Aims: Smartphone Augmented Reality (AR) enables social applications, but single-point Inverse Kinematics (IK) avatar tracking limits pose expressiveness and introduces positional errors. We introduce DPIK, a dual-point tracking system combining hand IK with face tracking, and evaluated whether it improves tracking accuracy, embodiment, and user experience over single-point IK.

Methods: DPIK uses the front and back cameras of ARKit to track the face of the user and hand/device pose, driving avatar hand IK and hip/head positioning. In a within-subjects study (N=20), we compared DPIK against our prior single-point IK system (ARIKA) and full-body motion capture (ground truth) across positional/rotational accuracy, embodiment, and user experience. We also examined temporal drift in tracking error and Spearman correlations between error and embodiment/user experience scores.

Results: DPIK significantly outperformed ARIKA in positional accuracy for 18 of 19 joints and reduced head rotational error by over . A temporal drift analysis found that neither ARIKA nor DPIK exhibited statistically significant growth in positional error over time. DPIK received significantly higher overall user experience ratings than ARIKA. Embodiment differences were not statistically significant, though effect sizes were moderate-to-large. Exploratory correlations suggested lower DPIK embodiment scores for Acceptance and Control with higher positional error, but these did not survive multiple-comparison correction; positional error did not predict user experience ratings for either technique.

Conclusion: DPIK improves tracking accuracy and user experience over ARIKA, with tracking fidelity selectively shaping embodiment rather than overall user experience, highlighting a distinction between perceptual ownership and holistic evaluation of smartphone AR avatar systems.

Advanced age is associated with immune decline and remodeling, including loss of adaptive reserve, impaired host defense, and chronic low-grade inflammation. Yet the immune phenotype of long-lived individuals (LLIs), especially centenarians, shows that immune aging is not a uniform process. Rather than reflecting global rejuvenation, longevity-associated immunity is better understood as selective preservation of immune competence, with selected cellular features retaining youth-like characteristics under the constraints of extreme age. The most direct cellular evidence comes from innate effector functions, including preserved natural killer (NK)-cell cytotoxic surveillance and neutrophil chemotaxis, phagocytosis, and redox control. T-cell findings are more heterogeneous, including maintenance of a non-inverted CD4/CD8 ratio and partial naive CD4⁺ T-cell reserve, while Th17/Treg data provide more limited support for preserved regulatory-inflammatory balance. Myeloid and antigen-presenting-cell programs may further support clearance and antigen handling, although direct functional evidence remains more limited. Molecular studies point to candidate support layers rather than proven causal mechanisms, including coordinated immune-cell states and communication, survival and apoptosis-regulatory programs, ribosome-inflammation balance, autophagy-lysosomal and mitochondrial quality control, and buffering of inflammatory and senescence-associated signals. Importantly, some immune changes reported in LLIs fall outside the youth-like frame: cytotoxic and effector-memory T-cell states and repertoire remodeling, humoral shifts, and complement changes are better interpreted as adaptive remodeling whose occurrence and significance depend on lifelong immunological experience. This framework places selective preservation of immune competence at the center of LLI immune biology while distinguishing it from experience-shaped adaptive remodeling.

Aims: Ferroptosis, an iron-dependent form of regulated cell death, has emerged as a major contributor to neuronal injury following ischemic stroke. Because our previous cancer-cell screens identified ataxia-telangiectasia mutated (ATM), a DNA damage response kinase, as a ferroptosis regulator, we investigated whether ATM inhibition protects neural tissue after ischemic stroke and examined determinants of therapeutic response.

Methods: ATM inhibitors, including the brain-penetrant clinical compound AZD1390, were evaluated in cultured cancer and neuronal cells, oxygen-glucose-deprived organotypic rat and mouse brain slices, and permanent middle cerebral artery occlusion models using multiple inbred and Rabep2-genotype mouse strains. Cell viability, cytotoxicity, lipid peroxidation, ferroptosis-associated markers, infarct volume, and collateral vessel density were assessed. Topical AZD1390 was also tested in mice with impaired collateral networks.

