring enables early, noninvasive detection of infectious disease spread by identifying airborne viral particles in shared environments. Integrating sampling, sensing, and data analysis, this perspective outlines an integrated framework for transforming epidemic responses from reactive testing to proactive surveillance. It synthesizes current technological advances and deployment experiences to identify key challenges in detection efficiency, data management, and societal trust. This marks a shift from clinical diagnosis to environmental surveillance, transforming epidemic responses from testing individuals to monitoring shared air. By enabling earlier interventions, these systems help reduce transmission, protect vulnerable groups, and limit disruptions to daily life and the economy.

The growing imperative to ensure food safety, preserve ecological integrity, and mitigate public health risks associated with pesticide residues has driven a critical demand for highly sensitive optical sensors. In this regard, optical biosensors, including fluorescence (FL), colorimetry (CL), surface-enhanced Raman scattering (SERS), surface plasmon resonance (SPR), and chemiluminescence strategies, have been developed for pesticide detection. This review aims to provide a comprehensive summary of both fundamental knowledge and advancements in the field of optical biosensors for pesticide detection. The advantages of these biosensors are highlighted, such as excellent sensitivity, high specificity, and on-site application. Subsequently, a detailed overview of the sensing mechanism of optical biosensors based on different molecular recognition elements [e.g., enzymes, antibodies, aptamers, molecularly imprinted polymers (MIPs), and supramolecular host–guest complexes] is provided. Finally, perspectives are offered on the current challenges and future directions of pesticide biosensors. This review is expected to serve as a fundamental guide for researchers in the field of optical biosensors for pesticide detection and to provide insights and avenues to enhance the performance of existing sensing mechanisms in applications across diverse fields.

Precise diagnosis and management of lower extremity dysfunction disorders hinge on continuous gait monitoring. Nevertheless, the existing wearable devices fall short as they grapple with insufficient sensing precision, inadequate energy endurance, and ineffective intelligent data analysis. Here, we report a fully integrated, biomimetic smart insole that incorporates 3 synergistic innovations to overcome these challenges. First, inspired by the hierarchical mechanosensory apparatus of mantis legs, we design dual-microstructure capacitive sensors with a detection limit of 0.10 Pa and a maximum detection range of 1.4 MPa. This sensor can distinguish pressures across a wide range from subtle to substantial and exhibits robust mechanical stability over 12,000 cycles, making it highly suitable for insole applications and outperforming current flexible pressure sensors. Second, we realize energy-autonomous operation by integrating nano-perovskite solar cells with high-capacity lithium–sulfur nanobatteries, achieving an average photocharging efficiency of 11.21% and energy storage efficiency of 72.15%. Third, embedded artificial intelligence algorithms interpret the spatiotemporal pressure data transmitted via a 16-channel wireless module. These models achieve 96.0% accuracy in detecting foot arch abnormalities and 97.6% accuracy in classifying 12 pathological gait patterns. Collectively, these 3 advances, including bioinspired high-resolution sensing, sustainable energy interfacing, and intelligent mechanodiagnosis, establish a closed-loop wearable platform validated in clinical studies. This system offers promising applications in early disease screening, personalized rehabilitation, and remote healthcare.

Lunar far-side samples returned by the Chang’e-6 mission offer unprecedented insights into regolith properties within the South Pole–Aitken basin, essential for advancing lunar exploration and in situ resource utilization. This paper presents an integrated characterization framework combining high-resolution x-ray micro-computed tomography with semisupervised machine learning to reconstruct and analyze 349,740 individual particles at high throughput. Morphological analysis demonstrates that far-side regolith exhibits greater irregularity than previously characterized near-side samples, with a median particle diameter of 60.51 μm and a mean 3-dimensional sphericity of 0.74—values distinct from those reported for Apollo and Chang’e-5 materials. Discrete element method simulations incorporating these high-fidelity morphologies under representative lunar surface confining pressures (5 to 15 kPa) reveal a high internal friction angle of 47.96° and a cohesion of 1.08 kPa. These parameters exceed Surveyor mission estimates and align with the upper range of Apollo program values, indicating enhanced mechanical strength and cohesion in far-side regolith. The superior mechanical properties arise primarily from pronounced particle irregularity promoting strong mechanical interlocking, potentially augmented by cementation from abundant glassy agglutinate phases. These findings establish critical geotechnical benchmarks for lunar far-side materials, providing essential design parameters for future robotic and crewed missions, landing site selection, and infrastructure development.

