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Pyrolysis is a relatively mature process for recycling plastic waste, yet predictive kinetic models remain elusive due to the enormous number of radical reaction pathways, intermediates, and products. Starting from elementary hydrogen abstraction, random and chain-end β-scission reactions, we construct continuum population balance equations (PBEs) and discrete species balance equations (SBEs) to model polypropylene (PP) pyrolysis for realistic initial molecular weight distributions (MWDs) and reactor time and length scales. The framework accounts for the separate but coupled MWDs of alkanes, α-olefins, and α,ω-olefins polymers, along with the amounts of volatile alkanes and olefins generated during the reaction. We parameterized the model using rate constants from prior ab initio calculations. The model predicts the evolution of the polymer MWD, the degree of double-bond functionality, the number of scission events, and the amounts of volatile alkane and alkene products as a function of time. The predictions agree with experimental MWD data and resolve prior questions about the double-bond functionality (f) of volatile and nonvolatile products. We discuss how the model can help design processes to obtain products of the desired molecular weight and functionality.

To evaluate whether the application of cell-free adipose liquid extract (ALE) synergistically enhances the therapeutic efficacy of vascularized lymph node transfer (VLNT) by reconstructing the lymphatic-vascular network and restoring the lymph node immune niche in a rat lymphedema model. A rat hindlimb lymphedema model was established involving popliteal lymph node excision. Animals were randomized into four groups: Control, ALE only, VLNT only, and VLNT combined with ALE (VLNT + ALE). ALE was prepared using a mechanical emulsification and filtration protocol. Edema resolution was monitored by limb circumference. Lymphatic drainage function was visualized via indocyanine green (ICG) lymphography. Histological assessments included Masson's trichrome and immunofluorescence for LYVE-1 (lymphangiogenesis), CD31 (angiogenesis), and MECA-79 (high endothelial venules, HEVs) to evaluate structural and functional regeneration. The VLNT + ALE group achieved the most rapid and significant edema regression compared to VLNT or ALE alone. ICG lymphography revealed that the combined therapy orchestrated the formation of continuous, linear lymphatic channels, effectively eliminating dermal backflow. Histologically, ALE treatment significantly increased the density of both LYVE-1+ lymphatic vessels and CD31+ blood vessels, suggesting a dual-regenerative effect on the microenvironment. ALE directly promoted tube formation in human lymphatic endothelial cells (HLECs), confirming its pro-lymphangiogenic activity in vitro. Crucially, within the transplanted lymph nodes, ALE treatment restored the expression of MECA-79+ HEVs to levels comparable to healthy young nodes. This indicates that ALE not only supports graft survival but also preserves the essential lymphoid microarchitecture required for immune surveillance. Cell-free ALE synergistically enhances the therapeutic efficacy of VLNT by promoting vascular-lymphatic coupling and restoring the functional immune niche of transplanted nodes. As a readily available, safe, and cell-free biologic adjuvant, ALE represents a promising translational strategy to optimize surgical outcomes in secondary lymphedema.

Spinal cord injury (SCI) causes severe and often permanent neurological deficits, including neurogenic lower urinary tract dysfunction. Although restoration of bladder function is a major clinical priority after SCI and would profoundly improve care and quality of life, it remains underrepresented in neurotrauma research. Central to this pathology is Repulsive Guidance Molecule a (RGMa), a potent inhibitor of axonal outgrowth and neuronal differentiation that is upregulated following central nervous system injury. In this study, we evaluated the therapeutic efficacy of elezanumab, a human anti-RGMa monoclonal antibody tested in clinical trial for acute SCI, on bladder function in a clinically relevant bilateral impact-compression model of traumatic thoracic SCI in female rats. Quantitative urodynamic and cystometric analyses demonstrated that elezanumab administered initially at 3 h post-SCI and then weekly for 6 weeks significantly reduced urinary retention, reflex bladder activity, and intravesical pressure in SCI rats. Morphological assessment revealed that RGMa neutralization limited pathological bladder hypertrophy, with reductions in bladder mass correlating with reduced urine retention. Neuroanatomical mapping via retrograde tracing, together with exploratory transsynaptic tracing, was consistent with increased supraspinal connectivity in pathways involved in micturition. Moreover, elezanumab promoted axonal plasticity of descending catecholaminergic and serotonergic fibers within the lumbosacral spinal cord. These structural changes were associated with reduced bladder pressure and improved neurological recovery. Together, these findings suggest that RGMa inhibition via elezanumab promotes recovery within key components of the micturition circuitry following traumatic SCI.

