Search Results (2,645)

Dengue Virus (DENV) induces assembly of the NOD-like receptor (NLR) family pyrin domain containing-3 (NLRP3) inflammasome and autophagy, which are closely interconnected processes playing crucial roles in lipid metabolism and DENV replication. However, the autophagy–NLRP3 activation interplay during DENV infection in human endothelial cells remains incompletely understood. We aimed to elucidate effects of NLRP3 activation on autophagy during DENV-2 infection. We investigated how autophagy-related molecules are altered by NLRP3 inhibition and how this regulation affects lipid metabolism, through the master lipid transcription factors SREBP-1 and 2, which increase the expression of their target lipid-synthesizing genes such as fatty acid synthase (FAS) in a model of microvascular endothelial cells (HMEC-1). We demonstrated a dynamic interplay between inflammasome activity and autophagy in DENV-infected HMEC-1 cells: autophagy increases early during infection and decreases as inflammasome activity increases. NLRP3 inflammasome inhibition affects viral replication. Glyburide (an inflammasome inhibitor) treatment partially inhibited DENV-induced NLRP3 inflammasome activation. Non-structural viral protein expression (NS3 and NS5) and infectious viral-particle formation were significantly reduced. NLRP3 inhibition also downregulated SREBP-1 and SREBP-2 activation. These findings provide new insights into the modulation of the interconnected NLRP3 inflammasome, autophagy, and lipid metabolism pathways, presenting a promising therapeutic strategy for severe clinical forms of dengue. Full article

Bacterial biofilms are critical contributors to chronic infections and antimicrobial resistance. Among the diverse extracellular matrix components, extracellular DNA (eDNA) and amyloid proteins have recently emerged as pivotal structural and functional molecules. Both individually contribute to biofilm stability and antibiotic tolerance, yet their cooperative roles remain underappreciated. This review aims to summarize current knowledge on the origins and functions of eDNA and amyloid proteins in biofilms, to highlight their molecular interactions, and to discuss how their synergistic effects promote biofilm-mediated resistance to antimicrobial agents. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases up to September 2025. Keywords included “biofilm”, “extracellular DNA”, “amyloid proteins”, “matrix”, and “antimicrobial resistance”. Relevant original research and review articles were systematically screened and critically analyzed to integrate emerging evidence on eDNA–amyloid interactions in bacterial biofilms. Current studies demonstrate that eDNA originates primarily from autolysis, active secretion, and host-derived DNA, while amyloid proteins are produced by multiple bacterial species, including Escherichia coli (curli), Pseudomonas aeruginosa (Fap), Bacillus subtilis (TasA), and Staphylococcus aureus (phenol-soluble modulins). Both molecules independently strengthen biofilm integrity and provide protective functions against antimicrobial agents. Importantly, recent evidence shows that eDNA can act as a nucleation template for amyloid fibrillation, while amyloid fibers stabilize and protect eDNA from degradation, creating a dense extracellular network. This synergistic eDNA–amyloid assembly enhances biofilm robustness, impedes antibiotic penetration, sequesters antimicrobial peptides, protects persister cells, and facilitates horizontal gene transfer of resistance determinants. The interplay between eDNA and amyloid proteins represents a central but underexplored mechanism driving biofilm-mediated antimicrobial resistance. Understanding this cooperative network not only deepens our mechanistic insights into bacterial pathogenesis but also highlights novel therapeutic targets. Strategies that disrupt eDNA–amyloid interactions may offer promising avenues for combating persistent biofilm-associated infections. Full article

Autophagy is a highly conserved catabolic process in eukaryotic cells that maintains cellular homeostasis by degrading damaged or superfluous intracellular components. Autophagy plays a dual, paradoxical role during viral infection. However, for most viruses, the induction of autophagy provides a favorable intracellular environment for the full completion of their life cycles. Most viruses that benefit from autophagy adopt a “regulate but not destroy” strategy, i.e., they initiate the autophagic process while suppressing their immune system through mechanisms such as blocking autophagosome-lysosome fusion. This allows them to avoid self-elimination while redirecting other functions of the autophagic machinery—for instance, utilizing autophagy-derived structures such as autophagosomes and double-membrane vesicles (DMVs) as specialized sites for viral genome replication, particle assembly, and maturation. The maintenance of cellular homeostasis by autophagy is crucial for the establishment of viral infection, as it provides a viable cellular microenvironment for viral replication; after infection occurs, inhibiting the degradative function of autophagy becomes a key strategy for viruses. Although canonical degradative autophagy exerts a negative effect on most viruses, redirected nondegradative autophagic structures and repurposed autophagic mechanisms are essential for the efficient replication of various viruses. In-depth analysis of this dynamic virus-autophagy interplay will provide important insights for elucidating virus-host interactions and developing autophagy-targeted antiviral strategies. Full article