Triple-negative breast cancer (TNBC) represents a notably aggressive form of breast cancer, distinguished by heightened invasiveness and an important propensity for metastasis. The expression of ubiquitin D (UBD) is significantly increased in lung metastases associated with TNBC, correlating with unfavorable patient outcomes. Functional assays indicate that UBD promotes invasion, migration, and pulmonary colonization of TNBC cells in vivo. At the mechanistic level, UBD preserves matrix metalloproteinase 3 (MMP3) levels by inhibiting proteasomal degradation. A proteomic analysis has identified MMP3 as a crucial downstream mediator of UBD. Concurrently, chromatin immunoprecipitation and luciferase reporter assays demonstrate that the Spi-B transcription factor (SPIB) directly interacts with the UBD promoter, leading to the activation of its transcription. Collectively, these findings identify the SPIB/UBD/MMP3 axis as a pivotal regulator of TNBC metastasis, indicating its value for prognostic evaluation and targeted therapy.

Plasmacytoid dendritic cells (pDCs) are innate immune cells that produce type I interferons (IFNs) upon sensing nucleic acids via Toll-like receptor 9 (TLR9). Synthetic oligodeoxynucleotides CpGA and CpGB are widely used TLR9 agonists, yet only CpGA robustly induces IFN-α in pDCs. In contrast, CpGB drives much less IFN production. The mechanism underlying this ligand-specific response is not known. Here, we identify PIEZO1, a mechanosensory ion channel, as a regulator for this ligand-specific response. We show that CpGA, unlike CpGB, self-associates into large aggregates that generate membrane tension during cellular uptake, activating PIEZO1. This triggers calcium influx and localized F-actin assembly, retaining CpGA in early endosomes to sustain IRF7 activation and IFN production. PIEZO1 deficiency or inhibition abolishes CpGA-induced IFN responses, while PIEZO1 activation enhances IFN production by CpGB. Our findings reveal a hitherto unknown biophysical checkpoint in TLR9 signaling, where PIEZO1 translates membrane tension into spatially controlled TLR9 signaling. This study uncovers a novel role for mechanosensing in nucleic acid immunity, with implications for modulating IFN responses in infections and autoimmunity.

As pioneering immunotherapy approaches, chimeric antigen receptor T cell (CAR-T) and natural killer cell (CAR-NK) therapies have shown notable clinical effectiveness when addressing different kinds of hematologic malignancies. For example, the application and efficacy of CAR-T cell therapy in acute lymphocytic leukemia, large B cell lymphoma, mantle cell lymphoma, and multiple myeloma have been widely recognized. In addition, the safety and feasibility of CAR-NK therapy when used to treat refractory/recurrent large B cell lymphoma have been verified. In particular, CD19-targeted CAR-T cell therapy has achieved marked efficacy and breakthrough progress in treating relapsed and refractory B cell leukemia and lymphoma. Although CAR-T cell therapy has achieved significant effectiveness in treating these diseases, patients still face challenges, including primary resistance and secondary recurrence after treatment. The complex mechanisms of resistance and recurrence involve multiple factors, such as target cells, CAR cell characteristics, and immune suppression conditions. This review examines resistance and recurrence mechanisms in CAR-T and CAR-NK therapies while exploring current therapeutic strategies and future research directions.

The NLRP3 inflammasome is a pivotal component of the innate immune system, responding to infections and cellular damage. Its dysregulation has been implicated in numerous inflammatory diseases, although the mechanisms controlling its activation remain incompletely elucidated. Recent studies have highlighted the importance of posttranslational modifications, such as ubiquitination and SUMOylation, in regulating inflammasome activation. In this study, we demonstrate that SENP6, a SUMO-specific protease, negatively regulates NLRP3 inflammasome activation by promoting K48-linked polyubiquitination of NLRP3. SENP6-deficient macrophages exhibit enhanced NLRP3 activation and increased secretion of interleukin-1β (IL-1β) and IL-18, resulting in amplified inflammatory responses. Mechanistically, SENP6 interacts with NLRP3 and promotes its degradation through the autophagy–lysosomal pathway via K48-linked polyubiquitination. We further identified that SENP6 deSUMOylated NLRP3 at specific lysine residues (K23, K204, and K689), which was essential for maintaining NLRP3 stability. Additionally, SENP6 recruits the E3 ubiquitin ligase MARCHF7 to promote NLRP3 ubiquitination and subsequent degradation. In vivo, SENP6 deficiency exacerbates NLRP3 activation and lung inflammation in lipopolysaccharide-induced endotoxic shock-associated lung injury, and enhances inflammatory responses in alum-induced peritonitis. Our findings reveal a novel mechanism whereby SENP6 modulates NLRP3 inflammasome activation via SUMOylation, ubiquitination, and degradation, providing new insights into potential therapeutic strategies for inflammasome-related pathologies.

