Robotic exoskeletons have emerged as promising motion-assistive technologies to meet the growing demand for structured, personalized cancer rehabilitation. This review critically examines their application in enhancing functional recovery, alleviating cancer-related fatigue, and improving quality of life among cancer patients and survivors. We first outline current evidence-based exercise strategies in cancer rehabilitation, followed by an analysis of how robotic exoskeletons complement and extend these approaches by restoring mobility, strengthening musculature, and supporting psychological well-being. Additionally, we assess how well they combine with multimodal interventions like nutritional, psychological, and digital therapeutics and their benefits. The convergence of artificial intelligence, wearable sensors, and telemedicine is also reshaping the landscape of remote, adaptive rehabilitation. Despite encouraging preliminary data, widespread clinical adoption remains limited due to challenges related to cost, exoskeleton system accessibility, safety, and long-term efficacy. We call for large-scale clinical trials, interdisciplinary collaboration, and policy reforms to promote equitable access to robotic-assisted rehabilitation. Collectively, this review offers a comprehensive perspective on the technical principles, therapeutic potential, and future directions of robotic exoskeletons as innovative tools in cancer recovery.

Biomacromolecules are now widely employed in the therapy of major diseases such as tumors, infections, cardiovascular diseases, metabolic diseases, and autoimmune diseases. Although significant advances have been made in their application, their administration is largely dependent on professional injection, which causes pain, massive medical waste, and high medical burden. As a novel delivery system, microneedles pierce the stratum corneum to assist in intradermal drug delivery, exhibiting minimal invasiveness, high delivery efficiency, and improved patient compliance. The evolution of biomaterials and tissue engineering has broadened microneedle utilization to encompass oral and cardiovascular therapies. Herein, we discuss research advancements regarding the development of biomacromolecule-laden microneedles for treating major diseases. We present detailed examples on how to devise functional microneedles to cross drug delivery barriers in the skin, heart, and blood vessels for improved therapeutic outcomes. Furthermore, we discuss the critical barriers in industrial-scale fabrication and transitioning into clinical practice of microneedles, aiming to provide insightful solutions. Moreover, we explore the future applications of microneedles, including the development of microneedle tacks, robots, and biomimetics to combat intractable diseases. We believe that this review will aid in the designing of microneedles for biomacromolecule delivery, opening up a new avenue for the treatment of major diseases.

Precisely targeting mitochondria to regulate macrophage fate has emerged as a critical therapeutic paradigm for managing inflammation-related pathologies. Mitochondria, while known for producing ATP, have been increasingly recognized for their critical involvement in immune cell differentiation and activation. As key innate immune effectors, macrophages dynamically adapt to microenvironmental cues through metabolic reprogramming and phenotype polarization, processes fundamentally controlled by mitochondrial homeostasis. Organelle-specific therapeutic advances now position mitochondria-targeted strategies as precision interventions with spatiotemporal advantages over conventional approaches. Crucially, these rationally designed systems demonstrate remarkable potential not only to direct macrophage differentiation toward anti-inflammatory phenotypes but also to reprogram the immune microenvironment concurrently, thereby achieving a breakthrough in precision medicine for inflammatory disorders. This review analyzes mitochondrial homeostasis mechanisms in pathophysiology, establishing design principles for targeted therapies. We classify emerging mitochondrial modulation approaches into indirect regulation and direct targeting, evaluating their impacts on macrophage plasticity and therapeutic efficacy. Critical translational challenges are examined, including single-cell-centric regulation, the complexity of mitochondrial interactions in macrophages, and the inefficiency of traditional trial-and-error strategies. The proposed artificial intelligence (AI)-driven methods such as deep learning-based material design, metabolic network modeling, and advanced small-molecule synthesis can accelerate the development of targeted mitochondrial therapies and enhance clinical feasibility. This synthesis aims to accelerate the development of mitochondrially engineered immunotherapies through rational design principles and standardized evaluation protocols.