Diabetic foot wounds disproportionately affect patients from ethnic minorities and lower-socioeconomic status, many of whom face barriers to accessing diabetes technology. To evaluate whether short-term virtual glucose monitoring (VGM) has the potential to improve clinical outcomes in this high-risk population, we implemented a pilot VGM program within a safety-net health system. We enrolled 40 hospitalized patients with diabetic foot wounds into a 3-month postdischarge VGM program that included 2 clinic visits and remote glucose monitoring every 1 to 2 weeks. Clinical outcomes were compared with a retrospective preintervention cohort of 78 similar patients. Although both groups had similar HgbA1c at diagnosis (VGM 10.6 &#xb1; 1.8% vs preintervention 11.1 &#xb1; 2.0%, P = .20), the HgbA1c at 3 to 6 months was lower in the VGM cohort (7.6 &#xb1; 1.1% vs 8.5 &#xb1; 2.0%, P < .01). Wound healing occurred more frequently in the VGM participants, with 68% achieving wound closure by 3-4 months versus only 47% in the preintervention cohort (P = .04). Nonsignificant reductions in emergency department visits and hospital readmissions for wound complications or hypoglycemia were observed in the VGM versus the preintervention cohort. The VGM program allowed for more timely and frequent opportunities to adjust diabetes medications and address social barriers to care. A short-term postdischarge VGM program has the potential to not only increase access to diabetes technology but also meaningfully improve clinical outcomes among patients with diabetic foot wounds in a safety-net health setting. Such program may offer a scalable strategy to reduce rates of complications and lower healthcare costs in a safety-net health system.

Plants frequently encounter recurring, sequential and combined environmental stresses, yet their adaptive capacity cannot be explained solely by immediate signalling and short-term acclimation. Increasing evidence indicates that prior stress exposure can leave molecular, metabolic and physiological imprints that alter the magnitude, speed and quality of later responses, thereby giving rise to stress memory and adaptive plasticity. In plants, these persistent states are increasingly linked to epigenetic regulation, including changes in chromatin accessibility, histone modifications, DNA methylation, RNA-directed DNA methylation and non-coding RNA-mediated control. However, stress memory is not determined by chromatin regulation alone. It is also shaped by metabolic and cellular reprogramming involving osmolyte accumulation, redox buffering, energy redistribution, protein quality control, autophagy, selective protein turnover and membrane remodelling, all of which help sustain cellular homeostasis during stress and recovery. In parallel, chloroplasts, mitochondria and the endoplasmic reticulum act as stress-sensitive organelles that relay their functional state to the nucleus through retrograde signalling, while long-distance systemic communication mediated by reactive oxygen species, calcium waves, electrical and hydraulic signals, hormones and peptides coordinates whole-plant acclimation. This review synthesizes these layers into a unified framework and argues that plant resilience under fluctuating environments depends on the interaction between stress memory, metabolic plasticity, organelle-derived signalling and systemic acquired acclimation. Particular attention is given to the distinction between transient acclimation and true memory, the balance between maintenance and resetting of stress-induced states and the developmental and fitness trade-offs associated with persistent preparedness. This review also highlights major gaps that continue to limit the field, including the lack of standardized criteria for defining stress memory, insufficient causal validation of epigenetic marks, weak integration of chromatin and metabolic states with whole-plant phenotypes, and the limited translation of memory-associated mechanisms into crop performance under realistic field conditions. Overall, this review provides a comprehensive framework for understanding how plants not only respond to stress, but also encode, retain and deploy information from prior exposure to optimize subsequent adaptation.