Autophagy is integral to the rapid proliferation of esophageal squamous cell carcinoma (ESCC), and its regulation presents a promising avenue for therapeutic intervention. Recent studies have elucidated the interplay between autophagy and glucose metabolism, while there is a paucity of anticancer drugs that concurrently target these 2 biological processes. In this study, we identified a natural compound, p-hydroxylcinnamaldehyde (CMSP), originally isolated from Cochinchina momordica seed (CMS) by our research team, which exhibits substantial anticancer activity against ESCC in both in vitro and in vivo models. The study demonstrates that CMSP induces apoptosis in ESCC cell lines and patient-derived organoid (PDO) models by disrupting autophagic flux. Mechanistically, CMSP specifically binds to the glycolytic enzyme LDHA in the cytoplasm, hindering its phosphorylation by blocking its membrane translocation and thereby disrupting its interaction with FGFR1. This inhibition results in decreased lactate production from glycolysis, reduced lysosomal acidity, and suppression of the AMPK/mTOR pathway, ultimately resulting in the blockade of autophagy and the induction of apoptosis. Furthermore, in vivo studies underscore the potential clinical application of CMSP in ESCC by disrupting autophagy. In summary, we propose a novel therapeutic strategy for the precision treatment of ESCC by simultaneously targeting glycolysis-mediated autophagy.

Head-mounted miniaturized microscopes have provided new capabilities for neuroscience by enabling neural imaging in freely behaving animals. The long-term application of these microscopes, however, is contingent upon specific and reliable cranial window designs. Here, we introduce optically guided and pre-assembled implantation (OGPI), a standardized cranial window technique designed for head-mounted miniaturized microscope imaging. OGPI employs a cost-effective, minimalist design and offers robust compatibility with miniaturized microscopes. This integrated method ensures precise implantation and supports chronic large-scale neural imaging in freely behaving animals for periods exceeding 8 months. The OGPI method is adaptable, supporting both semiautomated operation for enhanced throughput and manual operation for standard laboratory settings. Through behavioral assessments, we further demonstrate that animals with OGPI cranial windows exhibit preserved locomotor and spatial cognitive abilities. Leveraging this chronic window, we performed large-scale cortical imaging in mice engaged in a Y-maze navigation task. We found that the neurons’ tuning position, path, and acceleration were distributed in a “salt-and-pepper” pattern across multiple cortices. A subpopulation of neurons exhibiting conjunctive tuning to both spatial information and linear acceleration was identified, suggesting that the acceleration-tuned neurons required for the generation and updating of the spatial signal exist in the cortex. Further, population-level analyses of spatial representation in the cortex were conducted. A decoder and a classifier based on cortical activity accurately predicted the animal’s position and path. Altogether, our results establish OGPI as an enabling platform and a key methodological advancement for chronic imaging in freely behaving animals and reveal a widespread representation of spatial information in the cortex.

Fibroblast–myofibroblast transition (FMT) and the resultant renal fibrosis are central pathological features of chronic kidney disease (CKD). Epigenetic suppression of RASAL1 (Ras protein activator like 1), an antifibrotic regulator in fibroblasts, is a key driver of this process. However, the underlying mechanisms are only partially understood. Here, we identify histone deacetylase 3 (HDAC3) as a critical epigenetic suppressor of RASAL1 expression in FMT of renal fibrosis. In mouse models of renal fibrosis induced by unilateral ureteral obstruction and aristolochic acid I, RASAL1 suppression coincided with a preferential increase in HDAC3. Fibroblast-specific Hdac3 knockout mice exhibited preserved RASAL1 expression, attenuated FMT, and reduced renal fibrosis compared to wild-type controls. Consistently, pharmacological inhibition of HDAC3 with RGFP966 similarly restored RASAL1 expression, inhibited FMT, and alleviated renal fibrotic pathology. In cultured renal fibroblasts, HDAC3 overexpression or inhibition by RGFP966 inversely affected RASAL1 abundance and major FMT parameters, which was coregulated by the repressive transcriptional factor YY1 (Yin Yang 1). Notably, targeted silencing of RASAL1 abrogated the antifibrotic effects of HDAC3 inhibition both in vitro and in vivo, underscoring the functional significance of the HDAC3–YY1–RASAL1 axis in FMT and fibrogenesis. Given that FMT is a conserved feature of fibrotic diseases across multiple organs, restoring RASAL1 expression via HDAC3 and YY1 modulation offers promising therapeutic strategies for CKD and potentially broader fibrotic disorders.