Results: ATM inhibition reduced ferroptosis-associated lipid oxidative injury and protected neurons in multiple preclinical models of stroke. AZD1390 significantly decreased lipid peroxidation, protected neurons from cell death, and limited infarct volume in B6/J and B6/NJ mice, but not in BALB mice. Strikingly, treatment efficacy varied among mouse strains and correlated with differences in the collateral vascular network. The protective effect of systemic AZD1390 was similarly lost in Rabep2-knockout mice with deficient collateral networks. The efficacy of oral AZD1390 was associated with collateral vascular density. Early topical administration also reduced infarct volume in mice with limited collateral networks; however, differences in treatment timing and route prevent direct attribution of this effect to improved local drug delivery.

Conclusion: This work implicates ferroptosis-associated lipid oxidative injury in ischemic neuronal death, identifies ATM inhibition as a candidate translational strategy warranting further mechanistic validation, and highlights collateral vascular anatomy as a potential factor associated with therapeutic response. Collectively, these findings broaden the pathophysiological and translational framework for ferroptosis-targeting strategies in stroke.

Pancreatic cancer is a highly aggressive and lethal malignancy with an exceptionally poor prognosis. Its clinical management is severely hampered by insidious early symptoms, strong invasiveness, intrinsic chemoresistance, and limited efficacy of conventional therapies. Carbon dots (CDs) have shown great promise in precision cancer theranostics owing to their excellent optical properties, high biocompatibility, controlled drug loading and release capabilities and customizable targeting features. This review critically examines the major therapeutic barriers in pancreatic cancer management, systematically summarizes the applications of CDs in pancreatic cancer imaging, targeted drug delivery, hyperthermia and pH-responsive theranostics, analyzes the current limitations of CD-based nanosystems, and discusses future development directions. This work aims to provide a rigorous theoretical foundation for the rational design and development of novel CD-mediated precision intervention strategies for pancreatic cancer.

The incorporation of multiple stereogenic elements into a single molecule can profoundly influence its biological and physical properties. However, the direct enantioselective synthesis of atropisomers bearing both axial and central chirality remains a significant challenge. Herein, we report an efficient kinetic resolution strategy based on a Michael addition/O-alkylation cascade between racemic bromonitroalkenes and 2-naphthols. This methodology enables the simultaneous synthesis of atropisomers featuring multiple stereogenic elements while recovering axially chiral bromonitroalkene building blocks with excellent stereoselectivities (up to 98% ee and > 20:1 dr, with a selectivity factor S up to 259). The reaction accommodates a broad range of electronic and steric substituents on both the nitroalkene and the naphthol components, as well as variation of the fused aromatic ring system. The synthetic utility of the approach was further demonstrated through gram-scale synthesis, parallel resolution, and the transformation of the recovered (aR)-bromonitroalkene into diverse atropisomeric architectures and the construction of various bis-axially chiral atropisomers via central-to-axial chirality transfer. A plausible transition-state model was proposed to rationalize both the stereochemical outcomes and the role of DABCO as a co-catalyst. This work provides a practical and versatile platform for accessing structurally complex molecules with multiple stereogenic elements and expands the synthetic toolbox for constructing chiral molecular architectures.

Aims: Circular RNAs (circRNAs) act as vital miRNA sponges and participate in the pathogenesis of various complex diseases. Most existing computational methods focus on sequence-level prediction of circRNA-miRNA interactions, while few tools can accurately locate interaction sites at the nucleotide level.

Methods: In this study, we propose CMIFCG, a novel model combining fully convolutional neural networks (FCN) and bidirectional gated recurrent units (BiGRU) for nucleotide-level prediction of circRNA-miRNA interaction sites. We adopted one-hot encoding for sequence preprocessing, utilized stacked convolutional modules to extract high-order features, and integrated BiGRU to capture sequential association features. The decoding module with skip connections restores feature maps to the original sequence size for precise site prediction. We constructed four datasets with different sequence lengths and negative samples to evaluate model performance.

Results: Experimental results show that CMIFCG achieves optimal performance than other baseline models, and excessive module stacking causes performance degradation. Motif analysis confirms that the predicted motifs match well with known miRNA sequences. Partial predicted interactions are further verified via public databases.

Conclusion: In summary, CMIFCG model enables effective fine-grained identification of circRNA-miRNA interaction sites, providing a new tool for exploring circRNA regulatory mechanisms and disease-related molecular pathways.