Aging, caused by a variety of exogenous stimuli and internal factors, leads to a gradual and irreversible decline in the function of the organism. The aging process involves complex gene regulation, in which transcription factors may play a key role as core regulatory elements. In this study, the single-cell transcriptome of skin revealed homeobox C10 (HOXC10) as a core element in the transcription factor regulatory network associated with skin aging. In vivo and vitro, the expression of HOXC10 was down-regulated in senescent fibroblasts and aging tissues, and overexpressed HOXC10 delayed cell senescence and skin aging. Mechanistically, HOXC10 targeted the promoter region of frizzled 6 (FZD6) to reduce its expression and therefore activated the Wnt/β-catenin signaling pathway to delay aging. Finally, by using the Connectivity Map approach, we explored simvastatin as a functional mimic of HOXC10 and demonstrated its antiaging ability in vitro and vivo. In conclusion, our results establish the role of HOXC10/FZD6/Wnt signals in skin aging and identify simvastatin as a potential therapeutic strategy to delay aging.

Alternative splicing (AS) is the central mechanism of transcriptional regulation and generates diverse splice variants that influence protein structure, function, and intracellular activity. AS plays critical roles in tissue differentiation, organ development, and disease progression. This review focuses on the pivotal roles of AS in bone biology, highlighting its regulatory effects on osteoblasts, osteoclasts, chondrocytes, bone matrix remodeling, and bone remodeling, as well as the involvement of AS-related RNA-binding proteins in these processes. We also emphasize bone-specific AS events and their physiological importance in skeletal development and maintenance. Furthermore, the pathological role of AS is emphasized in bone-related tumors such as osteosarcoma, Ewing sarcoma, and chondrosarcoma. This review also explores aberrant AS mechanisms in bone metastatic cancers, including prostate, bladder, and breast cancers, with an in-depth analysis of their roles in tumor progression and alterations in the bone microenvironment. This review provides a comprehensive perspective on how AS factors, signaling pathways, and mechanical stimulation collaboratively regulate bone cells under both physiological and pathological conditions, paving the way for identifying potential intervention strategies. The mechanisms of AS in other pathological bone conditions, such as osteoporosis, osteoarthritis, and hereditary bone disorders, are also summarized. The potential applications of targeting AS in the diagnosis and treatment of bone diseases are discussed, offering insights into the underlying mechanisms and clinical translational potential.

Osteosarcoma, a primary malignant bone tumor originating from mesenchymal cells, is the most prevalent bone malignancy in children and adolescents. Current standard treatment involves aggressive surgical resection aimed at maximal tumor removal; however, this inevitably creates extensive bone defects that substantially impair patients’ quality of life. Furthermore, the risks of postoperative tumor recurrence and metastasis critically influence therapeutic outcomes. With the continuous advancement of biomaterials, their applications in postsurgical osteosarcoma management have increased substantially. Biomaterial-based strategies are enabling diverse antineoplastic function and bone regeneration strategies. However, previous biomaterial strategies have typically focused on osteogenic or antitumor functions in isolation. The current research frontier is shifting toward developing integrated strategies that simultaneously achieve both effective tumor suppression and functional bone regeneration. This review strategically categorizes these emerging strategies into 3 distinct approaches: (a) Traditional bifunctional strategies: Integrating coloaded osteogenic and antitumor agents within a carrier. (b) Enhanced antitumor bifunctional strategies: Incorporating components or designs that actively boost the potency of the antitumor modality beyond simple codelivery. (c) Temporally controlled sequential strategies: Engineered to perform antitumor and pro-regeneration functions in a defined, sequential order. By critically analyzing the cutting-edge biomaterials employed in these strategies, we assessed their potential for clinical translation, emphasized the ongoing technical barriers, and outlined the challenges for future development.

