The precise evaluation of real-world thermoelectric cooling (TEC) performance is vital for both the development of TEC devices, and for the rational design of TEC materials. Due to the relatively limited temperature difference (ΔT) that a single-stage TEC can achieve, the classical analytical formulae for thermoelectric cooling are commonly used with averaged material properties in the cooling performance evaluation. Nevertheless, this could cause remarkable errors in evaluations of the cooling power, even under a ΔT as low as 10 K. In this work, a cumulative model for thermoelectric cooling is proposed to evaluate the maximum coefficient of performance (COP) as well as the maximum cooling power of a TEC device under finite temperature differences, with the temperature dependence of material properties being fully considered. The inherent deficiencies in predicting the maximum cooling power by both the classical formulae and the original cumulative model are identified, and effective refinements are implemented to reduce the prediction error. Eight thermoelectric materials with state-of-the-art ZT values near room temperature are assessed for electronics cooling scenarios within a cold side temperature (T_c) range of 300-350 K. In comparison to the classical formulae, the proposed model predicts the maximum COP with comparably satisfying accuracies (±2%), while significantly improves the prediction accuracy of the maximum cooling power from approximately ±30% to within ±5% over a ΔT range of 10-70 K. This work fills the gap between thermoelectric material properties and device-level cooling performance, and is beneficial to the development and application of thermoelectric conversion technology for cooling purposes.

Photodynamic therapy (PDT) induces immunogenic cell death (ICD) through reactive oxygen species (ROS) generation, bridging localized tumor ablation with systemic antitumor immunity. However, the tumor microenvironment (TME) erects three barriers that intercept the PDT-immune cascade at distinct levels. The biochemical barrier, defined by chronic hypoxia and elevated antioxidant defenses, restricts ROS accumulation below the ICD threshold. The physical barrier, constructed by dense extracellular matrix and activated cancer-associated fibroblasts, confines photosensitizers to the tumor periphery and excludes effector immune cells. The immunosuppressive barrier, mediated by tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells, neutralizes immune activation signals even after successful ICD induction. These barriers are deeply coupled: breaching any single layer yields limited benefit when the others remain intact. This review examines how barrier-oriented PDT-immunotherapy strategies, particularly nanoplatform-enabled approaches, can relieve these three barriers and restore the PDT-immune cascade.

Aims: Spatially resolved omics technologies enable investigation of cellular interactions within their local microenvironments (neighbourhoods) directly in situ. Although several computational methods have been developed for neighbourhood analysis, significant limitations remain in how neighbourhoods are defined and interrogated. Here, we present Kandinsky, a toolkit that provides a flexible and versatile framework for defining and analysing cell neighbourhoods.

Methods: We developed Kandinsky to improve flexibility in neighbourhood analysis and maximise compatibility with a wide range of spatial omics data. We therefore implemented multiple approaches for identifying cell- or spot-based neighbourhoods that serve as input for four analytical modules: differential gene or protein expression analysis, neighbourhood clustering, co-localisation/dispersion, and spatial hot and cold areas. In addition to its core functionality, Kandinsky enables the execution of external tools within the same analytical framework.

Results: We applied Kandinsky to real and simulated spatial datasets to benchmark its performance against existing methods and demonstrate its ability to uncover biologically meaningful spatial interactions. Kandinsky achieved competitive performance in terms of accuracy, memory usage, and runtime. In real datasets, it suggested transcriptional changes associated with acinar-to-beta cell reprogramming in the healthy pancreas; recapitulated stromal, immune, and tumour-associated clusters in pancreatic cancer; revealed the spatial co-localisation of myoepithelial cells with specific breast cancer subpopulations; and confirmed the association between regions of high CD74 expression and immune cell infiltration.

Conclusions: Kandinsky is a flexible and versatile toolkit for neighbourhood analysis that facilitates the exploration and interpretation of complex spatial omics data.