Proton exchange membrane water electrolysis (PEMWE) is regarded as a practical hydrogen production method due to its advantages such as smaller resistance loss, higher current density, and higher hydrogen purity. However, the efficiency of PEMWE technology is severely hindered by the slow kinetics and the high reaction barrier of the oxygen evolution reaction (OER). Therefore, developing cost-effective, efficient, and stable OER electrocatalysts is urgently needed. The RuO₂-based elec-trocatalysts have been proven to be promising alternatives to Ir-based catalysts due to their excellent electrocatalytic activity and high adaptability in acidic environ-ments. This review comprehensively summarizes and discusses the morphological control strategies, advanced modification strategies, and structural synergy of RuO₂ catalysts. Furthermore, the composition and industrial development status of PEMWE are elaborated, along with the current research progress of RuO₂ as an an-ode in electrolysis. Finally, relevant suggestions for RuO₂ research and practical ap-plications are presented, the challenges facing practical deployment are analyzed, and future research directions are outlined.

Aims: Ferroptosis is a form of cell death associated with uncontrolled lipid peroxidation of polyunsaturated fatty acids (PUFAs) leading to membrane destruction. We previously showed that dietary dihomo-gamma-linolenic acid (DGLA) induces ferroptosis in Caenorhabditis elegans germ cells in a dose-dependent manner, and that the sensitivity of germ cells to dietary DGLA is altered by many genetic, dietary, and chemical interventions.

Methods: The severity of germ cell death was documented after dietary supplementation of DGLA, vitamin B12, methionine, and choline to wild type and mutant Caenorhabditis elegans (C. elegans). The presence of germ cells, gametes, and embryos was visualized in young adult worms with 4′,6-diamidino-2-phenylindole (DAPI).

Results: The addition of vitamin B12 rescued DGLA-induced cell death. For this protection, vitamin B12 functions as a cofactor for methionine synthase (METR-1). In addition, dietary methionine and choline rescued germ cell death in the context of low-B12 diets as well as in ferroptosis-sensitive metr-1 and sams-1 mutant strains. The pcyt-1 mutant worms, with reduced capacity for phosphatidylcholine (PC) synthesis, were not responsive to dietary vitamin B12-mediated rescue of DGLA-induced ferroptosis, providing evidence that PC synthesis and homeostasis play key roles in ferroptosis susceptibility. Oleic acid supplementation rescues DGLA-induced cell death in wild type, but not in pcyt-1 mutant strains.

Conclusion: These studies reveal the requirement for dietary vitamin B12 and sufficient PC synthesis in protection from dietary DGLA-induced ferroptosis, highlighting the importance of phospholipid metabolism in ferroptosis regulation.

Ferroptosis is an iron-dependent form of regulated cell death that has attracted considerable attention as a promising therapeutic strategy because of its ability to eliminate tumor cells. However, tumors are multicellular ecosystems in which malignant cells coexist with diverse stromal and immune cell populations that critically shape tumor progression, anti-tumor immunity, and therapeutic responses. Emerging evidence indicates that ferroptosis exerts fundamentally distinct biological effects across these non-malignant cell populations, extending far beyond direct tumor cell killing. In this review, we propose a cell type-centered conceptual framework in which the consequences of ferroptosis are determined primarily by cellular context rather than by ferroptosis itself. While ferroptosis resistance enables certain cell types, such as fibroblasts and macrophages, within the tumor microenvironment (TME) to maintain tumor-promoting functions, ferroptosis compromises the persistence and effector activity of cytotoxic lymphocytes, including CD8⁺ T cells and natural killer cells. Conversely, ferroptosis in neutrophils and polymorphonuclear myeloid-derived suppressor cells may generate oxidized lipid mediators that paradoxically reinforce immune suppression despite reducing cell abundance. Therefore, in this review, we integrate recent advances in understanding ferroptosis across major nonmalignant cell populations within the TME, focusing on its effects on cell fate, functional plasticity, and anti-tumor immunity. We further discuss how these insights may guide the development of precision ferroptosis-based therapies that selectively target tumor-promoting cell states while preserving protective immune responses.