Osteoarthritic cartilage tissue displays a characteristic imbalance in trace element metabolism closely associated with the production of oxidative stress. This study revealed the pivotal role of iron-overload-triggered and selenoprotein-catalyzed lipid peroxidation in osteoarthritis pathogenesis. Based on this discovery, we innovatively pioneered the integration of Fe²⁺-capturing (attack) nanocatalysts and selenium-enriched (defense) polypeptides (selenomethionine [SeMet]) into a hydrogel platform. Polyvinylpyrrolidone-assembled magnesium hexacyanoferrate (MgHCF) nanoparticles enabled efficient Fe²⁺ chelation to counteract ferroptosis. SeMet utilization by the selenoprotein glutathione peroxidase 4 is required to prevent hydroperoxide-induced ferroptosis. Furthermore, a dynamically cross-linked network was constructed from oxidized hyaluronic acid (OHA) and hyaluronic acid–adipic acid dihydrazide (HA-ADH), enhanced by grafting SeMet onto the OHA chain and encapsulating MgHCF into the polymeric matrix. MgHCF@OHA/HA-ADH/SeMet hydrogels exhibited injectable, self-healing, and sustainable drug release capabilities. The platform promoted the anti-lipid peroxidation process and restored the mitochondrial homeostasis of chondrocytes under inflammatory stimulation via the phosphoinositide 3-kinase/Akt/forkhead box O1 pathway. In vivo investigations showed its anti-inflammatory activity, ferroptosis-inhibiting capacity, and ability to reverse cartilage degeneration. This work establishes a therapeutic paradigm based on trace element synergy, providing a translatable disease-modifying candidate.

Chronic unpredicted mild stress (CUMS) and obesity are well-known risk factors for breast cancer (BC). However, their underlying correlation and potential mechanisms remain unknown. Herein, CUMS was found to promote BC growth and metastasis with increased adipocyte lipolysis, reactive oxygen species (ROS) burst, and mitochondrial fission. Metabolomic analysis identified tryptophan (TRP) as the main responding metabolite, which markedly induced macrophage M2 polarization and CXCL1 expression, and in turn promoted adipocyte lipolysis. Molecular investigation showed that CXCL1 triggered KEAP1 m⁶A demethylation via FTO (fat mass and obesity-associated protein) up-regulation, subsequently reducing NRF2 expression to exacerbate ROS burst and mitochondrial fission. Furthermore, either siCXCL1 or FTO inhibition markedly inhibited CUMS-induced BC progression, accompanied by suppression of adipocyte lipolysis, ROS production, and mitochondrial fission, as well as KEAP1 m⁶A demethylation. Our findings highlight the novel signaling of TRP/TAM/CXCL1 in mediating adipocyte lipolysis underlying CUMS-induced BC progression, and KEAP1 m⁶A demethylation presents a promising therapeutic target.

The synthesis of complex organic macrocycles, particularly large and rigid variants, has long been hampered by low yields, poor selectivity, and arduous purification stemming from stepwise approaches. Sánchez-Naya et al. present a transformative “clip-off” strategy in Science, liberating preformed macrocycles from the pores of designed covalent organic frameworks. By strategically incorporating cleavable bonds into specific covalent organic framework linkers and utilizing precise ozonolysis, near-quantitative yields of macrocycles with ring sizes ranging from 114 to 162 atoms have been achieved. This strategy leverages reticular chemistry to control size and functionality, establishing crystalline frameworks as molecular blueprints.

Modern electrical infrastructure relies heavily on insulation materials. Critical examples include polyimide films in microelectronics, epoxy resins in transformers, silicone rubber on outdoor insulators, and polyolefins in power cables. These solid insulation materials have high resistivity, which provides reliable assurance of the safe operation of equipment and power grids. However, both their production and end-of-life disposal place an important environmental burden. In light of the growing prevalence of sustainability principles and circular economy concepts, researchers and industry experts are re-evaluating every stage of the insulation life cycle. This includes synthesis processes, raw materials, energy consumption, and generation of toxic by-products, alongside performance durability and health impacts during use. Ultimately, disposal or recycling methods must also be considered.

Prostate cancer (PCa) progression is driven by intricate molecular mechanisms involving dysregulated signaling networks and posttranslational modifications of key regulatory proteins. In this study, we identify a novel oncogenic pathway wherein cyclin-dependent kinase 12 (CDK12) physically interacts with and phosphorylates forkhead box A1 (FOXA1) at serine 234 (S234). Phosphorylation at this residue markedly enhances FOXA1 transcriptional activity, leading to up-regulation of downstream targets including murine double minute 2 (MDM2), a critical negative regulator of the p53 tumor suppressor. Mechanistically, this CDK12–FOXA1–MDM2 axis destabilizes p53, attenuates apoptotic signaling, and promotes PCa cell survival and proliferation. Therapeutic targeting of CDK12 using the small-molecule inhibitor THZ531 or RNA interference effectively abrogates FOXA1 phosphorylation, restores p53 stability, reactivates apoptotic pathways, and suppresses tumor growth. Notably, the identification of S234 as a functional phosphorylation site in FOXA1 reveals a previously uncharacterized posttranslational regulatory mechanism in PCa biology. These findings establish the CDK12–FOXA1–MDM2 axis as a pivotal driver of PCa progression and underscore the therapeutic potential of targeting FOXA1 phosphorylation to restore tumor suppressor function and induce apoptosis in PCa. Our work provides a mechanistic framework for developing precision therapies aimed at disrupting this oncogenic cascade in PCa.