Thermal transport at the nanoscale is fundamentally important and crucially impacts a range of applications from electronic chip cooling to advanced energy technology. Inspired by the rise of twistronics, twist engineering has recently emerged as a powerful approach to control nanoscale heat flow, which leverages interlayer rotation in van der Waals materials as a new degree of freedom. Here, we first briefly introduce the basic principles of twist engineering. Subsequently, we discuss various experimental techniques and computational approaches for investigating phonon-mediated heat conduction, together with key results and physical mechanisms for the active manipulation of both out-of-plane and in-plane transport. Furthermore, we review advances in the twist-induced modulation of photon-mediated thermal radiation, distinguishing strategies that tune intrinsic optical responses from those utilizing extrinsic couplings. We conclude with remarks on the opportunities and challenges for future exploration of twist-engineered thermal management and energy conversion.

P2-type layered manganese-based oxides are promising cathode materials for sodium-ion batteries (SIBs) but suffer from structural instability and irreversible phase transitions. This study demonstrates that iron doping in P2-Na_2/3Li_1/6Fe_1/6Mn_2/3O₂ (NLFM) effectively reconfigures the structural and redox chemistry. Structural and electrochemical analyses reveal that Fe³⁺ incorporation expands the Na⁺ interlayer spacing, enhances reversible cationic (Fe³⁺/Fe⁴⁺) and anionic redox activity, and promotes a dominant surface-controlled charge storage mechanism. Consequently, the NLFM cathode delivers a high initial capacity of 225 mAh·g^-1 at 0.1 C, an impressive initial Coulombic efficiency of 110.21%, and superior cycling stability (73.6% capacity retention after 100 cycles at 1 C). Furthermore, Fe doping effectively mitigates the Jahn-Teller distortion and mitigates the reversible P2 to O2 phase transition at high voltages. This work highlights the multi-functional role of iron doping in stabilizing the structure and optimizing the redox chemistry of P2-type cathodes, providing an effective strategy for developing high-energy and durable SIBs cathodes.

Ferroptosis is an iron-dependent form of programmed cell death defined by the lethal accumulation of lipid peroxides. Accumulating evidence indicates that ferroptosis plays a critical role in a wide range of pathological processes, including tumor progression, ischemia-reperfusion injury, and neurodegenerative diseases. The key determinants of cellular susceptibility to ferroptosis are the homeostasis of iron and lipid metabolism, whose maintenance relies heavily on the precise regulation of inter-organelle communication networks. In this review, we focus on the spatial biology of ferroptosis regulation. From three core dimensions, iron homeostasis modulation, lipid metabolism remodeling, and redox balance maintenance, we systematically dissect the mechanisms by which signal crosstalk and functional coordination among multiple organelles (lysosomes, endoplasmic reticulum, mitochondria, plasma membrane, nucleus, lipid droplets, Golgi apparatus and peroxisome) govern ferroptosis initiation, signal amplification, and cellular defense responses. Comprehensive elucidation of this multi-organellar coordinated regulatory network will not only advance our fundamental understanding of ferroptosis execution but also provide a holistic perspective for the development of organelle-targeted therapeutic strategies against human diseases.

Quantum theory departs from classical physics in its treatment of correlations, most prominently through the phenomena of contextuality and nonlocality. Once regarded primarily as foundational curiosities, these efects are now understood as key operational resources for quantum computation, communication, and simulation. Although traditionally investigated in distinct settings, recent theoretical and experimental advances have revealed deep conceptual, mathematical, and operational connections between them. This review presents a unified perspective on these developments based on sheaf-theoretic and graph-theoretic frameworks, which provide theory-independent characterizations of statistical correlations. These approaches clarify the structural relationship between contextuality and nonlocality, facilitate the formulation of experimentally testable inequalities, and guide implementations in realistic physical platforms, with particular emphasis on photonic systems. By bridging abstract theoretical structures and concrete experimental realizations, this review sheds light on the nonclassical foundations of quantum correlations and their emerging role in quantum technologies.

Ferroptosis is a form of regulated cell death driven by iron-dependent lipid peroxidation, and is therefore intrinsically coupled to cellular redox metabolism. Progression of ferroptosis is regulated by an integrated network of metabolic signaling pathways that involve inter-organellar communication. In this Review, we synthesize recent progress in the field that have advanced our understanding of the metabolic determinants of ferroptosis. We discuss key metabolites which participate in the execution and prevention of ferroptosis, describe major signaling axes that impinge on regulating these metabolic activities to determine cellular ferroptosis sensitivity, and highlight how compartmentalized metabolism within and across distinct intracellular organelles collectively shape ferroptosis progression. Together, this Review aims to provide a framework that unifies metabolic state, signaling plasticity and organellar cooperation as a mechanistic basis of ferroptosis, underscoring its implications in the pathogenesis of various diseases including cancer.

Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation. Inducing ferroptosis in tumor cells has emerged as a crucial strategy for cancer treatment and overcoming therapeutic resistance. Ferroptosis suppressor protein 1 (FSP1), identified in recent years, is a key ferroptosis-inhibitory factor that operates independently of glutathione peroxidase 4 (GPX4). FSP1 is highly expressed in multiple malignant tumors, and its expression levels are tightly associated with unfavorable patient prognosis, treatment resistance, and tumor progression. Specific stresses within the tumor microenvironment, including hypoxia, metabolic stress, and the development of drug resistance, can drive a shift in ferroptosis resistance mechanisms from GPX4-dependent to FSP1-dependent pathways. Such plasticity renders FSP1 a druggable target in specific cancer genotypes or at particular stages of tumor progression. Indeed, genetic or pharmacological inhibition of FSP1 has yielded potent antitumor effects across diverse preclinical models. This review systematically summarizes the structural characteristics of FSP1, the molecular mechanisms through which it suppresses ferroptosis, the multilayered regulatory networks controlling its activity, and its roles in different malignancies. We deeply analyze the plasticity of FSP1 dependency in tumor cells in vivo and comprehensively review the latest preclinical progress on small-molecule FSP1 inhibitors and related combinatorial therapeutic strategies. This review aims to establish a theoretical framework to support the clinical translation of FSP1-targeted antitumor strategies.

Alzheimer’s disease (AD) and related dementias are closely associated with alterations in microglial states. These microglial changes occur in response to amyloid-β (Aβ) accumulation and aberrant tau phosphorylation and can either protect against or exacerbate AD progression, depending on factors such as disease stage, genetic background, and environmental influences. This review focuses on recent advances in understanding the protective functions and features of microglia during the early stages of AD, while highlighting the outstanding questions regarding how these protective states deteriorate and become dysfunctional as the disease progresses. Interestingly, epidemiological studies have suggested an inverse relationship between AD and cancer incidence, and in this context we provide a comparative analysis of microglial phenotypes in AD and cancer to speculate how insights from anti-tumor microglia may inspire new strategies for reprogramming microglia to combat AD and related dementias.

Myeloid cells are central components of innate immunity and are highly responsive to environmental and lifestyle-associated cues. Among them, neutrophils are the most abundant circulating leukocytes in humans and have rapid turnover, traditionally leading to the view that they act mainly as short-lived effector cells. However, emerging evidence indicates that neutrophils can participate in trained immunity like responses through upstream reprogramming of hematopoietic stem and progenitor cells and the bone marrow niche. In this review, we discuss how lifestyle-associated factors shape neutrophil-associated immunity within the broader context of myeloid immune regulation, with a particular focus on long-term neutrophil functional reprogramming. We summarize current evidence that lifestyle and metabolic factors shape neutrophil production, mobilization, tissue recruitment, and effector programs. We further highlight that lifestyle induced neutrophil reprogramming is context dependent and may be either adaptive or maladaptive. Finally, we propose future directions for translating lifestyle-based immune modulation into strategies that limit chronic inflammation while preserving antimicrobial defense.

Selenium is an essential trace element that maintains cellular redox homeostasis through its incorporation into selenoproteins, including glutathione peroxidase 4, a key regulator of ferroptosis. Although selenium deficiency has long been linked to oxidative stress and lipid peroxidation, its significance in the context of ferroptosis has not been fully appreciated. In this review, building on our previous studies, we revisit selenium deficiency and impaired selenoprotein biosynthesis through the lens of ferroptosis. We summarize our findings that selenium deficiency induces a non-apoptotic, vitamin E- and deferoxamine-sensitive form of cell death associated with lipid peroxidation, and that selenium-deficient cells accumulate not only phospholipid oxidation products but also cholesterol oxidation products. We also discuss the possibility that cholesterol oxidation may represent a broader feature of membrane lipid peroxidation, as similar products are observed in cells exposed to the radical initiator. In addition, we highlight SECIS-binding protein 2 deficiency as a human model of impaired selenoprotein biosynthesis, in which increased linoleic acid and cholesterol oxidation products, together with their responsiveness to vitamin E, indicate progressive lipid oxidative damage in vivo. Finally, we discuss recent findings on peroxiredoxin 6 and arsenite, which suggest that toxicological disruption of selenium metabolism can suppress selenoprotein biosynthesis and increase ferroptosis sensitivity. By integrating these findings with recent advances in ferroptosis research, this review provides a perspective on how impaired selenium metabolism contributes to lipid oxidative damage and ferroptotic vulnerability.