DNA replication and transcription operate on the same chromatin template and inevitably interfere with one another, giving rise to transcription-replication conflicts (TRCs), an important endogenous source of replication stress and genome instability. Although head-on (HO) conflicts are generally more disruptive than co-directional (CD) encounters, orientation alone does not determine the outcome. Gene architecture, transcriptional activity, replication timing, chromatin environment, DNA topology, and R-loop dynamics can all influence whether an approaching replication fork pauses, collapses, or traverses a transcribed region. Recent single-molecule, genomic, and biochemical studies further suggest that some CD encounters can be traversed under favorable topological and transcriptional conditions, although the mechanisms that permit such bypass and their broader biological significance remain incompletely understood. Here, we discuss TRC control within an operational framework comprising prevention, resolution, tolerance, and recovery. We examine how cells coordinate replication and transcription in space and time, regulate R-loop formation and turnover, protect or remodel challenged forks and chromatin, and modify or remove transcription complexes at conflict sites. We also consider how emerging single-molecule and multi-omic approaches can distinguish transient fork pausing from persistent pathological conflicts. Finally, we discuss the contributions of TRCs to cancer-associated chromosomal instability, cellular senescence, and neurodegenerative disease, and highlight the questions that must be resolved to understand how cells preserve genome integrity when replication and transcription compete for the same DNA template.

DNA replication constantly faces obstacles that threaten genome stability. Faithful duplication requires replication forks to smoothly process template damage, chemical or topological blocks, and repair intermediates. Traditionally, replication-associated lesions are described by their initial structures (nicks, gaps, etc.). However, their S-phase identities are highly transitional: a template single-strand break (SSB) can become a one-ended double-strand break (DSB) upon fork arrival, a replication fork stalled by a template block can reverse, restart, or collapse, and a repriming event leaves a post-replicative single-stranded DNA (ssDNA) gap. The biological consequence of a lesion depends heavily on its structural transitions and how it is "routed" through distinct repair, bypass, or cleavage pathways. In this review, we shift our focus from static structural identities to dynamic lesion routing, emphasizing the coordination between SSB repair (SSBR) and DSB repair (DSBR). We first summarize the major sources of replication-associated strand lesions, and then discuss how strand lesions are managed across three processing windows: SSBR before fork encounter, the overlap zone in which gaps and stressed forks can be buffered without immediate DSB conversion, and broken-fork/DSBR-centered processing after DSB formation, including homologous recombination (HR)-mediated restart, break-induced replication (BIR)-like synthesis, or end joining. Depending on the routing network, lesion processing can result in accurate completion, delayed resolution or salvage, mutagenic completion, structural genome scars, or cytotoxic genome instability. Finally, we discuss how this dynamic framework refines our understanding of DNA damage response (DDR)-targeted cancer therapies, drug resistance, and treatment outcomes in different genetic or therapeutic contexts.

At cryogenic temperatures, thermal transport is predominantly governed by long-wavelength acoustic phonons with exceptionally long intrinsic mean free paths, leading to significant departures from the diffusive transport behavior characteristic of room temperature. Understanding these transport mechanisms is essential for emerging technologies, including quantum computing, cryogenic electronics, and aerospace systems. This review summarizes the fundamental physics governing phonon-mediated thermal transport in the cryogenic regime. We first introduce the classical Casimir-Knudsen framework for geometry-limited transport and then discuss how this picture is modified by reduced dimensionality, competing scattering mechanisms, collective phonon transport, and wave effects. Particular emphasis is placed on the physical origins of thermal-conductivity behaviors that deviate from the conventional T³ scaling. We further examine the implications of cryogenic phonon transport for self-heating and thermal management in electronic and quantum devices. Finally, we identify key unresolved questions, particularly regarding predictive modeling and thermal management in cryogenic quantum devices. By providing a unified overview of recent advances, this review aims to stimulate further progress in the fundamental understanding and engineering of thermal transport at cryogenic temperatures.

Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation. Its execution depends not only on the amount of lipid peroxides, but also on where oxidizable lipids, redox-active iron, reactive oxygen species, and antioxidant defenses are distributed within cells. This review summarizes current evidence for organelle-resolved regulation of ferroptosis and oxidative stress, with emphasis on the endoplasmic reticulum, peroxisomes, mitochondria, lysosomes, lipid droplets, and phase-separated condensates. We discuss how lipid remodeling, ether lipid synthesis, mitochondrial metabolism and local antioxidant defense, ferritinophagy, lysosomal lipid peroxidation, and lipid droplet-mediated fatty acid buffering influence ferroptosis sensitivity. We also summarize how organelle-specific redox defenses and stress-adaptive signaling pathways may shape therapeutic responses. Together, these studies show that ferroptosis is regulated by coordinated changes in lipid metabolism, iron handling, and antioxidant capacity across distinct subcellular compartments.

Aims: Severe COVID-19 is characterized by marked heterogeneity in lung pathology, including diffuse alveolar damage, inflammation, and fibrosis. However, how spatially organized cellular interactions contribute to these divergent pathological outcomes remains incompletely understood. We aimed to define the spatial organization of cellular microenvironments in severe COVID-19 lungs and identify niche-specific cellular interactions associated with distinct histopathological states.

Methods: We applied imaging-based single-cell spatial transcriptomics to post-mortem lung tissues from patients with severe COVID-19 and control subjects, enabling high-resolution mapping of cellular composition, spatial neighborhoods, and predicted ligand-receptor interactions within intact tissue architecture.

Results: Analysis of 76,973 cells identified 20 distinct cell populations and revealed marked heterogeneity between COVID-19 samples, corresponding to different histopathological states. Spatial niche analysis identified discrete macrophage-associated microenvironments. Fibrotic niches were enriched in CHI3L1/MMP9^hi macrophages spatially associated with COL1A1⁺ fibroblasts and basal cells. Ligand-receptor inference predicted macrophage-derived TGF-β and galectin-3 signaling as drivers of pathogenic fibroblast activation and extracellular matrix remodeling. In contrast, alveolar niches contained SPP1^hi macrophages exposed to epithelial-derived cues, including WNT ligands and GM-CSF, consistent with differentiation toward an alveolar macrophage-like state.

Conclusion: Severe COVID-19 lungs are organized into distinct spatial niches associated with divergent immunopathological trajectories. Imaging-based spatial transcriptomics provides a framework to link histopathological states with localized cellular interactions and macrophage-driven tissue remodeling programs.

The tumor immune microenvironment (TIME) is a principal determinant of tumor progression, metastatic dissemination, and therapeutic response. Cellular senescence, primarily through the senescence-associated secretory phenotype (SASP), progressively reshapes the TIME toward immunosuppressive and therapy-resistant states. Here, we propose an integrative framework of “senescence-associated transcriptional reprogramming” comprising three mechanistic layers: endogenous inflammation-driven signaling centered on the cGAS-STING-NF-κB-IFN hub; lineage-specific epigenetic lock-in in immune cells; and metabolic-epigenetic coupling. We further discuss mechanism-guided, temporally optimized senolytic and senomorphic strategies, particularly relevant to elderly cancer patients, to rationally reverse senescence-driven tumor immune tolerance and enhance current immunotherapies.

Electrochromic devices (ECDs), featuring passive optical modulation, backlight-free operation, and bistable low-power characteristics, are promising candidates for energy-efficient display applications. However, wide-gamut color modulation in electrochromic displays is hampered by both the narrow spectral tunability of conventional materials and the fabrication complexity of existing wide‑gamut devices. Herein, we develop an approach to achieving reversible wide-gamut color switching by depositing ellipsoidal metallic nanoparticles and an electrochromic WO₃ layer in series. Specifically, the dielectric environment surrounding the metallic nanoparticles is dynamically altered by electrochemically modulating the refractive index of the WO₃ layer, enabling precise tuning of the localized surface plasmon resonance absorption peak. As a result, a broad collective color gamut spanning the visible spectrum is achieved through Ag NP dimension engineering. In addition, the Ag nanoparticles (NPs)/WO₃ working electrode exhibits a low electrode-level average coloration power density of 4 W m^-2. We believe the results demonstrated in this work provide a new strategy for electrochromic display devices.