Carbon aerogels (CAs) had been well applied in extreme condition thermal insulation, but achieving a balance between mechanical robustness and thermal insulation remains challenging. We present a novel strategy to fabricate carbon aerogels with tunable mechanical properties and thermal insulation properties by tailoring their skeleton architecture via molecular assembly. Carbon precursor aerogel with thick neck particle packing structure was obtained by strong hydrogen-bonding-induced self-assembly between polyurethane-urea oligomer (PUU) and phenolic resin (PF), and carbon aerogel retained robust interparticle connections after pyrolysis, resulting in excellent mechanical properties. The presence of PUU leads to denser packing of resin molecules, promotes graphitization of the carbon and formation of nanocrystalline structures at 1400 °C, resulting in optimized compression modulus and strength. The closed pore structure of carbon skeleton was further studied by Small-Angle X-ray Scattering (SAXS), while moderate pore width (0.4–0.6 nm) optimizes the balance between strength (110 MPa) and thermal conductivity (0.30 W/(m·K)). This work demonstrates that molecular-level assembly combined with pyrolysis control enables precise tuning of carbon aerogel structures and properties, providing new insights for high-temperature thermal insulation applications. Full article

Astrocytes and microglia constitute nearly half of all central nervous system cells and are indispensable for its proper function. Both exhibit striking morphological and functional heterogeneity, adopting either neuroprotective (A2, M2) or proinflammatory (A1, M1) phenotypes in response to cytokines, pathogen-associated molecular patterns (PAMPs)/damage-associated molecular patterns (DAMPs), toll-like receptor 4 (TLR4) activation, and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling. Crucially, many of these phenotypic transitions arise during the earliest stages of neurodegeneration, when glial dysfunction precedes overt neuronal loss and may act as a primary driver of disease onset. This review critically examines glial-centered hypotheses of neurodegeneration, with emphasis on their roles in early disease phases: (i) microglial polarization from an M2 neuroprotective state to an M1 proinflammatory state; (ii) NLRP3 inflammasome assembly via P2X purinergic receptor 7 (P2X7R)-mediated K⁺ efflux; (iii) a self-amplifying astrocyte–microglia–neuron inflammatory feedback loop; (iv) impaired microglial phagocytosis and extracellular-vesicle–mediated propagation of β-amyloid (Aβ) and tau; (v) astrocytic scar formation driven by aquaporin-4 (AQP4), matrix metalloproteinase-9 (MMP-9), glial fibrillary acidic protein (GFAP)/vimentin, connexins, and janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling; (vi) cellular reprogramming of astrocytes and NG2 glia into functional neurons; and (vii) mitochondrial dysfunction in glia, including Dynamin-related protein 1/Mitochondrial fission protein 1 (Drp1/Fis1) fission imbalance and dysregulation of the sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (Sirt1/PGC-1α) axis. Promising therapeutic strategies target pattern-recognition receptors (TLR4, NLRP3/caspase-1), cytokine modulators (interleukin-4 (IL-4), interleukin-10 (IL-10)), signaling cascades (JAK2–STAT, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphoinositide 3-kinase–protein kinase B (PI3K–AKT), adenosine monophosphate-activated protein kinase (AMPK)), microglial receptors (triggering receptor expressed on myeloid cells 2 (TREM2)/spleen tyrosine kinase (SYK)/ DNAX-activating protein 10 (DAP10), siglec-3 (CD33), chemokine C-X3-C motif ligand 1/ CX3C motif chemokine receptor 1 (CX3CL1/CX3CR1), Cluster of Differentiation 200/ Cluster of Differentiation 200 receptor 1 (CD200/CD200R), P2X7R), and mitochondrial biogenesis pathways, with a focus on normalizing glial phenotypes rather than simply suppressing pathology. Interventions that restore neuroglial homeostasis at the earliest stages of disease may hold the greatest potential to delay or prevent progression. Given the complexity of glial phenotypes and molecular isoform diversity, a comprehensive, multitargeted approach is essential for mitigating Alzheimer’s disease and related neurodegenerative disorders. This review not only synthesizes pathogenesis but also highlights therapeutic opportunities, offering what we believe to be the first concise overview of the principal hypotheses implicating glial cells in neurodegeneration. Rather than focusing on isolated mechanisms, our goal is a holistic perspective—integrating diverse glial processes to enable comparison across interconnected pathological conditions. Full article