The ubiquitous contamination of airborne nanoplastics (<100 nm), particularly polystyrene nanoplastics (PS NPs), has emerged as critical determinant regarding respiratory health. As inhalation exposure represents a primary route of human contact, the pulmonary toxicological profiles of PS NPs remained poorly characterized, with underlying mechanisms lacking. In this study, we systematically investigated the pulmonary toxicological mechanisms of PS NPs for inducing acute–subacute lung injury. PS NPs markedly reduced cell viability of lung epithelial cells (BEAS-2B cells) and macrophages (RAW 264.7 cells) in a dose-dependent manner. Further investigations revealed that PS NPs induced a hierarchical oxidative stress paradigm that redox imbalance triggered by reactive oxygen species (ROS) burst led to the cascade activation of compensatory nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, up-regulation of pro-inflammatory cytokines, mitochondrial dysfunction, and apoptosis. Furthermore, the in vivo toxicities of PS NPs were validated by the acute and subacute pulmonary injury on rodent models, which was characterized by obvious inflammatory cell infiltration and pulmonary fibrosis. These results indicated that hierarchical oxidative stress mediated PS NPs-induced acute–subacute lung injury. This also raised a warning that susceptible individuals with long-term plastic exposure should receive regular pulmonary monitoring.

Sepsis remains a leading global cause of death, with immune heterogeneity’s molecular mechanisms poorly understood. This study analyzed 1,862 human peripheral blood samples, constructing a molecular interaction disturbance network that first revealed the network biology underlying sepsis immune heterogeneity. We identified 3 sepsis subtypes with marked different prognostic characteristics, with the C1 subtype showing the worst prognosis characterized by severe CD4⁺ T cell exhaustion—validated across 10 independent cohorts. Integrating single-cell transcriptomics from over 450,000 cells, proteomics, and functional validation, we identified monocyte-derived matrix metalloproteinase-9 (MMP9) as a key regulator driving CD4⁺ T cell dysfunction. Mechanistically, MMP9 modulates T cell exhaustion through dual mechanisms: promoting leukocyte-associated immunoglobulin-like receptor-1 (Lair-1) aggregation on T cell membranes, directly inhibiting zeta chain of T cell receptor associated protein kinase 70 (ZAP70) phosphorylation in T cell receptor signaling, while impairing Ca²⁺-release-activated Ca²⁺ channel function and intracellular calcium clearance, causing calcium dysregulation that blocks nuclear factor of activated T cells (NFAT) activation and nuclear translocation. The selective MMP9 inhibitor MMP9-in-1 effectively reversed T cell dysfunction, restored calcium homeostasis and NFAT nuclear translocation, markedly enhanced CD4⁺ T cell interleukin-2 and interferon-γ production, and reduced programmed cell death protein 1 expression. This work establishes a comprehensive translational framework from molecular network disturbances to clinical phenotypes, advancing sepsis immunopathophysiology understanding and providing effective targets for the treatment of sepsis patients.

Sepsis is a life-threatening disease characterized by systemic inflammation and endothelial barrier dysfunction, leading to multiorgan failure and high mortality. This review provides a comprehensive overview of the pathological mechanisms underlying sepsis-induced endothelial dysfunction, focusing on glycocalyx degradation, endothelial cell death, increased vascular permeability, and coagulopathy. During sepsis, the endothelial glycocalyx (EG) is disrupted, leading to increased vascular permeability and impaired microcirculation. Endothelial cells undergo various forms of cell death, including apoptosis, pyroptosis, ferroptosis, and autophagy, which are driven by inflammation and oxidative stress. These processes are further complicated by the activation of coagulation pathways and the formation of intravascular thrombi. The interaction between endothelial cells and immune cells amplifies the inflammatory response, contributing to the persistence of systemic inflammation. We also discuss emerging therapeutic strategies aimed at protecting endothelial cells, modulating inflammation, and improving coagulation function, including glycocalyx protectants, anti-inflammatory agents, anticoagulants, and endothelial repair mechanisms. Future research should focus on translating these therapeutic approaches into clinical practice to improve outcomes in patients with sepsis.