Zeolite materials, featuring well-defined pore architectures, tunable framework structures, ion-exchange capability, and favorable thermal stability, have been widely utilized in catalysis, adsorption, and separation processes. Recent advances in synthetic strategies and functional modification have further extended their utility into a diverse range of emerging interdisciplinary fields. This review systematically surveys recent progress in zeolite synthesis and applications, with particular emphasis on elucidating the relationships among synthetic strategies, structural modulation, and resultant performance. Representative synthetic approaches, including hydrothermal, sonochemical, microwave-assisted, mechanochemical, dry-gel conversion, and molten-salt synthesis, are discussed in terms of their effects on crystal size, morphology, pore hierarchy, and framework composition. The emerging applications of zeolite materials in biomedicine, energy storage and conversion, and intelligent sensing are subsequently examined. In biomedical contexts, zeolite materials have shown promise in drug delivery, bone regeneration, diagnostic imaging, and wound hemostasis, attributable to their controllable loading behavior, favorable ion-release properties, and biocompatibility. As for energy-related applications, they have been employed in electrochemical energy storage, separator modification, hydrogen storage, and thermal energy storage, achieved through precise pore structure regulation and interface engineering. In the realm of intelligent sensing, zeolite materials have evolved from passive sieving media into active functional components with enhanced selectivity and signal responsiveness. This review provides a comprehensive overview of recent advances in the synthesis and functional applications of zeolites and discusses their prospects across a broad range of emerging interdisciplinary fields.

Aims: Human leukocyte antigen (HLA) polymorphism influences immunity by balancing protection against pathogens with the preservation of self-tolerance. This balance has been proposed to affect longevity, and associations with HLA variants have been reported. However, studies in this field have often yielded inconsistent findings due to small sample sizes and low-resolution genotyping methods. We aimed to identify HLA alleles linked to longevity while overcoming these previous limitations.

Methods: We performed high-resolution HLA genotyping using targeted sequencing (HLA-seq) in 1,265 long-lived individuals (long-lived individuals (LLI); ≥ 94 years) from Germany and compared their HLA allele frequencies with those of a large control population of 3.4 million individuals from the German Bone Marrow Donor Registry (DKMS) using χ² (chi-square) tests.

Results: Six HLA alleles were significantly associated with longevity. Of those, two exhibited the most robust associations: A*01:01g (odds ratio (OR) = 0.87; 95% confidence interval (CI): 0.80-0.95; adj. P = 0.02) and DRB1*13:02g (OR = 1.24; 95% CI: 1.10-1.41; P = 0.01). DRB1*13:02g was replicated in the UK Biobank after Bonferroni correction, whereas A*01:01g showed directionally concordant nominal support but did not remain significant after multiple-testing correction.

Conclusion: Both DRB1*13:02g and A*01:01g have previously been implicated in dementia-related phenotypes. These observations support the hypothesis that HLA variation may influence longevity partly through pathways linked to neurodegeneration. This study provides a high-resolution (2-field) HLA dataset for a longevity cohort, which should be valuable for future investigations.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine and metabolic disorder, in which the interaction between insulin resistance (IR) and hyperandrogenism (HA) is a major driver of reproductive and metabolic complications. Accumulating evidence suggests that chromatin remodeling may represent a regulatory layer linking metabolic stress, inflammation, steroidogenic gene expression, and androgen receptor activity. Research indicates that chromatin remodeling may be a key regulatory factor linking metabolic stress, inflammation, steroidogenic gene expression, and androgen receptor activity. This review systematically summarizes current evidence on chromatin remodeling in PCOS-related IR and HA, focusing on histone modifications, DNA methylation, ATP-dependent remodeling complexes, transcription factors, and non-coding RNA-mediated regulation. We distinguish between direct evidence from PCOS tissues and cells and indirect evidence from metabolic, endocrine, and hormone-responsive disease models, proposing a hierarchy of evidence. Available data suggest that chromatin remodeling may influence insulin signaling genes, adipogenesis, ovarian steroidogenic enzymes, and co-transcriptional networks involving Forkhead box protein O1 (FOXO1), Peroxisome Proliferator-Activated Receptor γ (PPARγ), nuclear factor-kappa B (NF-κB), androgen receptor (AR) signaling, and SWI/SNF-related complexes. However, PCOS-specific functional validation remains limited, particularly in theca cells, granulosa cells, adipose tissue, and cell-type-resolved chromatin. Integrating multi-omics, single-cell epigenomics, and CRISPR-based epigenome editing may help identify causal chromatin regulators and clinically relevant PCOS subtypes. We further discuss how computational biomedical approaches, including bioinformatics, Artificial Intelligence (AI), machine learning, and multi-omics integration, can enhance mechanistic inference, biomarker discovery, and PCOS subtype stratification. A chromatin-centric framework may deepen our understanding of the IR-HA cycle and support future biomarker discovery and precision interventions in PCOS.