This study develops a life-cycle techno-economic analysis and optimization framework for hybrid deep ground source heat pump (GSHP) systems, addressing the limitations of existing evaluations that often neglect subsurface thermal attenuation and rely on simplified heat transfer models. A coupled heat transfer model is established by combining the finite difference method for the borehole interior with the segmented finite line-source model for the surrounding ground, enabling long-term simulation of fluid and ground temperature evolution. The energy model is integrated with a life-cycle economic evaluation to calculate net present value, levelized cost of heating/cooling, payback period (PP), and internal rate of return. A Bayesian optimization algorithm is further employed to identify optimal system configurations under multiple objectives. The framework is applied to a hybrid geothermal system in Xi’an, China, incorporating mid-deep boreholes with auxiliary air-source heat pumps or gas boilers. Results show that long-term thermal attenuation significantly affects economic performance, with a 2 °C increase in fluid temperature extending the PP by approximately 0.3 years. User-side load uncertainty also has a substantial impact, as a 10% deviation from the design load can shift the optimal PP by about 2 years. Sensitivity analysis identifies the GSHP installed capacity ratio and borehole number as the most influential parameters. Compared with pure geothermal systems, the hybrid geothermal–gas boiler configuration achieves the shortest PP, demonstrating the framework’s effectiveness for robust low-carbon system design.

The microenvironment of solid tumors is characterized by dynamic availability of oxygen and persistent, complex inflammatory signaling. Accumulating evidence suggests that hypoxia and inflammation actively influence tumor progression and therapeutic response. In physiological conditions, hypoxic and inflammatory responses function as evolutionarily conserved protective mechanisms. Acute hypoxia promotes temporary metabolic adaptation to preserve tissue viability, while acute inflammation facilitates clearance of damaged or abnormal cells and restores homeostasis. In tumors, by contrast, hypoxia and inflammation become chronic and unresolved. Persistent activation of these protective signals gradually renders the microenvironment permissive to the sustained adaptation of abnormal cells rather than eliminating them. This transition from clearance to tolerance reshapes cellular metabolism, immune cell behavior, and tissue organization within the tumor microenvironment. As a result, tumor cells increasingly adapt to metabolic stress and evade effective immune surveillance, contributing to malignancy and therapy resistance. Interestingly, some subterranean species, including the naked mole rat and blind mole rat, show natural cancer resistance. They either evolved adaptations counteracting inflammation, or take the immune response to their advantage to prevent cancer. These anti-cancer mechanisms are a result of adaptation to their hypoxic subterranean habitats. In this review, we examine the fundamental features of hypoxia and inflammation in tumors, explore their functional interplay, and discuss how these mechanisms are evaded or harnessed by cancer resistant subterranean mammals. We further propose a simple clearance to resistance framework that links acute protective stress responses, chronic tumor-promoting adaptation, and naturally evolved cancer resistance.

Aging and cancer represent divergent fates of a common stress response. Senescence initially restrains malignancy through stable cell-cycle arrest and immune clearance, yet persistence of senescent cells and their secretory phenotype (SASP) paradoxically drives tumor progression, therapeutic resistance, and immune evasion via chronic inflammation and metabolic reprogramming. Functional genomic screening has evolved from bulk RNA interference to precision CRISPR modalities, including knockout, interference, activation, and base editing, and onward to single-cell and in vivo platforms. These technological advances have transformed our capacity to dissect cellular state transitions and network dependencies with unprecedented resolution. Here, we trace this technological evolution and synthesize its impact on aging and cancer research, with emphasis on chromatin regulation, metabolic rewiring, the SASP, nucleocytoplasmic transport, therapeutic response, and the tumor microenvironment. We emphasize that the current evidence derives predominantly from preclinical functional screens and computational predictions. We propose shifting from gene-centric discovery toward context-dependent network analysis. Integrating precise editing, in vivo screening, single-cell multi-omics, and emerging AI-assisted design may provide information and a design basis for future combined strategies that simultaneously target vulnerabilities in senescent cells and malignant populations.

