Search Results (1,499)

Background: Venous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism, is increasingly recognized as a thromboinflammatory disorder involving coagulation, innate immunity, endothelial dysfunction, and vascular homeostasis. Emerging evidence suggests that gut microbiome-related inflammatory and metabolic signals may influence pathways potentially relevant to VTE through intestinal barrier dysfunction, microbial translocation, and microbiome-derived metabolites. This review critically examines the direct and indirect evidence relating gut dysbiosis to mechanisms potentially relevant to venous thrombogenesis. Methods: A structured literature search of PubMed, Scopus, and Web of Science was conducted from database inception to February 2026. Observational, translational, experimental, preclinical, and selected genetic studies were narratively synthesized across heterogeneous evidence types. Results: Available evidence suggests that intestinal barrier dysfunction and microbial translocation may increase systemic exposure to lipopolysaccharide and other microbial products, potentially contributing to inflammatory signaling and procoagulant responses. Proposed downstream effects include tissue factor (TF) activation, platelet reactivity, neutrophil extracellular traps (NETs) formation, complement signaling, endothelial perturbation, and impaired balance of anticoagulant and fibrinolytic pathways. Microbiome-derived metabolites, including trimethylamine N-oxide (TMAO), phenylacetylglutamine (PAGln), bile acids, and short-chain fatty acids (SCFAs), have been linked, mainly in experimental or non-VTE settings, to thrombosis-related biology. However, most evidence remains indirect, associative, or experimental, whereas direct human VTE-specific evidence is limited and heterogeneous. Conclusions: The gut microbiome–VTE axis is biologically plausible and supported mainly by mechanistic and indirect evidence, but current data are insufficient to support strong causal conclusions. Further longitudinal, well-phenotyped, mechanistically informed studies are needed to determine whether microbiome-related pathways have measurable clinical relevance in human VTE. Full article

As a new performance evaluation system, ESG has garnered significant goodwill and tax benefits for a set of benchmark enterprises through its forward-looking corporate values and overall enhancement of public trust. However, as more companies pay attention and invest more in ESG, the pursuit of these ratings also entails increasing costs. Whether the impressive upward trend in ESG ratings genuinely enriches and enhances a company’s reputation, or if the ratings driven by ESG costs are unsustainable over the long term, remains uncertain. In the pursuit of sustainable development, several enterprises may find themselves in a predicament where ESG ratings are on the rise while corporate performance is declining. This paper selects listed companies in China’s petrochemical industry, which exhibit the distinctive characteristics of ESG and corporate performance divergence, as its research sample. It aims to identify the quantitative features of this performance–ESG divergence dilemma and empirically uncover its causes and development pathways. The findings of this research will guide enterprises back to the path of ESG alignment, providing a theoretical foundation for ensuring that companies adhere to a high-quality ESG development path. Furthermore, it offers insights into addressing the gaps in the rating system behind the phenomenon of inflated ESG scores and presents policy-oriented perspectives to help enterprises avoid the pitfalls mentioned above. Full article

Endovascular therapies have transformed cardiovascular medicine, yet restenosis, thrombosis, and device failure remain common and poorly predictable complications. Increasing evidence suggests that immunothrombotic processes critically shape vascular recovery after device implantation. This includes neutrophil extracellular trap (NET) formation, innate immune polarization, and endothelial damage responses. Concurrently, advances in artificial intelligence (AI) are increasingly enabling continuous multimodal monitoring and adaptive clinical decision-making throughout the medical device life cycle. Here, we propose the concept of immunologically adaptive endovascular devices: a closed-loop paradigm in which patient immune status informs device selection, device–tissue interactions are interpreted via mechanistic biomarkers, and real-world monitoring dynamically updates risk and management. The study introduces (i) an immune–device interaction phenotype taxonomy linking device design features to measurable thrombo-inflammatory trajectories, (ii) a mechanistic framework defining interface signaling processes that enhance or resolve NET-driven responses, (iii) a minimum evidence model encompassing preclinical testing, clinical validation, and post-market surveillance, and (iv) a reference AI architecture for risk prediction, drift detection, and safety monitoring. This study also outlined testable predictions and a translational roadmap toward precision endovascular intervention and next-generation adaptive cardiovascular devices. Full article