Spatial transcriptomics (ST) maps gene expression within intact tissues, but its cost and technical complexity limit broad adoption. A growing body of deep-learning methods now seeks to infer ST directly from routine histology images, especially hematoxylin and eosin (H&E)-stained slides, with the aim of turning archived pathology material into virtual molecular data. This review examines more than 40 ST prediction models, comparing their data requirements, modelling strategies, evaluation practices, and translational potential. Recent advances in model architecture, histology foundation models, and higher-resolution in situ ST platforms have improved prediction performance and expanded the range of potential applications. However, most current methods still show limited robustness and generalisability, with performance constrained primarily by the quantity, quality, and diversity of available ST training data. Comparisons between models also remain difficult due to inconsistent pre-processing pipelines, training datasets and evaluation strategies. The field is increasingly recognising that progress depends not only on more sophisticated models, but also on standardised benchmarks, improved data harmonisation and clearer evaluation frameworks. Despite these limitations, ST prediction is already showing utility in research settings, including biomarker discovery, tissue domain inference, molecular super-resolution and large-scale analysis of archived histology cohorts. Emerging applications also include patient stratification, virtual molecular profiling and multi-modal pathology systems that integrate histology, transcriptomics and language models. As datasets continue to expand and models become more reliable, ST prediction has the potential to become an important component of next-generation digital pathology workflows.

Hormesis, the biphasic dose-response by which mild stressors trigger adaptive programs that leave cells better defended, has become the standard lens through which geroscience interprets lifespan-extending interventions. However, the supporting evidence comes largely from young or middle-aged animals. This review argues that the hormetic window, i.e., the range of stimulus intensities that an organism can convert into net benefit, is set not by chronological age but by integrated adaptive reserve, which is shaped jointly by aging biology, cumulative life-history exposures, and comorbidity burden. Because stress-response pathways involving nuclear factor erythroid 2-related factor 2 (NRF2), heat shock factor 1 (HSF1), forkhead box O (FOXO), adenosine monophosphate (AMP)-activated protein kinase (AMPK), autophagy, and the telomere-associated DNA damage response are progressively attenuated, and because immune resilience governs the sensing, resolution, and repair phases of any adaptive response, the window both narrows and shifts toward lower doses. Doses clearly restorative in youth can therefore fall on the damaging side of the curve in old age, and two individuals of identical chronological age may respond very differently. We apply this framework to five paradigms: mitohormesis, caloric restriction, thermal stress, exercise, and genotoxic stress, and show that the stimulus generally retains its signal in old age while the downstream amplification machinery becomes rate-limiting. Interventions with explicitly age-dependent effects, including senolytics, nicotinamide adenine dinucleotide (NAD⁺) precursors, partial reprogramming, B-cell lymphoma-extra large (Bcl-xL) overexpression, and stem-cell-derived extracellular vesicles, are examined as complementary probes of the same principle. The review closes with implications for geriatric trial design: comprehensive geriatric assessment combined with molecular biomarkers, longitudinal monitoring of a moving window, explicit safety thresholds, and sex-disaggregated analysis.

Organic anti-corrosion coatings are extensively used to protect metallic structures, but conventional coatings mainly serve as passive barriers and offer limited information on concealed interfacial degradation. Once corrosive media pass through pores, cracks, or local delamination, under-coating corrosion may begin before visible rusting or coating blistering becomes evident. Early, in situ, and real-time monitoring of coating degradation is therefore necessary for assessing coating performance, clarifying failure mechanisms, and supporting timely maintenance. This review presents recent advances in corrosion monitoring technologies for anti-corrosion coatings. Electrochemical sensing methods, including electrochemical impedance spectroscopy, electrochemical noise monitoring, and galvanic corrosion sensors, are examined with respect to their signal mechanisms, sensor configurations, and suitability for service-state assessment. Optical and electromagnetic sensing techniques are subsequently reviewed for nondestructive and spatially resolved detection of under-coating corrosion. Special attention is given to corrosion-sensing coatings that introduce responsive molecules or micro/nanocontainers into coating matrices to realize pH- or metal ion-triggered fluorescent and colorimetric warning. Finally, the major remaining challenges and future research directions are discussed, including high-sensitivity detection, long-term signal stability, multi-signal coupling, quantitative interpretation, and engineering implementation of intelligent coating systems.