To compare polymerization shrinkage and shrinkage stress of highly filled flowable resin composites with conventional low filled and bulk-fill flowables. Fifteen flowable resin composites with A2-shade were tested. For each material, shrinkage depth (&#xb5;m) was measured using a topography-based cavity method (n&#x2009;=&#x2009;10), and peak polymerization shrinkage stress (MPa) using a bonded-disc test (n&#x2009;=&#x2009;5) under a standardized light-curing protocol. Data were analyzed with one-way ANOVA, Tukey's post-hoc tests, and Pearson's correlations. Shrinkage depth ranged from 84.08&#x2009;&#xb1;&#x2009;14.66&#xa0;&#x3bc;m to 169.81&#x2009;&#xb1;&#x2009;6.93&#xa0;&#x3bc;m, whereas stress ranged from 2.84&#x2009;&#xb1;&#x2009;0.28&#xa0;MPa to 6.34&#x2009;&#xb1;&#x2009;0.56&#xa0;MPa. Shrinkage and stress were negatively correlated (r&#x2009;=&#x2009;-&#x2009;0.749, p&#x2009;=&#x2009;0.0013). "Bulk-fill" status showed no association with shrinkage stress (r&#x2009;=&#x2009;-&#x2009;0.136, p&#x2009;=&#x2009;0.628) or shrinkage depth (r&#x2009;=&#x2009;0.199, p&#x2009;=&#x2009;0.476). Highly filled flowables tended to reduce shrinkage but often developed higher stress, whereas some low filled bulk-fills reduced stress despite higher shrinkage. Shrinkage and stress should be considered independently, as material category labels and viscosity classes are not reliable predictors of material behavior. Polymerization shrinkage and peak shrinkage stress varied markedly among both low filled and highly-filled flowable composites, and the 'bulk-fill' designation was not a reliable predictor of either outcome. Clinicians should therefore select materials according to their specific shrinkage and stress profiles in relation to cavity geometry, rather than relying solely on category labels, especially when maintaining interfacial integrity is critical. Not applicable.

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Bioelectrical signals, particularly endogenous direct-current electric fields (EFs), constitute a pivotal yet often underappreciated class of physical cues within the cellular microenvironment. Macrophages, as central effectors of the innate immune system, exhibit remarkable plasticity in response to physicochemical stimuli. Accumulating evidence indicates that both endogenous and applied direct current EFs can significantly modulate key macrophage behaviors, including electrotaxis, phenotypic polarization (M1/M2), and phagocytic activity. While the precise molecular architecture remains to be fully delineated, current research suggests a multi-layered regulatory network involving surface charge redistribution, polarized activation of growth factor receptors, and signal transduction mediated by voltage-gated or mechanosensitive ion channels, which subsequently converge on downstream pathways such as phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase (MAPK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-&#x3ba;B). A rigorous dissection of the biophysical and molecular mechanisms governing these responses is essential for elucidating the role of physical signaling in tissue repair, chronic inflammation, and the tumor microenvironment. Furthermore, distinguishing the mechanistic nuances between physiological endogenous fields and therapeutic applied fields provides a critical theoretical foundation for developing next-generation, bio-mimetic immunomodulatory strategies. Future efforts should focus on characterizing the in vivo spatiotemporal dynamics of EFs, unraveling cell-type-specific response mechanisms, and assessing the translational feasibility of these fundamental insights.

Several aquatic invertebrates commonly used in standardized ecotoxicological bioassays exhibit cryptic diversity, a factor often overlooked in environmental risk assessment. Cryptic diversity raises concerns about the reproducibility and comparability of bioassay results. The calanoid copepod Eurytemora affinis is a cryptic species complex broadly distributed across the Northern Hemisphere in estuarine waters (0.5-20 PSU, Practical Salinity Unit). Thus, it represents a promising bioindicator species for assessing environmental risk in estuarine ecosystems. This study aims to assess the extent to which the cryptic diversity and the ecotoxicological responses observed within the E. affinis cryptic complex may compromise its usefulness in environmental risk assessment (ERA). The ecotoxicological responses of two E. affinis cryptic species (clades), the European (E) and the North Atlantic (NA) clades, originating from the Seine (France) and the St. Lawrence (Canada) estuaries, respectively, were assessed. Both clades were exposed to benzo[a]pyrene (BaP) using a standardized semi-chronic larval bioassay for 96&#x2009;hr. Endpoints assessed included naupliar survival, growth and development. Median lethal concentrations (LC50) were calculated. The results showed that the E clade was 2.5-fold more sensitive than the NA clade with LC50 values of 8.41 and 22.24&#x202f;&#xb5;g&#x202f;L-1, respectively. Benzo[a]pyrene also had a greater effect on growth and development of the nauplius stages from the E clade compared to the NA clade. Such differential sensitivity is likely due to genetic divergence, phenotypic plasticity or environmental factors during sampling. Despite the observed inter-clade variation, the magnitude remains within the acceptable range of environmental variability considered in ERA. This study provides valuable insights into the implications of cryptic diversity for the use of E. affinis in ecotoxicological bioassays and supports its application within the ERA framework.