The integration of multiband and multimode systems has substantially increased the complexity of electromagnetic interference, revealing critical limitations of existing absorbers in tuning efficiency and structural resilience. Here, we propose a nested microaerogel strategy to simultaneously improve the mechanical strength and microwave absorption (MA) performance of polyimide (PI) aerogel. By incorporating pomelo-peel-derived cellulose micronetworks and helical carbon nanocoil microaerogels to construct a gradient-nested framework, the long-standing issues of filler agglomeration and structural shrinkage in aerogels are effectively resolved. The aerogel combines low density, impact resistance, and thermal insulation with remarkable MA performance. The compressive strength reaches 1.3 MPa, which is about 20 times higher than pristine PI aerogel. Furthermore, it exhibits a minimum reflection loss of −50.16 dB, a broad effective absorption bandwidth of 7.44 GHz, and an ultrawide tunable range of 5.6 to 16.4 GHz. Benefiting from its exceptional mechanical properties and pressure-dependent tunability, the aerogel establishes a clear correlation between compression-induced capacitive response and MA performance. These features highlight its potential as a new generation of intelligent microwave absorbers with integrated sensing and adaptive regulation capabilities.

Exigent demands for multifunctional composites integrating proficient thermal management and electromagnetic shielding functionalities arise directly from the accelerating sophistication and power intensification of modern electronic systems. Drawing inspiration from the efficient grasping tentacles of sea anemones, this study pioneers a bioinspired strategy for thermal and electromagnetic management in high-power electronics: architecting bioinspired carbon nanotubes (CNTs) interfaces on copper foam. Notably, the sea anemone tentacle-like CNTs architected on copper foam not only anchor abundant poly(styrene-ethylene-propylene-styrene)/n-docosane to enhance the composites’ latent heat capacity and leakage resistance but also interconnect with expanded graphite to establish multi-path thermal conduction networks while creating electromagnetic wave-reflecting heterogeneous interfaces. By leveraging CNTs as structural bridges, this design integrates the copper foam, expanded graphite, and polymer matrix into a continuous composite (CuFCE-2), achieving superb thermal conductivity (4.71 W/m·K). Consequently, CuFCE-2 excels in thermal management, suppressing chip temperatures by 60.6 °C (transient shock) and 15.7 °C (steady state). Critically, synergistic coordination across these bioinspired heterogeneous interfaces achieves prominent electromagnetic interference shielding, averaging 111.1 dB in the X-band (8.2 to 12.4 GHz). Collectively, the straightforward preparation method and exceptional properties of CuFCE-2 endow it with substantial application potential in electronics and communications, aerospace and defense, as well as new energy and energy storage systems.

Abdominal aortic aneurysm (AAA) is a life-threatening aortic disease without effective pharmacological therapies. Mounting evidences suggested that RNA-binding proteins (RBPs) exert pivotal roles in various diseases including AAA. The public human AAA microarray dataset and the RBP database were used to screen the involved RBPs during AAA formation. The integrated analysis identified zinc finger protein 36 (ZFP36) as a potential mediator of AAA. Underexpression of ZFP36 was observed in aortic vascular smooth muscle cells (VSMCs) within aneurysms from patients and angiotensin II (AngII)-induced mice. Zfp36 deficiency in VSMCs augmented extracellular matrix (ECM) degeneration, VSMC phenotypic switch, and apoptosis, which promoted AAA formation in the AngII-infused model. In contrast, VSMC-specific overexpressing Zfp36 inhibited AAA formation. Mechanically, guanylate binding protein 2 (GBP2), a GTPase related to interferon-γ signaling, was identified as a direct target gene of ZFP36 by analyzing the bulk sequencing data. We confirmed that ZFP36 regulates VSMC phenotypic switch via manipulating Yes-associated protein1/TEA domain transcription factor 1 (YAP1/TEAD1) signaling in a GBP2-dependent manner. Additionally, we further verified that dexamethasone (Dex) could promote glucocorticoid receptor nuclear translocation and Zfp36 transcription. In vivo Dex administration prevented AAA formation in a ZFP36-dependent manner. These findings revealed the regulatory role of ZFP36/GBP2/YAP1/TEAD1 signaling in VSMC phenotypic switch and AAA formation, and provided a novel strategy (Dex) for AAA treatment.