Vasculogenic mimicry (VM) is a microcirculation pattern that has a crucial effect on hepatocellular carcinoma (HCC) metastasis. In this study, leveraging the GeneCard and The Cancer Genome Atlas databases, we identified ATPase inhibitory factor 1 (IF1) as a potential regulator of VM formation. Our research findings indicate that IF1 can promote HCC cell tube formation in vitro and enhance HCC VM and lung metastasis in vivo. Transcriptome sequencing combined with in vivo experiments revealed that IF1 knockdown elevates miR-20a-3p expression. Lentivirus-mediated miR-20a-3p overexpression reversed IF1-induced VM. Dual-luciferase reporter gene assays showed that estrogen receptor 1 (ESR1) acts as a transcription factor of the miR-20a-3p precursor. Further mechanistic studies revealed that excessive reactive oxygen species accumulation caused by IF1-induced mitochondrial metabolic reprogramming can inhibit ESR1 expression by promoting DNA methylation of its promoter. G protein subunit alpha Z (GNAZ), a miR-20a-3p target protein, can promote VM by phosphorylating components of the ERK pathway. Collectively, these results delineate a novel IF1/ESR1/miR-20a-3p/GNAZ axis in HCC VM and metastasis, providing potential therapeutic targets.

Since the skin is the largest organ of the human body, skin injuries may result in substantial social and economic burdens. Skin wound management remains a substantial challenge due to the complex nature of the healing process involving inflammation, tissue proliferation, and remodeling. Coordinated interactions between cells, extracellular matrices, and cytokines drive regeneration, while cell metabolism—an essential pillar of physiological activity—regulates key biological processes like proliferation, angiogenesis, immune responses, and tissue regeneration. Modulating metabolic pathways provides a promising alternative to conventional therapies. However, understanding of the role of cell metabolism in wound healing remains to be fully elucidated. Further exploration of their cross talk will not only establish a robust theoretical foundation for innovative treatments but also open avenues for promoting scar-minimizing regenerative healing and bringing new prospects for clinical practice.

Hepatic lipid dysregulation drives metabolic dysfunction-associated steatotic liver disease (MASLD); nonetheless, the precise regulatory mechanisms remain incompletely elucidated. In this study, we examine the function of EVA1A, a known hepatocellular carcinoma tumor suppressor, in hepatic lipid metabolism. Hepatic EVA1A was markedly down-regulated in individuals diagnosed with MASLD, as well as in mice subjected to a high-fat diet. Hepatocyte-specific knockout of Eva1a in mice resulted in significant hepatic steatosis, accompanied by disrupted fatty acid metabolism, marked by increased fatty acid uptake and compromised β-oxidation, while hepatic Eva1a overexpression reversed these metabolic changes and largely alleviated fatty liver in ob/ob mice. Mechanistically, EVA1A deficiency activates mTORC1 (mechanistic target of rapamycin complex 1)–PPARγ2 (peroxisome proliferator-activated receptor γ2) signaling to up-regulate CD36 transcription. Concurrently, it transcriptionally represses the S-depalmitoylase APT1 while enhancing palmitoyl acyltransferases ZDHHC4/5, boosting CD36 palmitoylation. This dual action promotes CD36 plasma membrane localization for fatty acid uptake, reducing its mitochondrial distribution and impairing β-oxidation. Collectively, these results establish EVA1A as an essential regulator of hepatic lipid homeostasis, coordinating fatty acid uptake and β-oxidation by modulating CD36 expression and palmitoylation. Therefore, targeting the EVA1A–CD36 axis represents a promising therapeutic strategy for MASLD.