Astrocytes are among the first cellular responders to central nervous system injury, yet the mechanisms governing their earliest responses remain incompletely understood. Here, we investigated astrocyte dynamics during the first hours after focal cortical injury induced by cortical devascularization in rats. We observed a rapid and spatially restricted increase in glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) immunoreactivity surrounding the ischemic core as early as 1.5-3.5&#x2009;h post-lesion, in association with blood-brain barrier disruption and edema-related changes. Within the injury core, astrocytes displayed differential GFAP detection by monoclonal and polyclonal antibodies, together with the appearance of lower-molecular-weight GFAP fragments both in&#xa0;vivo and after oxygen-glucose deprivation in&#xa0;vitro, suggesting GFAP cleavage in severely damaged astrocytes. At the chromatin level, astrocytes proximal to the lesion exhibited reduced histone H3 acetylation, particularly histone 3 acetylation at lysine 9 (H3K9ac), a phenomenon recapitulated in cultured astrocytes exposed to hypo-osmolar stress. This reduction was transient, reversible upon recovery, and prevented by histone deacetylase (HDAC) inhibition. Functionally, hypo-osmolar stress conditioned astrocyte responses to subsequent stimuli, attenuating nuclear factor kappa B (NF-&#x3ba;B) activation and complement 3 (C3) induction after lipopolysaccharide exposure while enhancing proliferative capacity during recovery. Together, these findings identify edema-associated osmotic stress as an early regulator of astrocyte epigenetic state and functional plasticity, suggesting that astrocytes exposed to edema are primed to adopt distinct responses that may contribute to tissue repair and scar formation following brain injury.

Reprocessable and recyclable polyolefin (PO) vitrimers can be used as alternatives to conventional non-recyclable thermosets. While recent studies have successfully demonstrated dynamic network formation in virgin POs, the application of dynamic covalent chemistry in post-consumer mixed POs remains unexplored. Herein, we report the first reactive melt extrusion approach that utilizes nitroxide-mediated silyl ether chemistry to produce post-consumer high-density polyethylene (HDPE) and polypropylene (PP) blended vitrimers. Key findings show that the fully formulated 75:25 wt./wt. HDPE/PP vitrimer creates a covalently crosslinked network with a storage modulus of >1 MPa at 220&#xb0;C. Thermomechanical benchmarking against a permanent epoxy-ester thermoset reveals that the upcycled vitrimer combines thermoset-like dimensional stability above 180&#xb0;C with dynamic melt-reprocessability, albeit with a modulus above its melting transition that is lower than the permanent network. For the first time, 2D wideline separation (2D WISE) solid-state NMR was used to qualitatively validate highly phase-selective crosslinking. This is the first study that establishes vitrimer formation from mixed post-consumer PO blends, thus providing a scalable upcycling pathway for municipal solid waste.

Following radiation injury, intestinal epithelial cells adapt through cellular plasticity to regenerate and repopulate the damaged epithelium by activating Yap, a key effector protein of the Hippo signaling pathway. However, the impact of pharmacologically targeting the Hippo pathway on the regeneration of the irradiated intestinal epithelium remains poorly understood. Here, we investigated this question using NCGC-023, a selective and potent small-molecule inhibitor of Yap's upstream regulators LATS1/2. NCGC-023 treatment significantly increased active Yap protein expression in human enteroids and protected them against ionizing radiation (IR) in vitro. In mice, transient treatment with NCGC-023 before IR reduced radiation-induced DNA damage, suppressed premitotic apoptosis and aberrant mitosis in intestinal crypt cells, facilitated regenerative reprogramming of the damaged intestinal epithelium, and improved survival of mice subjected to IR doses that precipitate gastrointestinal acute radiation syndrome (GI-ARS). Mechanistically, NCGC-023 treatment before IR upregulated key signaling pathways controlled by LATS1/2, including Yap-dependent regenerative responses involving Il-33 and Yap-independent cellular responses to heavy metals mediated by metallothioneins. Moreover, NCGC-023 treatment did not exacerbate delayed injury in multiple organs of mice that survived 4 months post-irradiation. Together, these results demonstrate that transient NCGC-023 treatment before high-dose IR promotes the regeneration of the damaged intestinal epithelium. This proof-of-concept study supports further development of LATS1/2 inhibitors as prophylactic medical countermeasures for GI-ARS.