The topological Hall effect (THE), a transport signature emerging from chiral spin textures induced by structural symmetry breaking and the Dzyaloshinskii–Moriya interaction (DMI), represents a rich frontier in condensed matter physics with promising applications in spintronic devices. To enhance the DMI and thereby induce THE in SrRuO₃ (SRO), we introduce a structural-symmetry-breaking strategy that disrupts the Ru–O termination at the rigid substrate interface. This disruption triggers a transition from a rigid epitaxial interface to a freestanding membrane with unsaturated surface bonds, resulting in asymmetric surface terminations (Sr–O on top and Ru–O at the bottom). Unlike its rigid counterpart, which shows no detectable THE, the freestanding SRO exhibits a pronounced THE signal, persisting up to 100 K while preserving high crystallinity and electronic coherence. The ability to generate robust THE in transferable oxide membranes has direct implications for next-generation spintronics, offering compelling prospects for creating low-power magnetic memory and logic devices based on chiral spin textures.

Zincology, the rigorous cross-disciplinary study of zinc metabolism and its multifaceted biological and applied roles in health and disease, delivers a transformative framework for resolving long-standing uncertainties in biomedical research. As a central regulator of cellular function and a versatile element in applied fields, zinc dyshomeostasis underpins diverse high-burden pathologies, including renal, metabolic, cardiovascular, and neurodegenerative disorders, yet its mechanisms remain fragmented across disciplines. This Perspective marks the first formal definition of Zincology as a distinct cross-disciplinary discipline, clarifying zinc’s context-dependent dual role: systemic deficiency exacerbates biological injury through compromised antioxidant defense and inflammation, while local excess drives pathogenesis—exemplified by the Zn–protein kinase B (AKT)–forkhead box protein O1 (FOXO1)–glucose-6-phosphatase catalytic subunit (G6PC) axis in kidney disease. We synthesize Zincology’s core principles to integrate systemic and local zinc metabolism, dissect its pathogenic role in the aforementioned disorders, and outline cross-disciplinary research directions with implications extending beyond biomedicine. Leveraging Zincology’s multidisciplinary rigor, we establish zinc homeostasis as a unifying framework for deciphering disease mechanisms, with kidney disease serving as a paradigmatic model to validate its core tenets, bridging fragmented basic, clinical, industrial, and environmental research to address global critical unmet medical and societal needs. Notably, Zincology extends beyond biomedicine to encompass engineering, ecology, and other frontier fields, representing a comprehensive cross-disciplinary system that links basic science with diverse applied domains.

Biological stress responses operate across multiple scales, yet the coordination mechanisms remain poorly characterized. Here, we present comprehensive systems-level characterization of coordinated plant and endophytic microbiome responses during xenobiotic stress, integrating ultrastructural analysis, proteomics, and microbiome profiling in rice seedlings exposed to ciprofloxacin. We discovered a sophisticated multi-level defense system with chloroplasts as a key hub within a highly integrated cross-organellar network, comprising 36% of all differentially expressed proteins. The system operates through 3 integrated mechanisms: (a) differential cellular accumulation patterns showing 14-fold tissue-specific differences, (b) reactive-oxygen-species-associated metabolic processes with reduced toxicity of transformation products, and (c) restructuring of endophytic bacterial communities toward stress-resistant genera. This work indicates that biological systems deploy hierarchical, integrated responses spanning from organellar to ecosystem levels. The chloroplast-centered response represents a comprehensive characterization of multicompartmental responses with implications across multiple biological fields. Our findings illustrate how multidisciplinary systems approaches can uncover emergent properties of multiscale biological responses invisible to single-scale analyses, providing a framework for investigating multiscale responses across diverse biological systems.

Intracranial hemorrhage (ICH) represents a subtype of stroke characterized by increased mortality and disability rates. Early evacuation of the hematoma is essential for the effective management of ICH. Currently, minimally invasive surgery (MIS) has emerged as a promising alternative to traditional craniotomy by offering advantages, such as reduced operating time, minimal surgical trauma, and accelerated recovery. Nonetheless, postoperative rebleeding remains an important complication that adversely affects the functional outcomes and survival rates of the affected patients. Thus, acquiring a thorough understanding of postoperative rebleeding following MIS for ICH is crucial for enhancing neurological functional outcomes. This review aimed to synthesize current evidence regarding the definition of postoperative rebleeding following MIS for ICH, elucidate the mechanisms contributing to this phenomenon, and identify the associated risk factors, including both surgical and patient-related factors. In addition, the review discusses contemporary strategies for the prevention and management of postoperative rebleeding. Furthermore, it explores prospective advances in dynamic risk prediction and early detection of postoperative rebleeding using artificial intelligence and real-time biosensors. This review offers a reference for clinical practice and guides future studies aimed at reducing the risk of postoperative rebleeding after MIS for ICH, thereby enhancing the outcomes of patients.