K-Rev Interaction Trapped protein-1 (KRIT1) is a scaffold protein that forms functional protein complexes involved in physiologically important signaling networks. While it is primarily recognized for its association with Cerebral Cavernous Malformations (CCMs), KRIT1 may also play critical roles in tumor formation and the acquisition of malignant phenotypes, regulating cell adhesion, cytoskeletal dynamics, and angiogenesis. In this study, we investigated the role of KRIT1 in cancer cell migration and metastasis, with a focus on identifying novel interacting proteins and characterizing the intracellular signaling pathways activated upon its loss. By using a yeast two-hybrid screening, we identified Kinesin Family Member 1C (KIF1C), a protein involved in regulating podosome and invadopodium elongation, as a novel binding partner of KRIT1, and the interaction was confirmed in melanoma and epithelial cancer cells. In silico docking and interaction interface analyses supported the KRIT1–KIF1C interaction, providing structural insight into the binding mode as shown experimentally. We also found that SRC and focal adhesion kinase (FAK) phosphorylation, as well as Ras homolog family member A (RhoA) expression, represent additional pathways affected by the loss of KRIT1. This study confirms our earlier hypothesis that KRIT1 functions as a tumor suppressor and uncovers a compelling link between its loss and enhanced cancer aggressiveness. Full article

Diffractive optical elements with a trigonometric phase dependence on radius are considered. They allow the formation of multiple local light segments on the optical axis. The dependence of the focal distribution on the optical element parameters is studied analytically and numerically. It is shown that by varying the parameters, both the positions and relative magnitudes of the foci can be independently changed. A detailed comparison of a sinusoidal lens with a parabolic one is performed. Binarization of a sinusoidal lens leads to non-obvious effects: this process does not create new foci, but significantly changes the energy distribution between the foci. In particular, the intensity can increase at positions where the focal magnitude was very small before binarization. Moreover, the trigonometric elements have very interesting chromatic dispersion features: changing the wavelength leads to significant variations in the ratio of the focal energies, which is not typical of parabolic lenses. The obtained results are promising for the field of multiplexing optical information transmission channels, increasing the depth of focus, laser material processing and optical trapping. Full article

Natural fungal polysaccharides are increasingly explored as bioactive compounds capable of orchestrating complex regenerative responses during tissue repair. This study aimed to evaluate the in vivo wound-healing efficacy and molecular mechanisms of a topical polysaccharide formulation derived from Bovistella utriformis (Calvatin 2%) using complementary murine, zebrafish, and proteomic approaches. Phylogenetic analysis based on ITS sequences confirmed the taxonomic identity of the Chilean specimen. In a murine full-thickness excisional wound model, Calvatin 2% significantly accelerated wound contraction and re-epithelialization compared to both saline and base-cream controls, achieving near-complete closure by day 10. Label-free quantitative proteomic analysis of wound tissue by UHPLC-HRMS identified 2432 high-confidence proteins, with 171 upregulated and 153 downregulated proteins in the Calvatin versus control comparison (p < 0.01). Functional enrichment revealed strong activation of innate immune response, complement activation, coagulation cascades, and acute-phase response pathways, while lipid metabolism, mitochondrial energy production, and muscle-related processes were significantly downregulated. KEGG pathway analysis further highlighted complement and coagulation cascades and neutrophil extracellular trap formation as the most prominently affected pathways. In a zebrafish laser-induced wound model, Calvatin induced early and sustained regenerative responses, reaching over 93% wound closure by 18 days post-lesion, significantly outperforming both PBS and vehicle-treated groups. Chronic oral administration of polysaccharides did not induce major hepatic inflammatory responses, supporting systemic safety. Overall, these findings indicate that B. utriformis polysaccharides are associated with modulation of immune- and repair-related pathways together with tissue reprogramming processes that may contribute to accelerated cutaneous regeneration, positioning Calvatin as a promising bioactive formulation for wound-healing applications. Full article