Solidification cracking is a critical defect in Cu–steel dissimilar laser welding for cylindrical lithium-ion battery busbar assembly, yet the metallurgical role of phosphorus (P) in crack formation has not been quantitatively established. In this study, the influence of phosphorus in the coating layer on weld solidification behavior was clarified by preparing Cu substrates with four different coating conditions—Ni–P-coated Cu (10 and 50 μm) and pure Ni-coated Cu (10 and 50 μm)—and performing high-speed single-mode fiber-laser welding under identical heat-input conditions. Shear-tensile testing, EPMA-based microstructural analysis, and Thermo-Calc solidification calculations were combined to correlate P segregation with solidification cracking susceptibility. The Ni–P 10 μm coating generated severe solidification cracking compared with the pure Ni 50 μm coating, which was attributed to excessive P enrichment in the terminal liquid phase (up to 8.8 mass%). This enrichment significantly expanded the mushy-zone width to approximately 869 K, yielding a highly solidification crack-susceptible fusion zone. In contrast, 50 μm pure Ni coatings produced narrow mushy-zone widths (200–400 K) and extremely low residual P levels (~0.1 mass%), resulting in fully crack-free microstructures. The 50 μm Ni coating exhibited the highest shear-tensile strength and largest rupture displacement among all conditions, confirming that suppression of P segregation directly improves both structural integrity and mechanical performance. Overall, this study demonstrates that phosphorus enrichment critically governs the solidification-cracking susceptibility of Cu–steel dissimilar welds by widening the solidification temperature range. Eliminating P from the coating layer and applying an adequately thick pure Ni coating constitute highly effective strategies for achieving crack-free, mechanically robust welds in lithium-ion battery busbar manufacturing. Full article

Co-reactants are essential in co-reactant-based electrochemiluminescence (ECL) systems because they generate reactive intermediates that can oxidize or reduce ECL luminophores, thereby driving ECL emission. In the context of ECL, gold nanoclusters (Au NCs) have emerged as innovative luminophores, owing to their tunable electronic structures and excellent biocompatibility. However, their efficiency in ECL applications is often compromised by challenges such as limited excited-state generation and non-radiative losses. To tackle these practical challenges, advanced co-reactant engineering strategies have been developed to improve the performance of Au NCs in ECL systems. This review begins with a brief overview of the mechanisms of ECL. Subsequently, a systematic overview of various co-reactant engineering strategies is presented, including: (1) using innovative co-reactants to replace traditional ones due to their lower toxicity and better biocompatibility; (2) applying co-reaction accelerators to reduce the onset potential and improve the production of reactive intermediates from co-reactants; (3) combining co-reactants with luminophores or creating integrated nanostructure assemblies of co-reactants, co-reaction accelerators, and luminophores to achieve shorter electron transfer paths and reduced energy loss for stable high-intensity ECL emission; (4) utilizing host-guest strategies that encapsulate co-reactants within cavities to stabilize radical intermediates and minimize environmental quenching. This review provides a comprehensive overview of recent developments in co-reactant engineering for Au NCs-based ECL systems, thereby encouraging further exploration and understanding of these systems and expanding their potential applications. Full article

Photonic integrated circuits play a crucial role in almost every aspect of modern life, such as data storage, telecommunications, medical diagnostics, green energy, autonomous driving, agriculture, and high-performance computing. To fully harness their benefits, an efficient coupling mechanism is required to successfully launch light into on-chip waveguides from fibers. This study introduces low-loss coupling strategies and their implementation for silicon nitride integrated photonics. Here we present an overview of coupling technologies, optimized designs, and a fabrication technique for inverse tapers, which enable effective coupling for both transverse-magnetic and transverse-electric modes. We measured the coupling losses of 0.15 dB for UHNA-7 fiber at 1550 nm per facet for single-mode 220 × 1200 nm waveguides. We also designed, fabricated, and experimentally characterized a multi-tip taper, yielding 1.5 dB per facet at 1550 nm with broadband stability over 1500–1600 nm. We believe that our approach is universal and can be used both for individual fiber and fiber arrays coupling and for subsequent assembly of fiber with a chip, ensuring minimal losses. Full article