Apoptosis and autophagy are fundamental pathophysiological programs governing cell fate decisions under stress, particularly during anticancer therapy. However, the interplay between apoptosis and autophagy in cancer chemoresistance remains incompletely understood. Here, we identify the apoptosis-related protein in the transforming growth factor-β signaling pathway (ARTS) as a key molecular transferring apoptotic signal to autophagic machinery to promote cell survival and chemoresistance. ARTS was highly expressed in chemoresistant breast cancer tissues and was associated with poor patient prognosis. ARTS conferred resistance to doxorubicin and docetaxel by inducing protective autophagy in vitro and in vivo cancer models. Mechanistically, upon proapoptotic signaling triggered by chemotherapeutic agents, ARTS translocated from the mitochondrial intermembrane space into the cytosol, where it induced autophagy through triggering seven in absentia homolog 1-mediated degradation of Livin and subsequent engagement of the mouse double minute 2 homolog (MDM2)–p53 axis, thereby promoting cancer cell survival. Pharmacologic inhibition of caspases or autophagic flux attenuated ARTS-mediated chemoresistance. Overall, this study delineates an apoptosis-dependent ARTS–Livin–MDM2–p53 pathway that drives autophagy and confers chemoresistance in breast cancer.

Majorana zero modes (MZMs) localized in vortex cores of topological superconductors are widely regarded promising building blocks for fault-tolerant quantum computation. However, their unambiguous detection is hindered by the extremely small energy spacing separating them from conventional Caroli-de Gennes-Matricon states. Using a microscopic Bogoliubov-de Gennes approach, we demonstrate that nonmagnetic impurities, rather than suppressing, can substantially enhance the energy gap between MZMs and other vortex core excitations. The robustness of MZMs against local perturbations ensures that while conventional states are shifted by impurity-induced potentials, the MZMs remain intact. This results in a pronounced zero-bias peak in the local density of states. Our results dispute the widespread assumption that large \mathrm{\Delta }/E_F values—where \mathrm{\Delta } is the superconducting gap and E_F is the Fermi energy—are required to detect MZMs, and instead indicate that purposefully engineered pinning centers in conventional s-wave superconductors offer a practical and experimentally accessible alternative.

Copper complexes hold a promise for electroluminescent applications, owing to their dual emissive feature based on the moderate spin-orbital coupling effect of Cu⁺ ion for controllable singlet–triplet conversion. However, efficient red dual emission from copper complexes remains an important challenge, because emission wavelengths and thermally activated delayed fluorescence (TADF)/phosphorescence (PH) ratios are simultaneously correlated to electronic effects. Herein, fluorine atoms with suitable electron-withdrawing inductive effect were introduced into a typical tridentate phosphine ligand coordinated CuI skeleton, namely, TTPPCuI, to reduce the lowest unoccupied molecular orbital (LUMO) energy levels, giving rise to narrowed energy gaps between the highest occupied molecular orbital and LUMO, corresponding to emission wavelengths red shifted from 574 to 603 nm. Fluorine atoms simultaneously enhance metal-ligand charge transfer, therefore adjusting positive and reverse intersystem crossing for dual emission balance, leading to TADF/PH ratios changing from 56/44 over 75/25 to 83/17. The devices based on these fluorinated CuI complexes realized efficient red electroluminescence with the maximum wavelength and external quantum efficiency beyond 600 nm and 20%, respectively. These results demonstrate that, based on electronic effects from functional groups, ligand engineering is a feasible way for comprehensively manipulating excited-state characteristics of dual-emissive copper complexes.

Because of their outstanding weak light detection ability, multiplication-type photodetectors have great application prospects in fields such as environmental detection, biological science, and night vision imaging. Traditional photomultiplication-type organic photodetectors (PM-OPDs) usually achieve a large external quantum efficiency (EQE) through the mechanism of interfacial trap-assisted charge tunneling injection but inevitably produce a large dark current. Here, we demonstrate a novel dual-function photon-regeneration multiplication-type organic photodetector (PRM-OPD) with photocurrent gain by absorbing additional photons generated by an integrated organic light-emitting diode unit. The optimized PRM-OPD exhibits a maximum EQE of 2,484% and maintains a low dark current density (J_d) of only 10⁻⁸ A/cm². More importantly, the resulting PRM-OPD can not only exhibit efficient detection performance but also directly detect the shape of the light spot, showing a dual-function working mode. Furthermore, by combining optical resonant microcavities, the response spectrum is successfully extended to the near-infrared region and a narrowband PRM-OPD with excellent performance is obtained. This designed device structure provides a new idea for the development of high-performance PM-OPDs.