Antibody polyreactivity refers to the ability of a monoclonal antibody to non-specifically bind to a diverse range of antigens. While this property may be an intrinsic mechanism of the immune response, it poses significant challenges in therapeutic antibody development, often leading to off-target effects, poor pharmacokinetics, and potential toxicity. This review compiles the data resources related to polyreactive antibodies and places a particular emphasis on computational models for predicting antibody polyreactivity. The latter includes empirical models based on physicochemical properties, traditional machine learning models, deep learning networks, and protein language models. Through delineating the complexity of antibody polyreactivity, this review emphasizes the critical role and growing potential of computational prediction tools in selecting and engineering antibody drug candidates at early stages, thereby reducing development risks and accelerating the development of safer and better therapeutic antibodies.

Aims: This study aimed to characterise the natural killer (NK; CD3^-CD16⁺CD56⁺) and monocyte compartments in 54 participants by analysing absolute cell counts in relation to age, sex, cytomegalovirus (CMV) serostatus, an established marker of immune ageing, and interleukin-6 (IL-6) values, as an indicator of inflamm-ageing.

Methods: The analysis was conducted in a cohort of Sicilians (28 females and 26 males) aged 19-110 years, including 20 adults (19-64 years), 15 older adults (68-88 years), 11 long-living individuals (93-104 years), and 8 semi- and supercentenarians (105-110 years; hereafter referred to as the oldest centenarians). Multiple negative binomial regression models were used to assess the independent effects of age, sex, CMV serostatus, and IL-6 concentrations on NK and monocyte counts.

Results: Although NK cells and monocytes are generally reported to increase with age, adjustment for covariates revealed that NK cell counts showed only a non-significant age-related trend. In contrast, no statistically significant independent association with age was detected for monocytes. A statistically significant sex effect emerged, with men exhibiting higher NK cell counts than women. Monocyte counts were significantly and positively associated with IL-6 levels.

Conclusion: These findings suggest that previously reported associations of advanced age, particularly extreme longevity, with higher NK-cell and monocyte counts may not be independent of sex, in the case of NK cells, or of chronic low-grade inflammation, as reflected by IL-6 levels, in the case of monocytes. Given the observational design, these results should be interpreted as adjusted associations rather than evidence of mediation or causality.

In the past decades, multi-functional materials have attracted significant attention for applications in electromagnetic interference (EMI) shielding, thermal management, and intelligent sensing. Extensive efforts have focused on developing conductive composites with enhanced functional performance. Increasing evidence indicates that the structural characteristics of conductive networks play a decisive role in determining material properties. Among various structural engineering strategies, oriented conductive networks have emerged as a highly effective platform for optimizing charge transport, heat transfer, and electromagnetic wave attenuation through the deliberate alignment of functional fillers. Unlike isotropic networks, oriented architectures provide new opportunities for achieving high performance with reduced filler loading by forming anisotropic transport pathways. This review systematically summarizes recent advances in multi-functional materials based on oriented conductive networks, with particular emphasis on the underlying structure–property relationships governing sensing, EMI shielding, and thermal management performances. The effects of filler characteristics, orientation degree, and structural features on functional properties are critically analyzed. More importantly, this review highlights oriented conductive networks as a universal structural design strategy for multifunctional materials and discusses emerging opportunities associated with advanced fabrication technologies, AI-assisted materials design, and integrated material–structure engineering. Finally, the remaining challenges and future perspectives regarding scalability, structural precision, reliability, and multifunctional integration are discussed to guide the future development of next-generation multifunctional composites.