Dopamine signaling through dopamine 1 receptors (D1Rs) and dopamine 2 receptors (D2Rs) regulates hippocampal synaptic plasticity underlying learning and memory, yet their subcellular localization within the hippocampus is unknown. Here, we performed electron microscopic immunocytochemistry to elucidate the distribution of D1R and D2R in subregions of the mouse hippocampus. In CA1 and CA3 stratum radiatum (SR), D1R- and D2R-immunoreactivity was found primarily on pyramidal cell dendritic spines and unmyelinated axons, and to a lesser extent in axon terminals and glia. In both regions, D1R-labeled terminals formed predominantly asymmetric (excitatory-type) synapses on dendritic spines, whereas D2R-labeled terminals formed mainly symmetric (inhibitory-type) synapses on pyramidal cell dendritic shafts. In the dentate gyrus (DG) hilus, D1R labeling was almost exclusively found in unmyelinated axons and glia. D2R immunoreactivity in the hilus similarly was present in unmyelinated axons and glia but was also detected in dendritic spines originating from mossy cells and in terminals forming symmetric synapses. These findings indicate that dopamine receptors are positioned to influence excitatory and inhibitory signaling in the murine hippocampus. As D1R and D2R exert opposing effects on neuronal signaling, their localization on pyramidal neuron compartments provides a structural substrate for bidirectional modulation of synaptic plasticity and pyramidal cell activity. In addition, the presence of D2Rs on inhibitory terminals contacting pyramidal neurons and hilar interneurons suggests a role in regulating inhibitory circuitry within the hippocampus.

This study aimed to establish new morphometric reference values for the styloid process of the temporal bone, with particular emphasis on age- and sex-related differences and standardized 3-dimensional spatial orientation. A retrospective analysis of CT angiographies of the supra-aortic vessels from 339 patients (678 styloid processes) was performed. Patient age and sex were documented. Measurements included styloid process length and diameter, angular orientation in 2 orthogonal planes, distance to the lesser horn of the hyoid bone, and ossification of the stylohyoid ligament. Statistical evaluation was conducted. CT angiographies of 176 male (51.9%) and 163 female (48.1%) patients were analyzed. The mean styloid length was 26.1&#xb1;10.4&#xa0;mm (left) and 26.5&#xb1;11.9&#xa0;mm (right). Length increased with age in both sexes and was consistently greater in males. The mean anterior-posterior angle was 70.4&#xb0;&#xb1;5.63&#xb0; (left) and 70.3&#xb0;&#xb1;5.9&#xb0; (right); increasing length correlated with a decreasing AP angle, indicating medial displacement of the tip. The mean lateral angle was 64.2&#xb0;&#xb1;6.45&#xb0; (left) and 64.2&#xb0;&#xb1;6.32&#xb0; (right); increasing length correlated with increasing lateral angle, corresponding to dorsal displacement. The mean diameter measured 3.81&#xb1;1.09&#xa0;mm (left) and 3.87&#xb1;1.16&#xa0;mm (right), with age-related enlargement. This study provides new morphometric reference values for the styloid process, demonstrating age-related elongation and thickening accompanied by dorsomedial deviation of the tip toward the adjacent neurovascular structures.In summary, CTA&#x2011;based morphometry of the stylohyoid complex provides a shared quantitative framework linking anatomical variation to clinical presentation in Eagle syndrome. Incorporating these standardized reference values into routine imaging reports may facilitate more consistent recognition of clinically relevant stylohyoid pathology and support targeted treatment decisions.

Ketamine, a non-competitive N-methyl-D-aspartate acid (NMDA) receptor antagonist, produces rapid and sustained antidepressant actions, but the underlying molecular mechanism remains unclear. The CX3CL1/CX3CR1 signaling is closely related to mood disorders, and this study aims to investigate its role in ketamine's antidepressant actions. We pharmacologically (AZD8797, a selective CX3CR1 antagonist) and genetically (intra-mPFC microinjection with AAV-CX3CR1-siRNA) manipulated the CX3CL1/CX3CR1 signaling and investigated their effects on ketamine's antidepressant-like effects in mice treated with corticosterone (Cort), and observed changes in synaptic plasticity in response to these manipulations. We found that 24&#x2009;h after drug injection, ketamine (10&#x2009;mg/kg, i.p.) significantly reversed the Cort-induced depression-like behaviors, and inhibited the overexpression of pro-inflammatory cytokines and microglial activation. Ketamine significantly improved the Cort-induced impairment in the dendritic complexity and spine densities. In addition, our ELISA results showed that ketamine significantly inhibited the activation of CX3CL1/CX3CR1 signaling, and ketamine attenuated the upregulation of CX3CR1 and CX3CL1 expression in Cort-treated HT22 and BV2 cells in vitro. Furthermore, pretreatment with AZD8797 (0.8&#x2009;mg/kg, i.p., twice a week) completely blocked ketamine's antidepressant-like behavioral effects and eliminated ketamine-induced enhancement in the synaptic plasticity; intra-mPFC microinjection with AAV-CX3CR1-siRNA also prevented ketamine's behavioral effects and beneficial effects on the synaptic plasticity. These findings demonstrated that CX3CL1/CX3CR1 signaling-mediated synaptic plasticity played essential roles in ketamine's antidepressant-like effects, which opened a new door to targeting chemokines to improve depression symptoms.