Background: Sepsis-induced acute lung injury (ALI) is a life-threatening condition with limited therapeutic options. Neutrophil extracellular traps (NETs) contribute to its pathogenesis. This study investigated whether polydatin (PD) protects against septic ALI by inhibiting NETs via the Nrf2/HO-1 pathway. Methods: A cecal ligation and puncture (CLP)-induced septic ALI mouse model and an LPS-stimulated neutrophil model were established. Lung injury was assessed by histology, lung wet/dry ratio, BALF protein, and inflammatory cytokines. Endothelial junction proteins and NETs markers were examined by Western blot, immunofluorescence, and SYTOX Green staining. Nrf2/HO-1 pathway activation and ML385 inhibitor experiments were performed for mechanistic validation. Results: PD dose-dependently attenuated lung injury, preserved endothelial junction proteins (ZO-1, VE–cadherin, occludin), and suppressed NETs formation in vivo. In vitro, PD activated Nrf2/HO-1, promoted Nrf2 nuclear translocation, reduced ROS, and inhibited LPS-induced NETs. These effects were abrogated by ML385, confirming pathway specificity. Conclusions: PD mitigates septic ALI by inhibiting NETs formation. In vitro mechanistic studies further suggest that this effect is mediated through activation of the Nrf2/HO-1 antioxidant pathway, positioning PD as a potential therapeutic candidate for sepsis-induced ALI. Full article

This research reveals the coupling mechanism between structural deformation and hydrocarbon accumulation. The Dibei area in the Kuqa Depression represents a key hydrocarbon exploration domain within the northern Tarim foreland basin. Although extensive studies on stratigraphy, sedimentology, and accumulation mechanisms have been conducted, the control of segmented deformation on traps remains poorly understood. Furthermore, the synergistic regulation mechanism involving paleo-uplifts, salt thickness, synsedimentation, and erosion is still ambiguous. Based on high-quality 2D and 3D seismic data, this study integrates tectonic evolution balanced restoration with physical modeling. We conducted two sets of 3D sandbox experiments: “differential paleo-uplift and salt thickness” and “synsedimentation-erosion.” This approach systematically investigates the control of tectonic evolution on trap formation. Results show a strong correspondence between the “subsalt–salt–supra-salt” structural deformation and trap types. The supra-salt layer is dominated by detachment fold traps, whereas the subsalt layer features thrust-fold anticline traps. The basement paleo-uplift governs structural segmentation and trap distribution. Salt thickness modulates strain partitioning and trap stability. Synsedimentation optimizes trap conditions via tectono-sedimentary coupling. Erosional unconformities serve dual functions as both migration pathways and seal beds. These four factors work synergistically throughout the entire petroleum system, from “trap formation–migration–accumulation–preservation.” It enriches the genetic theory of salt-related structures in foreland basins. The findings provide a reference for predicting favorable exploration zones, evaluating trap characteristics, and assessing resource potential in the Kuqa Depression. Full article