Over decades, nomenclature in erythrocyte cell death research has been unrefined. Recently, several attempts have been made to adapt the nomenclature suggested by the Nomenclature Committee on Cell Death (NCCD) guidelines to erythrocytes. Within the framework of the standardization of terms used in erythrocyte cell death studies, erythrocyte senescence and eryptosis, a regulated cell death of erythrocytes, have been defined and the formal distinction between both events has been recently established. Differences in their physiological role have been underscored, and markers that can be used to distinguish between erythrocyte senescence and eryptosis have been identified. As a further step, we aim to dissect cellular senescence in nucleated cells and erythrocytes, identifying their hallmarks, key triggers, molecular mechanisms, immunity-related effects, as well as physiological aspects. Available evidence suggests that cellular senescence in nucleated cells can be considered an active biological program, while erythrocyte senescence rather reflects a more passive, gradual accumulation of cellular damage. Fundamental mechanism-based and physiological differences between senescence in nucleated cells and erythrocytes highlighted in this mini-review indicate that the use of the term ‘erythrocyte senescence’ should be discouraged as misleading. Instead, the term ‘erythrocyte aging’ might be more appropriate.

Z-nucleic acid-binding protein 1 (ZBP1) is a cytosolic innate immune sensor that detects left-handed Z-DNA and Z-RNA, structures arising from endogenous retroelements, splicing stress, R-loops, viruses, or viral mimicry. Originally viewed as an antiviral receptor, ZBP1 has emerged as a sentinel of genomic and transcriptomic instability. Upon ligand binding, ZBP1 recruits receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and receptor-interacting serine/threonine-protein kinase 3 (RIPK3) via RIP homotypic interaction motif domains; in humans, RIPK1 acts as an essential scaffold to form the necrosome, which phosphorylates mixed lineage kinase domain-like pseudokinase (MLKL) and triggers necroptosis, a lytic, immunogenic cell death. This pathway is intimately regulated by reactive oxygen species (ROS): oxidative stress promotes RIPK1 activation, and necroptosis further drives a mitochondrial ROS burst, establishing a feed-forward amplification loop. In cancer, therapeutic induction of viral mimicry (e.g., using curaxins or splicing inhibitors) combined with tumor-localized ROS generation activates ZBP1-driven necroptosis, leading to the release of damage-associated molecular patterns and tumor antigens. This process converts immunosuppressive “cold” tumors into inflamed “hot” tumors, enhancing dendritic cell maturation, CD8⁺ T cell infiltration, and sensitivity to immune checkpoint blockade. Integrating epigenetic priming, nanomedicine, and patient stratification according to ZBP1/RIPK3/MLKL pathway status holds promise for overcoming therapeutic resistance. Thus, ZBP1-mediated nucleic acid surveillance represents a central innate checkpoint bridging genomic stress to antitumor immunity.

Immune checkpoint inhibitors, like PD-1/PD-L1 blockers, have revolutionized cancer treatment in recent years. However, these therapies still face many problems, such as low objective response rates and drug resistance, making clinical treatment very difficult. Numerous studies have demonstrated that the heterogeneity of the tumor microenvironment (TME), including various subtypes such as “cold tumors”, “hot tumors”, and “immune-rejecting tumors”, as well as complex immunosuppressive mechanisms, is a major factor leading to resistance to immunotherapy. Chemotherapy and radiotherapy can aid in treatment by inducing immunogenic cell death, but they often lead to PD-L1 upregulation, which causes treatment effects to vary over time and space and reduces their efficacy. Given their excellent biocompatibility, drug delivery capacity, and responsiveness to environmental factors, nanomaterials offer a novel opportunity to address this challenge. This review explores sequential nanoregulation strategies based on different types of TME, describes how functionalized nanocarriers, such as stimulus-responsive polymers, liposomes, and biomimetic nanoparticles, can be used to detect changes in the microenvironment, like pH, enzymes, and reactive oxygen species, and to precisely deliver drugs when needed. This will allow researchers to target key points of immune activation, thereby blocking immune checkpoint signaling. These specific strategies, which include antigen release, immune system activation, and blocking interventions, not only offer new approaches for overcoming PD-L1 resistance but also shed light on the challenges and opportunities associated with applying these strategies in clinical practice.