Nonviral intracellular delivery based on pulsed-electric-field-induced electroporation is one of the most effective and widely used platforms in basic biological and biomedical research. However, the conventional bulk electroporation technique has exhibited limited performance in improving delivery efficiency with a single type of pulse, especially for in vivo small interfering RNA (siRNA) delivery. Pulse modulation has been confirmed effective in facilitating intracellular delivery. Nonetheless, pore evolution and regulation during and after electric exposure plays an essential role in the effective intracellular delivery of molecules with variable sizes. Here, we propose a progressive electroporation (PEP) strategy on the basis of multiple-pulse combination, which decouples the perforation process and delivery process compared to conventional bulk electroporation, efficiently improving delivery efficiency with regulation of the perforated pores. We demonstrated an important correlation between delivery efficiency enhancement and delayed pore resealing by quantitative investigations. The performance of this disruption-and-field-enhancement method also showed delivery advantages over conventional chemical systems. Moreover, we validated the improvement for siRNA knockdown efficacy in vivo. Overall, PEP helps provide a unique insight into improving intracellular delivery, by regulating pore dynamics rather than just inducing perforation. This strategic advancement of PEP may pave the way for the development of advanced wearable delivery systems with reduced energy consumption.

Traditional solid metal catalysts in organic reaction have been hindered by drawbacks, including limited surface catalytic region, restricted reactant diffusion, catalyst deactivation, low atom utilization efficiency, and harsh reaction condition. To overcome these drawbacks, we introduce liquid metal into organic reaction. An efficient mechano-assisted reaction system was proposed integrating dynamic metal catalyst and liquid metal reaction medium. With a low-energy ball-milling process (at a speed of 270 rad·min⁻¹), the dynamic metal atoms in liquid state could achieve maximum atomic utilization and fast reaction kinetics compared to solid metal. Furthermore, liquid metal also act as reaction media. It not only offers a homogeneous electron-rich environment for reactants but also continuously disperses active metals to construct a multimetal catalytic system in one step. These would revolutionize the understanding of metal catalysts and reaction media, providing a novel platform for exploration of high-throughput catalysis and discovery of novel chemical reaction in future.

Highly pathogenic avian influenza H5N1 virus has spread to over 1,080 dairy farms across 18 states in the United States, resulting in 41 human infections and posing serious risks to both animal and public health. To address these risks, a hemagglutinin-based mRNA–lipid nanoparticle vaccine was developed, and its safety, immunogenicity, and protective efficacy in high-yielding lactating dairy cows were evaluated. The vaccine was well tolerated, had no adverse effects on health or milk production, and induced strong antibody responses. Two weeks after the second immunization, all the immunized cattle were fully protected against a high-dose H5N1 virus challenge. Notably, two-thirds of the cattle were still completely protected even at the 19th week after the first vaccination, when their serum antibody levels were very low. These data demonstrate that the mRNA vaccine confers robust, lasting protection against H5N1 virus in lactating dairy cows, providing a foundation for clinical trials.

Metabolism-regulating microspheres have evolved from conventional drug carriers into active platforms capable of spatiotemporally reprogramming pathological metabolic networks. Chronic diseases are increasingly understood to be driven by metabolic dysregulation, highlighting the need for therapeutic strategies that enable localized and precise metabolic intervention. This review systematically outlines the core design principles of these microspheres, emphasizing the synergistic integration of engineered chemical properties, such as ionic signaling, metabolite delivery, and pathway modulator release, with tailored physical characteristics, including stiffness, porosity, and size of the microspheres. Together, these features construct “metabolic instruction systems” that correct dysregulated pathways at the tissue level. Their versatile applications include orthopedic diseases, such as osteoporosis, osteoarthritis, and bone defects; ophthalmic conditions, including glaucoma and diabetic retinopathy; and gynecological disorders, such as premature ovarian insufficiency, ovarian cancer, and endometriosis. These systems target key metabolic abnormalities, such as glycolytic dysregulation, mitochondrial dysfunction, and oxidative stress, which are recognized as central drivers of disease pathogenesis across multiple organ systems. Despite considerable progress, clinical translation remains limited by tissue-specific delivery barriers, interindividual metabolic heterogeneity, and long-term safety concerns within dynamic metabolic networks. Emerging strategies, such as personalized formulations, artificial-intelligence-driven designs, and organ-on-a-chip validation platforms, are being developed to address these challenges. With ongoing interdisciplinary innovation, metabolism-regulating microspheres hold great promise as precise therapeutic modalities for a spectrum of chronic diseases rooted in metabolic imbalance, offering targeted and sustained metabolic correction.