The development of an immunosuppressive microenvironment is a critical factor in stomach carcinogenesis. Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) serve a pivotal function in mediating immune suppression. However, the precise mechanisms underlying PMN-MDSCs infiltration into the tumor immune microenvironment (TIME) and their immunosuppressive functions remain poorly understood. In this investigation, we observed that PMN-MDSCs were up-regulated during stomach carcinogenesis, with gastric cancer (GC) cells secreting CCL26 to promote the infiltration of PMN-MDSCs into the TIME via the CX3CR1 receptor. The infiltrating CX3CR1⁺ PMN-MDSCs secreted transforming growth factor-β1 (TGF-β1), which, through the SMAD2/3/SNAI1 signaling pathway, further sustained the secretion of CCL26 by GC cells, establishing a positive feedback loop. Additionally, CX3CR1⁺ PMN-MDSCs suppressed mTOR signaling via TGF-β1 and competed with CD8⁺ T cells for glucose, disrupting glycolysis and leading to T cell exhaustion. Notably, inhibition of CX3CR1 reduced the infiltration of PMN-MDSCs, improved anti-PD-1 therapeutic efficacy, and suppressed tumor growth. In conclusions, this study illustrated that the CCL26–CX3CR1 axis mediates a positive feedback loop between GC cells and PMN-MDSCs, promoting CD8⁺ T cell exhaustion and tumorigenesis. Targeting CX3CR1 on PMN-MDSCs could serve as a potential therapeutic strategy to prevent stomach carcinogenesis.

Organic piezoelectric materials have garnered increasing interest for biomechanical applications; however, their practical appeal has been limited by low piezoelectricity and low mechanical compliance. Recently, liquid–liquid interface polar engineering has emerged as a promising strategy to overcome these limitations. By utilizing polarity asymmetry at the liquid–liquid interface, this strategy enables precise control over molecular assembly and phase separation, thereby inducing high piezoelectric polarization of organic materials while maintaining their intrinsic mechanical compliance. This breakthrough paves the way for developing organic piezoelectric materials that exhibit both high piezoelectricity and high mechanical compliance, advancing their potential in biomechanical sensing, actuating, and energy harvesting.

The normal development of spermatogonial stem cells (SSCs) is essential for maintaining male fertility. Nevertheless, signaling molecules and pathways regulating the fate decisions of human SSCs remain elusive. We have reported that Opa interacting protein 5 (OIP5) is involved in controlling human SSC self-renewal and apoptosis. Notably, we found that insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) interacted with OIP5 in human SSCs. Our RNA sequencing (RNA-seq) and immunofluorescence–fluorescence in situ hybridization (IF-FISH) identified heme oxygenase 1 (HMOX1) as a downstream target of IGF2BP1 in human SSCs. Methylated RNA immunoprecipitation-binding qPCR (MeRIP-qPCR) and RNA stability assays revealed that IGF2BP1 could bind to HMOX1 mRNA and enhance its stability and HMOX1 expression level. Functional assays demonstrated that IGF2BP1 or HMOX1 silencing resulted in the decreased expression levels of ferroptosis-associated genes (e.g., SLC7A11 and SLC3A2), the increased intracellular reactive oxygen species (ROS) level and ferrous ion (Fe²⁺) content, and the impaired stemness maintenance of human SSCs. Additionally, we observed that IGF2BP1-mediated HMOX1 stabilization activated system Xc⁻, thereby inhibiting ferroptosis of human SSCs. Furthermore, IGF2BP1 gene variants were positively correlated with the occurrence of non-obstructive azoospermia (NOA). Collectively, these results imply a critical role of IGF2BP1/HMOX1 mRNA/system Xc⁻ axis in regulating human SSC ferroptosis, autophagy, and stemness maintenance. This study thus provides novel insights into the regulatory mechanisms of human SSC fate determinations and offers new targets for treating male infertility.

Quantum machine learning stands poised as a forefront application for near-term quantum devices, addressing scalability challenges posed by classical computers in handling large datasets. Gaussian boson sampling (GBS), an intricate quantum algorithm deemed computationally infeasible for classical counterparts, represents a substantial leap forward in computational tasks. However, to date, the benefits of GBS-assisted quantum unsupervised machine learning are not experimentally demonstrated. Here, we present the first experimental implementation of quantum unsupervised machine learning using the GBS protocol with a universal programmable integrated photonic chip. The experimental system contains 16 squeezing sources, a universal programmable unitary matrix network of 16 modes, and a multi-channel single-photon detector, producing substantial output data crucial for 2 typical types of unsupervised tasks: feature extraction and generative network. Compared to classical approaches, the study demonstrates quantum-enhanced capability in extracting complex features from high-dimensional spaces and improved performance in generating arbitrary curve points and reconstructing handwritten digit images. This work not only underscores the potential of GBS in expressing high-dimensional features but also charts a path toward practical implementations within scalable, dimension-enhanced quantum unsupervised machine learning frameworks. The quantum unsupervised machine learning paradigm, offering theoretical acceleration and reduced training parameters for high-dimensional datasets, shows significant promise for advancing real-world applications of quantum technologies.