Supercapacitors (SCs) are critical for high-power energy storage, yet their practical deployment is still limited by insufficient energy density. MXenes have emerged as promising electrode materials owing to inherent metallic conductivity, hydrophilic terminations, and intercalation pseudocapacitance, but suffer from layer restacking and oxidative degradation. Hybridizing MXenes with 3D carbon scaffolds offers a synergistic strategy by providing interlayer spacers, hierarchical ion transport pathways, and oxidation barriers. To the best of our knowledge, this review is the first to systematically couple the structural design of MXene/3D-carbon composites with machine learning (ML) guided optimization, summarizing recent advances in MXene/3D-carbon composite electrodes. This review systematically evaluates MXene etching routes and representative composite assembly strategies, and classifies existing systems into three structural categories, critically comparing their performance metrics, strengths, and inherent limitations. It further highlights the frontier applications of ML in performance prediction, compositional optimization, and mechanical design, along with current challenges, including data bias, the black-box nature of models, and the gap between idealized predictions and real synthesis. Overall, this work aims to provide a framework for integrating advanced synthesis strategies, 3D architectures, and data-driven tools toward the rational design of high-performance SCs.

Somatic mutations accumulate in tissues throughout life and are increasingly being recognized as contributors to aging. While their role in cancer has been extensively characterized, their occurrence and functional impact in the cardiovascular system remain poorly understood, partly due to technical limitations in detecting low-frequency and cell-specific variants. Recent advances in single-cell sequencing have begun to unveil how somatic mutations accumulate both in vascular resident cells, including vascular smooth muscle cells, and in circulating hematopoietic cells, such as those associated with clonal hematopoiesis of indeterminate potential. Both resident vascular cells and infiltrating immune cells harboring clonally expanded somatic mutations may influence vascular pathology. This mini-review summarizes the current knowledge on somatic mutation accumulation in the vasculature, focusing on recent studies and the techniques applied for their detection. In addition, we discuss emerging evidence for the functional relevance of somatic mutations in aging and age-related vascular disease.

Cancer recurrence remains a leading cause of mortality in patients with solid tumors. Early disseminated tumor cells (DTCs), which seed distant organs during the initial stage of tumor progression, are widely recognized as an important source of late metastatic relapse. Tumor cell dormancy, a reversible but prolonged non-proliferative state, enables DTCs to survive in metastatic tissues for years or even decades before re-entering the cell cycle and giving rise to overt metastases. Accumulating evidence indicates that dormancy is regulated by both cell-intrinsic mechanisms, such as epigenetic reprogramming and metabolic adaptation, and extrinsic cues from the tissue microenvironment. Among these extrinsic regulators, ageing has emerged as a critical determinant of DTC fate by profoundly remodeling tissue microenvironments through cellular senescence, chronic inflammation, extracellular matrix (ECM) remodeling, vascular dysfunction, stromal metabolic rewiring, and immune dysregulation. These ageing-associated alterations progressively erode dormancy-supportive niches, thereby leading to metastatic reactivation. In this Review, we summarize the molecular mechanisms governing tumor dormancy and discuss how ageing-associated microenvironmental remodeling contributes to the reactivation of dormant DTCs. We highlight the roles of the senescence-associated secretory phenotype (SASP), ECM remodeling, vascular deterioration, and organ-specific stromal ageing in regulating the maintenance and exit of tumor dormancy. We also discuss emerging translational opportunities, including dormancy-reinforcing therapies, senolytic strategies, liquid biopsy-based surveillance, and advanced experimental platforms such as single-cell and spatial technologies. Collectively, this Review provides a conceptual framework for understanding how ageing progressively modulates tumor dormancy and highlights potential strategies to prevent late metastatic recurrence.

The flight of insects exemplifies nature’s use of resonance to achieve large-amplitude, high-frequency motion with exceptional energy efficiency. Emulating this resonant amplification effect (RAE) in artificial systems remains a key challenge in soft robotics. Conventional dielectric elastomers (DEs) can be tuned electrically but rely on in-plane deformation. This generates insufficient inertial forces for resonance and thus requires rigid external frames, which consequently add fabrication complexity and reduces energy density. Here, we present a material-level approach to achieve intrinsic resonance amplification using space charge-driven dielectric elastomers (SC-DEs), which generate asymmetric electric fields and self-induced bending without external support. The optimized materials exhibited efficient actuation at low driving fields (~1 V μm^-1), with bending angles amplified from 20° to 150° through resonance without increasing field strength. This work establishes a framework for realizing resonance-amplified electromechanical actuation intrinsically within soft materials, offering new design routes toward lightweight, energy-efficient, and high-performance soft robotic systems.