Delayed abscess formation after orbital floor reconstruction using poly-L-lactic acid/hydroxyapatite (PLLA/HA) implants is exceedingly rare. A 49-year-old man presented with progressive diplopia and hyperglobus 4 years after orbital floor repair with a PLLA/HA implant. Imaging showed an encapsulated lesion displacing the globe with the implant appearing displaced within the lesion. Surgical exploration revealed a fibrous capsule containing purulent fluid and fragmented implant material. Staphylococcus epidermidis was cultured, and histopathology showed chronic inflammation and fibrosis. After complete removal of the implant and capsule, the patient experienced full resolution of diplopia and hyperglobus. This case highlights that late abscess formation can occur even with bioresorbable PLLA/HA implants, possibly related to degradation byproducts and systemic factors such as diabetes mellitus and smoking. Long-term follow-up and prompt surgical intervention are important for successful management.

Stimulated by retinoic acid 6 (STRA6) is widely recognized for its roles in the pathogenesis and progression of multiple cancers. However, its biological functions and molecular mechanisms in rectal cancer (RC) remain poorly understood. This study aims to elucidate the functional roles of STRA6 and investigate the mechanisms underlying its dysregulation in RC. We employed RNA-seq to identify differentially expressed genes. STRA6 expression levels and activation of the Wnt/&#x3b2;-catenin pathway in RC were assessed using reverse transcription-quantitative PCR and Western blotting. Functional implications of these genes were investigated through a series of assays, such as CCK-8, flow cytometry and transwell assays. Potential upstream transcription factors regulating STRA6 were predicted bioinformatically and validated using a dual-luciferase reporter assay. Finally, the in vivo relevance of these findings was evaluated in a xenograft mouse model. A marked increase in STRA6 and One cut domain family member 2 (ONECUT2) expression was observed in RC tissues, with particularly elevated levels detected in radiation -resistant RC tissues. Functionally, STRA6 overexpression enhanced RC cell proliferation, migration and invasion, while reducing apoptosis. Rescue experiments demonstrated that the oncogenic effects of ONECUT2 were partially reversed upon STRA6 knockdown. Mechanistically, ONECUT2 was identified as a transcription factor that binds directly to the STRA6 promoter and upregulates its expression, thereby activating the Wnt/&#x3b2;-catenin pathway to facilitate RC progression and radiation resistance. ONECUT2/STRA6 axis exerts an oncogenic function in RC through activation of Wnt/&#x3b2;-catenin pathway, suggesting its potential as a therapeutic target. STRA6 is widely recognized for its roles in the pathogenesis and progression of multiple cancers. but its role in rectal cancer (RC) remains unclear. This study clarified STRA6's function in RC and identified ONECUT2 as its upstream transcription factor regulating the Wnt/&#x3b2;-catenin pathway to facilitate RC progression and radiation resistance. The findings provide novel insights into the prognostic and functional role of STRA6 in RC and underscore its potential as a promising therapeutic target.

NK cells are classically defined by their rapid cytotoxicity against tumor cells and infected cells and by early inflammatory cytokine production. However, unconventional roles for NK cells as regulators of immunity and tissue homeostasis have recently been uncovered. Beyond their classical roles, NK cells can orchestrate leukocyte trafficking, curtail responses of other immune cells, remove protein aggregates, support pregnancy, and contribute to healthy tissue regeneration. We discuss the importance of these myriad functional activities of NK cells in infection, cancer, autoimmunity, atopic and allergic disease, pregnancy, tissue injury, and neurodegenerative diseases. The functional pleiotropy of NK cells provides new avenues of translational utility for these innate lymphocytes and represents an unexplored complexity in conventional clinical applications of NK cells against infection and cancer.