Tungsten oxide (WO₃) nanostructures have emerged as promising electroactive materials due to their high pseudocapacitance, structural versatility, and chemical stability, while reduced graphene oxide (rGO) provides excellent electrical conductivity and surface area. The strategic combination of these nanomaterials in hybrid electrodes has gained attention for enhancing the energy storage performance of supercapacitors. In this work, we report the fabrication and electrochemical performance of nanostructured multilayer films based on the electrostatic Layer-by-Layer (LbL) self-assembly of poly (amidoamine) (PAMAM) dendrimers alternated with tungsten oxide (WO₃) nanofibers dispersed in reduced graphene oxide (rGO). The films were deposited onto indium tin oxide (ITO) substrates and subsequently subjected to electrochemical reduction. UV-Vis spectroscopy confirmed the linear growth of the multilayers, while atomic force microscopy (AFM) revealed homogeneous surface morphology and thickness control. Electrochemical characterization by cyclic voltammetry (CV) and galvanostatic charge–discharge (GCD) revealed a predominantly electrical double-layer capacitive (EDLC) behavior. From the GCD measurements (PAMAM/rGO-WO₃)₂₀ films achieved an areal capacitance of ≈2.20 mF·cm⁻², delivering an areal energy density of ≈0.17 µWh·cm⁻² and an areal power density of ≈2.10 µW·cm⁻², demonstrating efficient charge storage in an ultrathin electrode architecture. These results show that the synergistic integration of PAMAM dendrimers, reduced graphene oxide, and WO₃ nanofibers yields a promising strategy for designing high-performance electrode materials for next-generation supercapacitors. Full article

p17, the human immunodeficiency virus type 1 (HIV-1) matrix protein traditionally associated with viral assembly, has been recently investigated for its extracellular functions linked to vascular damage. This review examines the molecular and pathogenic signatures by which p17 and its variants (vp17s) contribute to endothelial activation, aberrant angiogenesis, and vascular inflammation, highlighting their relevance even under effective antiretroviral therapy (ART). Specifically, p17 exerts chemokine-like activities by binding to chemokine (C-X-C motif) receptor-1 and 2 (CXCR-1/2) on endothelial cells (ECs). This interaction triggers key signaling cascades, including the protein kinase B (Akt)-dependent extracellular signal-regulated kinase (ERK) pathway and endothelin-1/endothelin receptor B axis, driving EC motility, capillary formation, and lymphangiogenesis. Variants such as S75X demonstrate enhanced lymphangiogenic potency, associating them with tumorigenic processes involved in non-Hodgkin lymphoma (NHL) pathogenesis. Importantly, p17 promotes endothelial von Willebrand factor (vWF) storage and secretion, implicating a pro-coagulant state that may trigger the increased thromboembolic risks observed in HIV-positive patients. Furthermore, p17 crosses the blood–brain barrier (BBB) via CXCR-2-mediated pathways, contributing to neuroinflammation by activating microglia and astrocytes and amplifying monocyte chemoattractant protein-1 (MCP-1) levels, therefore playing a critical role in the development of HIV-associated neurocognitive disorders. Hence, the elaboration of potential therapeutic strategies finalized at inhibiting p17/vp17s’ interaction with their receptors could complement ART by addressing HIV-related neurovascular morbidity. Full article

This study presents a strategy for enhancing hydrogel formation through SpyCatcher-mediated conjugation of nanoscale scaffold proteins. We demonstrate that SpyCatcher can facilitate hydrogel assembly with various nano-scaffolds of diverse structural configurations. By conjugating one, two, or three SpyCatcher units to the P9 protein nanoscaffold, hydrogel yield was substantially increased, allowing for the simultaneous co-immobilization of a larger number of enzymes. Characterization using cell-free biosynthesis, electron microscopy, and rheological analysis revealed that the resulting SpyCatcher-mediated nanoscaffold hydrogels exhibit soft solid-like behavior, high elasticity, and an “ink-bottle” pore morphology, which collectively promote and regulate enzymatic activity. Notably, hydrogels crosslinked via the P9 scaffold with two SpyCatcher units showed the most balanced properties, leading to a 149% increase in pyruvic acid production. These findings not only advance the efficient design of hydrogels for enzyme co-immobilization but also provide a foundation for developing more sophisticated models and expanding the scope of biocatalytic systems. Full article

Enterococcus alishanensis JNUCC 77 (=BLH10) was isolated from the flowers of Zinnia elegans collected at Ilchul Land, Jeju Island, Republic of Korea. Whole-genome sequencing was conducted to clarify its taxonomic position, genomic composition, and adaptive metabolic potential. The assembled genome comprised five contigs totaling 3.86 Mb, with a G + C content of 35.6% and 100% completeness. Genome-based phylogenomic analyses using the Type Strain Genome Server (TYGS) and digital DNA–DNA hybridization (dDDH) confirmed that strain JNUCC 77 belongs to E. alishanensis. Functional annotation revealed enrichment of genes related to transcriptional regulation, carbohydrate metabolism, replication, and DNA repair, suggesting a lifestyle adapted to oxidative and UV-exposed floral habitats rather than pathogenic competitiveness. Genome mining with antiSMASH identified two putative biosynthetic regions associated with terpenoid and isoprenoid metabolism, which are commonly linked to redox regulation and cellular protection. These genomic features indicate that E. alishanensis JNUCC 77 has evolved a metal-assisted, redox-regulated survival strategy suitable for floral microenvironments. Given its origin from vibrant flowers and its genomic potential for redox-protective metabolism, this strain represents an attractive microbial resource for future development of nature-inspired postbiotic and cosmeceutical ingredients that align with the clean and eco-friendly image of flower-derived biotechnologies. Full article