A microwave-coupled biphasic solvent system was developed for steerable liquefaction of pentoses and hierarchic separation of furfural by leveraging the dielectric properties of γ-valerolactone (GVL)/NaCl aqueous solution under microwave irradiation, during which more than 85.38 mol% of furfural yield was obtained from xylan at 140 °C for 20 min, compared to that of 78.1 mol% at 150 °C for 120 min under conventional heating conditions. Strikingly, the separation efficiency was improved under microwave conditions with the partition coefficients (R) of furfural ranging from 31.1 to 35.68, compared with 22.71 to 29.33 under conventional heating conditions. Moreover, the coupled effect on the substrate from the microwave was also explored. Notably, high heating power during the initial hydrolysis phase enhances the depolymerization of xylan glycosidic bonds, resulting in the rapid release of 87.89 mol% xylose from xylan. Meanwhile, the application of low heating power during the dehydration process effectively facilitates the production of furfural, which is promptly extracted into the organic phase, thereby minimizing product loss. Besides, the feasibility of the process was assessed using real biomass as the substrate, demonstrating low energy consumption attributed to the efficient microwave absorption by GVL and the NaCl aqueous solution. This approach offers a viable strategy for the efficient and scalable production of furfural.

Electronic waste contains gold at concentrations far exceeding natural ores, yet efficient and selective recovery remains challenging. Here, we present a covalent organic framework (COF), tetra-(4-aminophenyl)-porphyrin–4,4′-(thiazolo[5,4-d]thiazol-2,5-diyl)bis(2,5-dimethoxybenzaldehyde)–COF (TAPP-TZ-OMe-COF), in which thiazole and methoxy groups create abundant AuCl₄⁻ binding sites and modulate the electronic structure via donor–acceptor interactions and p–π conjugation. These features narrow the band gap, enhance charge separation, and accelerate photogenerated electron transfer, enabling synergistic adsorption and visible-light reduction of Au(III) to Au(0). TAPP-TZ-OMe-COF delivers a gold recovery capacity of 4,109 mg g⁻¹ and achieves 99.9% recovery from computer processing unit-board leachate with >10⁵-fold selectivity and excellent cycling stability. This molecular-engineering approach offers a generalizable blueprint for integrating adsorption and photocatalysis in COFs, advancing the recovery of gold from complex waste streams for sustainable resource reclamation.

Septic cardiomyopathy, a severe complication of sepsis, is characterized by high morbidity and mortality rates, and its effective management remains an important challenge. Although fibroblast growth factor 2 (FGF2) has been shown to exert cardioprotective effects, its role in septic cardiomyopathy has not been extensively investigated. To address this knowledge gap, FGF2 knockout (FGF2^−/−) mice were injected with lipopolysaccharide (LPS) to establish septic cardiomyopathy in vivo, and the resulting cardiac injury was evaluated after 72 h. The results demonstrated that LPS inhibited FGF2 expression in cardiomyocytes, and genetic ablation of FGF2 exacerbated myocardial inflammation, oxidative stress, apoptosis, and cardiac dysfunction. Notably, treatment with recombinant FGF2 (rFGF2) effectively reversed these detrimental effects. Proteomic analysis revealed that FGF2 significantly modulated mitophagy, and further verification assays confirmed that FGF2 prevented LPS-induced mitochondrial injury and followed apoptosis by activating FUNDC1-mediated mitophagy. Molecular studies demonstrated that rFGF2 triggered the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, leading to the activation of FUNDC1-mediated mitophagy, which in turn mitigated myocardial mitochondrial injury and apoptosis. These findings suggest that FGF2 exerts its cardioprotective effects in septic cardiomyopathy by activating the AMPK–FUNDC1-mediated mitophagy pathway, thereby providing a potential therapeutic strategy for mitigating sepsis-induced cardiac damage.