Cytoskeletal remodeling, particularly actin dynamics, is a central driver of tumor metastasis. However, actin-targeting agents have faced major translational barriers due to poor specificity and the absence of defined druggable sites. Here, we report a bladder tumor-targeting polyarginine peptide, R11, as a precision modulator of actin dynamics capable of disrupting the cytoskeletal architecture of bladder cancer (BCa) to suppress its lung metastasis potently and persistently. R11 directly interacts with actin, weakening the actin–plectin–vimentin/integrin β4 axis and initiating a cascade of cytoskeletal disorganization that ultimately impairs cellular motility and metastatic potential. Remarkably, nanoscale multivalent assemblies of R11 amplify these effects through enhanced multivalent binding to actin. This study unveils a new strategy for cytoskeleton-targeted intervention through peptide-based precision materials, highlighting R11 assemblies as a promising therapeutic platform for the treatment of metastatic BCa and potentially other cytoskeleton-dependent malignancies.

Drug-resistant bacterial infections threaten global health and economies. Stimulus-responsive antibacterial materials are promising for combating resistance and improving treatment precision. Among them, electroresponsive strategies stand out for being practical, economical, tunable, and safe. This perspective examines various strategies, including electroluminodynamic therapy, electrodynamic therapy, and electrocontrolled drug release, which enable precise antibacterial action with minimal side effects and demonstrate strong application potential. Finally, we outline current challenges and future directions to guide further research and practical applications.

Two-dimensional transition metal dichalcogenides (TMDs) are promising candidates for next-generation electronics, but their future application is hindered by the inherently slow growth kinetics of conventional vapor deposition methods, particularly for the synthesis of large-area single-crystal films. Here, we demonstrate a source-confined chemical vapor deposition strategy that enables the fast synthesis of centimeter-scale MoS₂ single-crystal films within just 10 min. An optimized sandwich-structured Mo source was employed to ensure a concentration-balanced metal supply under sodium chloride catalysis, followed by sulfurization to form MoS₂. The films nucleate uniformly and directionally on the miscut C/A sapphire substrate positioned 2 cm upstream of the Mo source, achieving high crystal quality with a low sulfur vacancy density of 8.49 × 10¹² cm⁻². Additionally, these films support the development of high-performance enhancement-mode MoS₂ field-effect transistors, exhibiting excellent transport performances, including a high on–off ratio of 10⁸, an average positive threshold voltage of 1.71 ± 0.32 V, an average mobility of 34.28 ± 0.46 cm² V⁻¹ s⁻¹, and an average subthreshold swing of 155.8 ± 33.7 mV dec⁻¹. Furthermore, high-performance rail-to-rail inverter gates and logic circuits with low power consumption (<0.3 nW) were successfully demonstrated, underscoring the potential of these MoS₂ films for integrated circuit applications. This work offers a scalable and reliable approach for the fast growth of large-scale TMDs single-crystal films, accelerating their future applications in next-generation electronics.

In liver ischemia–reperfusion injury (LIRI), macrophage clearance of apoptotic cells via efferocytosis is crucial to prevent excessive inflammation and tissue damage. Here, we investigate the role of nucleotide-binding oligomerization domain-like receptor protein 3/cysteine-aspartate protease-1 (NLRP3/Caspase-1) signaling in modulating macrophage efferocytosis during LIRI. We observed robust activation of the NLRP3/Caspase-1 pathway during the early phase of LIRI. Genetic ablation of Nlrp3 or Caspase-1 substantially reduced LIRI severity. Notably, myeloid-specific Nlrp3 knockout mice exhibited less severe LIRI compared to hepatocyte-specific Nlrp3 knockouts, whereas macrophage-specific overexpression of Caspase-1 exacerbated tissue injury. Mechanistically, NLRP3/Caspase-1 activation enhances a disintegrin and metalloprotease protein-17 (ADAM17)-mediated cleavage of Mer proto-oncogene tyrosine kinase (MerTK), leading to impaired efferocytosis. Pharmacological inhibition of ADAM17 restored macrophage efferocytic capacity and alleviated LIRI. Clinically, elevated serum levels of soluble MerTK (s-Mer) correlated with hepatic injury severity and Caspase-1 activation in patients after partial hepatectomy or liver transplantation. Our findings suggest a potential therapeutic strategy for LIRI prevention and treatment.