Ga-based liquid metal (LM), particularly gallium-based alloys, uniquely combines metallic conductivity with fluidic flexibility, offering attractive opportunities for biomedical technologies that are difficult to achieve with conventional solid-state metals. This review first summarizes the expanding applications of LM in microfluidics, flexible electronics, biosensing, drug delivery, and thermal therapy, highlighting the functional advantages arising from its fluidity, deformability, and electrical conductivity. However, the limitations that hinder broader biomedical implementation remain: although the native gallium oxide layer can stabilize LM structures, it also introduces challenges in oxidation control, wettability, interfacial adhesion, conductivity, and long-term reliability. Against this background, surface engineering is presented as a central strategy for addressing these limitations. We systematically review surface modification approaches based on small molecules, polymers, biological coatings, and related interfacial strategies for improving stability, biocompatibility, and functionality. We further discuss fabrication approaches for integrating surface-engineered LM into wearable platforms, including 3D printing and hydrogel-based architectures. Finally, persistent challenges involving surface tension, adhesion, nanoparticle aggregation, conductivity loss, electrochemical corrosion, mechanical mismatch, biocompatibility, and sterilization are critically evaluated together with corresponding solutions. This application-surface-engineering framework provides a roadmap for designing multifunctional, surface-engineered LM-based systems, while outlining future directions for translating these materials from laboratory studies to clinical and practical biomedical applications.

Joint disorders, such as osteoarthritis (OA) and rheumatoid arthritis (RA), significantly impair patients’ quality of life and pose persistent challenges for current clinical management. The articular cavity presents a uniquely challenging therapeutic environment characterized by dense avascular cartilage, stringent synovial barriers, rapid synovial fluid clearance, and complex dynamic mechanical loading. Conventional therapeutic strategies, ranging from systemic pharmacological administration and intra-articular (IA) injections to invasive surgical approaches, are severely constrained by poor local bioavailability, rapid drug clearance, off-target toxicity, and the inherent passivity of static scaffold designs. Consequently, there is an urgent need for intelligent platforms capable of responsively adapting to pathological microenvironments to orchestrate concurrent biochemical regulation and tissue reconstruction. This review summarizes recent advances in smart devices for joint tissue intervention and repair, focusing on multi-scale therapeutic strategies specifically for the management of arthritis and related joint disorders, encompassing microneedle (MN)-based systems and 3D-printed structural scaffolds. Finally, the primary translational bottlenecks and future perspectives of these technologies are outlined to guide next-generation joint therapeutics.

Adoptive cell therapy continues to encounter diverse hurdles in treating solid tumors, including poor infiltration, an immunosuppressive microenvironment, and tumor immune evasion, necessitating the endowment of effector cells with multiple functionalities. However, conventional cell-engineering techniques, including genetic editing and chemical modification, usually modulate a single functional axis to yield a monofunctional effector cell that can overcome only one physiological barrier, leading to insufficient solid tumor suppression. Recently, membrane-fusogenic liposomes have emerged as a multiplex engineering tool capable of directly producing multifunctional effector cells to simultaneously surmount multiple challenges for effective antitumor efficacy. Through a fusion process, this liposome concurrently achieves immune cell surface functionalization and intracellular delivery of bioactive molecules, thereby endowing effector cells with multiple functionalities within a single step. This minireview summarizes recent advances in the use of fusogenic liposomes for immune cell engineering to boost their therapeutic efficacy against solid tumors. We discuss their design principles and representative applications, and analyze their technical advantages and current limitations. Looking forward, we propose that membrane-fusogenic liposomes hold potential to advance the development of multimodal engineered immune cells for next-generation cancer immunotherapies.