Developing environmentally friendly, multifunctional waterproof and breathable membranes (WBMs) has attracted extensive attention and is of great significance but remains challenging. Herein, an environmentally friendly and multifunctional waterborne polyurethane WBM with self-healing and self-cleaning properties is developed in two steps. Firstly, by using polydimethylsiloxane (PDMS) as a hydrophobicity giver and tannic acid (TA) as a crosslinker, a dual-modified waterborne polyurethane (PTWPU) is prepared, which has high surface hydrophobicity due to the surface enrichment of siloxane segments and self-healing performance from the formation of a dynamic phenolic carbamate network. Secondly, by incorporating titanium dioxide (TiO₂) photocatalyst nanoparticles to increase internal porosity and establish hydrophilic pathways, a multifunctional waterborne polyurethane WBM (TPTWPU) is developed. This membrane features further enhanced surface hydrophobicity from generated micro-roughness and effective self-cleaning performance, because TA acts as an electron trap to promote the photocatalytic activity of TiO₂. The TPTWPU membrane shows good hydrophobicity (water contact angle of 115.3°) and satisfactory moisture permeability of 135.0 g/(m²·24 h), which is 61.2% higher than unmodified membranes. Furthermore, it exhibits efficient self-healing, with a recovery rate exceeding 80% within 2 h. This feasible strategy will provide guidance for materials design in multifunctional coatings for textiles and leather. Full article

Sodium metal batteries (SMBs) are promising energy storage systems, yet their practical application is hindered by unstable solid electrolyte interphases (SEIs) and safety issues associated with flammable electrolytes. Although the flame-retardant solvent trimethyl phosphate (TMP) is widely used in rechargeable batteries, its application in SMBs remains constrained due to uncontrolled and accumulated parasitic reactions with sodium metal anodes. Here, we propose a novel synergistic strategy that combines a fluorinated additive (FEC) with a low-cost, high-concentration NaClO₄ to stabilize the electrode–electrolyte interface in TMP-based electrolytes. This approach enables the formation of a robust, NaF-rich SEI while restructuring the Na⁺ solvation sheath to coordinately trap TMP molecules, thereby suppressing parasitic reactions between sodium metal and TMP. As a result, the Na|Na₃(VOPO₄)₂F cell achieves exceptional cycling stability with 89.04% capacity retention over 1000 cycles at 1C. This work provides a cost-effective and practical pathway toward safe and long-lasting SMBs using non-flammable phosphate electrolytes. Full article

The impact of anesthetic technique on long-term oncologic outcomes remains controversial. While early observational data suggested that regional anesthesia might reduce cancer recurrence, large randomized trials have failed to demonstrate consistent survival benefits. This apparent contradiction may not reflect biological neutrality, but rather a mismatch between trial design and the inflammatory biology of the perioperative period. Surgical resection provokes an acute and intense inflammatory surge characterized by sympathetic activation, cytokine release, neutrophil extracellular trap formation, endothelial activation, and transient suppression of cellular immunity. During this perioperative inflammatory window, circulating tumor cells encounter a biologically permissive microenvironment that may facilitate immune evasion, adhesion, and early metastatic niche establishment. The magnitude of this inflammatory response varies across patients and may represent a critical, yet under-recognized, determinant of tumor–host dynamics. Anesthetic and analgesic strategies influence this inflammatory cascade. By attenuating nociceptive signaling and sympathetic activation, regional anesthesia may modulate perioperative immune and immunometabolic pathways. However, it should not be framed as an anti-cancer therapy per se, but rather as a potential regulator of the transient inflammatory milieu that shapes early oncologic biology. We propose that prior neutral trials may reflect methodological misalignment, including heterogeneous tumor populations, absence of inflammatory stratification, and reliance on distant survival endpoints without mechanistic correlates. Future investigations should integrate perioperative immune phenotyping, inflammatory biomarkers, and tumor subtype stratification to determine whether modulation of acute surgical inflammation meaningfully alters early tumor–host interactions. Reconceptualizing the perioperative period as a biologically active inflammatory interface may refine the anesthesiologist’s role within perioperative oncology and open new avenues for precision-based perioperative modulation. Full article