The cost-effective upcycling method of waste anode graphite (SG) presents an important challenge within the field of spent lithium-ion battery recycling. In this study, waste graphite was recovered from waste lithium-ion batteries by a one-step mechanochemical method and the high-efficiency graphene-based adsorbent OMG17 was synthesized. Following this, titanium dioxide microspheres (TiO₂) were integrated through electrostatic self-assembly to create an in situ photo-regeneration adsorbent, referred to as OMG17@TiO₂. The synthesized OMG17@TiO₂ exhibits a well-developed pore structure, characterized by regular crack-like pores and an abundance of functional groups. Furthermore, OMG17@TiO₂ was fabricated into a membrane via the vacuum filtration method, enhancing its practicality for collection in water bodies. The results indicate that the adsorption capacities of OMG17@TiO₂ for methylene blue and rhodamine B reached 673.67 and 966.58 mg/g, respectively, as determined by the Langmuir isothermal model, significantly exceeding the performance of comparable graphitic adsorbents. Additionally, the regeneration efficiency achieved through ultraviolet (UV) irradiation was found to be as high as 70%. In contrast to traditional desorption methods, the in situ photo-regeneration approach offers distinct advantages in preserving the structural integrity of the material, including the maintenance of pore structure and recovery of specific surface area. Through density functional theory calculations and an examination of the adsorption mechanism, it was established that the pore structure and oxygen-containing functional groups are the primary determinants of the adsorption capacity, while the in situ degradation of pollutants within the pores via UV light serves as the principal mechanism for regeneration.

Postinjury restenosis is a common complication of peripheral arterial disease treated via endovascular techniques. Its pathogenesis mainly involves neointimal hyperplasia and persistent inflammation. Although antiproliferative drugs used clinically can temporarily slow restenosis, their effects are limited by short action duration and lack of precise regulation. In this investigation, tRF-49:69-chrM.Trp-TCA (tRF-Trp-TCA) was identified through sequencing data from an animal restenosis model, and its regulatory effects on endothelial cell migration and inflammation were confirmed. Additionally, we discovered that cabbage exosome-like nanoparticles (CELNs) could precisely target injured blood vessels in vivo, enhance the stability of nucleic acid therapeutics, and more effectively inhibit neointimal hyperplasia in a carotid artery balloon injury model. Our results demonstrated that tRF-Trp-TCA is crucial in restenosis induced by arterial injury and CELNs loaded with tRF-Trp-TCA effectively inhibit neointimal hyperplasia following carotid artery injury in rats, showing good biocompatibility. This study has, for the first time, identified the target tRF-Trp-TCA for treating restenosis after vascular injury and has also, for the first time, used CELNs as the delivery system. This discovery could provide new insights for noninvasive treatments or mitigation of restenosis post-endovascular therapy.

Osteonecrosis of the femoral head (ONFH) is a progressive and disabling condition characterized by bone microenvironmental dysregulation, including imbalanced bone remodeling, impaired angiogenesis, and dysregulated osteoimmunity. In hip-preserving surgeries for early-stage ONFH, the most common approach is core decompression with grafting. Although widely used synthetic scaffolds, such as ceramics and metals, provide structural support or partially improve blood supply, they cannot counteract the complex pathological microenvironment of ONFH, resulting in poor long-term efficacy. To address these limitations, bioactive scaffolds incorporating functional agents have been developed to modulate pathological abnormalities and improve regenerative outcomes. This review summarizes recent advances in bioactive scaffolds for ONFH, focusing on systems functionalized with small molecules, growth factors, stem cells, exosomes, and metal ions that regulate cellular behaviors and signaling pathways in ONFH microenvironment. Emerging evidence indicates that osteoclasts exhibit heterogeneity, influencing resorptive, angiogenic, osteogenic, and immunoregulatory processes. Building on these insights, we discuss osteoclast heterogeneity and its potential relevance to ONFH, proposing that future scaffold strategies may harness osteoclast-mediated regulation to restore the osteonecrotic niche. By integrating mechanistic insights with material design, bioactive scaffolds provide a framework for targeted microenvironmental modulation and functional bone regeneration in ONFH.