Background: Prolonged standing is common in industrial environments and may induce functional adaptations in the foot and postural system. This study aimed to evaluate short-term changes in foot posture and plantar pressure distribution after a working day in assembly line workers. Methods: Forty participants (31 males, 9 females; mean age 44 ± 7 years; BMI 26.1 ± 3.6 kg/m²) performed standing tasks during an 8 h shift. Static baropodometric measurements and 3D foot scans were obtained before and after the workday to assess plantar pressure, contact area, and arch height. The Spanish versions of the Cornell Musculoskeletal Discomfort Questionnaire (CMDQ) and the Foot Function Index (FFI) were used to evaluate discomfort and functional status. Paired t-tests were applied, and correlations were analyzed (p < 0.05). Results: Left-foot arch height decreased significantly after the workday (mean change = 0.6 mm; p = 0.027). Both mean and peak plantar pressures declined (p < 0.001), along with moderate reductions in contact area (p ≤ 0.05). The center of pressure shifted mediolaterally, and discomfort was most frequent in the lower back, knees, and feet. A positive correlation was found between arch height reduction and FFI score (r = 0.349; p = 0.028). Conclusions: Prolonged standing was associated with measurable adaptations in foot posture and plantar pressure, possibly indicating short-term fatigue or compensatory postural adjustments. These results emphasize the importance of assessing plantar load and foot morphology as indicators of potential functional responses to sustained standing and as possible targets for ergonomic and rehabilitation strategies. Full article

Cultured meat has progressed from early in vitro cell culture concepts to regulatory approvals and preliminary commercialization, with recent advancements propelled by interdisciplinary innovations in cell line engineering, serum-free media, bioreactor design, and three-dimensional (3D) assembly technologies. This review synthesizes recent developments from 2023 to 2025, utilizing peer-reviewed publications, patent analyses, regulatory frameworks, and media reports to assess global preparedness for large-scale production. Asia has emerged as a leading hub, with China, Japan, South Korea, and Singapore focusing on scaffold-based 3D cultures, bioinks, and serum-free strategies, complemented by national centers and pilot facilities. The United States leverages its technological advancements and established regulatory framework, as evidenced by recent Food and Drug Administration and United States Department of Agriculture approvals. However, potential complications related to political regional bans and legislation may arise. Europe and the UK prioritize defined media, cell optimization, and structured novel-food regulations, with early commercialization primarily in pet food. Looking ahead, the industrialization of cultured meat is anticipated to be driven by process engineering and hybrid product strategies, with initial pilot-to-demonstration facilities established in countries open to alternative food products. Premium and hybrid cultured meat products are expected to enter the market first, while whole-cut cultured meat is likely to remain a premium offering into the early 2030s. Full article

Driven by Industry 5.0, efficient obstacle avoidance of robotic arms in dynamic environments is a key bottleneck for human–robot collaboration in smart manufacturing. Traditional path planning methods such as Rapidly-exploring Random Tree and artificial potential field work stably in static settings but exhibit flaws including path oscillation and poor real-time performance under dynamic obstacles. Deep reinforcement learning adapts to environmental changes but is limited by low sample efficiency and high computational costs, failing industrial demands. This study proposes a collaborative framework integrating improved Rapidly-exploring Random Tree Star and Deep reinforcement learning. It uses Rapidly-exploring Random Tree Star to guide Deep reinforcement learning’s strategy exploration, reducing invalid sampling by 62%, and leverages Deep reinforcement learning’s global optimization to enhance dynamic obstacle prediction. The framework achieves a task success rate of 93.8%, surpassing traditional Rapidly-exploring Random Tree Star by 21.5%, with an average path length of 1.97 m and system energy consumption of 12.6 kWh. Experiments demonstrate superior performance in extreme dynamic scenarios, including a 94.7% success rate in multi-robot collaboration. Industrial cases confirm improvements in automobile manufacturing assembly cycle time to 8.4 s per task, yield rate to 98.7%, and reductions in energy consumption by 34% and human intervention by 85.6%, providing a reliable dynamic obstacle avoidance solution for Industry 5.0 applications. Full article