Charge-trapping memory (CTM) exhibits significant potential in high-density memory, yet reliability degradation resulting from the coupling of program/erase (P/E) cycles and electrical stress remains a key bottleneck for large-scale commercialization. This study focuses on a Au/Al₂O₃/TiO₂/p-Si CTM device, systematically investigating the device failure mechanism under continuously operating P/E cycles and constant voltage stress (CVS), with emphasis on elucidating the synergistic effect of bulk and interface defects on performance decay. Mechanistically, oxygen vacancies in TiO₂ serve as defect precursors, which form Frenkel pairs under electric field stress and further promote the formation of new defect precursors, thereby driving a self-sustaining defect evolution process. Interface traps, by contrast, arise from the cleavage of interfacial Si-H bonds triggered by electric field stress, resulting in a net elevation of the interface state density. The passive effects from the bulk and interface defects may give rise to issues, such as threshold voltage drift and decreased P/E speed. This work provides in-depth insights into the device failure mechanism of CTM, offering critical theoretical support for optimizing fabrication processes and enhancing long-term reliability. Full article

Spiral inertial microfluidic devices provide a simple, high-throughput approach for size-based particle separation; however, translating PDMS-optimized designs into monolithic, fully enclosed 3D-printed channels is often limited by printability and post-print channel clearing. In our previous PDMS study, a $400\times 120\mu \mathrm{m}$ spiral achieved high separation performance after computational optimization and experimental validation. To translate this high-performing PDMS concept into a faster and more cost-effective manufacturing approach, the same separation principle is transferred to a fully 3D-printed, closed-channel spiral device, and the geometry is re-optimized around manufacturability constraints. Printing trials showed that enclosed channels at $400\times 120\mu \mathrm{m}$ and $600\times 180\mu \mathrm{m}$ could not be cleared reliably due to trapped resin and frequent blockage, most often near the inner-outlet region. In contrast, $800\times 240\mu \mathrm{m}$ and $1200\times 360\mu \mathrm{m}$ channels were printed and flushed successfully, and $800\times 240\mu \mathrm{m}$ was selected as the smallest reproducibly functional cross-section. Particle-tracking simulations were then used to re-optimize spiral development length, showing that a 4-turn device provides limited collection for $12\mu \mathrm{m}$ targets (10%), intermediate lengths (5–7 turns) improve collection to 50%, and an 8-turn spiral achieves complete large-particle collection (100%) across tested target sizes (12–$24\mu \mathrm{m}$) while reducing small-particle crossover. Experimental validation of the 8-turn $800\times 240\mu \mathrm{m}$ device at $Q=6\mathrm{m}\mathrm{L} {\min }^{-1}$ using fluorescent polystyrene particles ($18\mu \mathrm{m}$ target; $6\mu \mathrm{m}$ background) yielded an average collection efficiency of 84% and an inner-outlet purity of 92%. Overall, these results demonstrate that spiral inertial separation can be retained in a monolithic 3D-printed format when the design is re-optimized around the smallest reliably clearable enclosed cross-section and sufficient spiral development length. Full article

Peritoneal dialysis (PD)-associated peritonitis in children represents a complex interplay between microbial virulence, host immune activation and progressive peritoneal membrane remodeling. It should not be viewed solely as an acute infectious episode, but as a process unfolding within a chronically conditioned immune environment shaped by prolonged exposure to glucose-based dialysis solutions, oxidative stress and persistent biofilm formation on the Tenckhoff catheter. Mesothelial cells act as immunologically active sentinel cells, recognizing pathogen-associated molecular patterns through Toll-like receptors and related innate pathways. Subsequent activation of nuclear factor kappa B, inflammasome signaling and neutrophil extracellular trap formation further amplifies local inflammatory responses. Repeated inflammatory stimulation promotes mesothelial–mesenchymal transition, angiogenesis and extracellular matrix deposition driven by transforming growth factor beta 1 and interconnected profibrotic networks. In pediatric patients, prolonged PD vintage during critical stages of growth may intensify cumulative structural injury and increase the risk of ultrafiltration failure or encapsulating peritoneal sclerosis. Emerging strategies targeting inflammation, fibrosis and biofilm persistence, together with earlier molecular risk detection, may support preservation of the peritoneal membrane. A unified host–pathogen framework may therefore deepen pathophysiological insight and facilitate more individualized therapeutic strategies in pediatric PD. Full article