Search Results (41,906)

Textile materials represent a versatile class of engineering substrates widely used in apparel, domestic products, and medical protective systems. Despite their extensive application, large-scale textile production has seen limited integration of fundamentally new functionalization strategies. In recent years, however, advances in materials science have enabled the development of textiles with tailored electrical, adaptive, and biological functionalities. This review summarizes recent progress in the functionalization of textile materials with a focus on approaches relevant to engineering and industrial implementation. Particular attention is given to conductive textiles designed for operation under extreme environmental conditions, including low-temperature climates. Methods for integrating electrically conductive elements into fibrous structures are discussed, highlighting their potential for sensing, thermal regulation, and energy-related applications such as powering portable electronic devices. Inkjet printing is presented as a scalable technique for high-resolution deposition of conductive patterns while preserving the mechanical integrity and aesthetic properties of textile substrates. In addition, adaptive and stimuli-responsive textile systems are reviewed, including materials capable of responding to thermal, optical, or chemical stimuli, with applications in camouflage, wearable systems, and multifunctional surfaces. The review further addresses the development of bioactive textiles, emphasizing antibacterial functionalization using organic and inorganic agents to mitigate the spread of pathogenic microorganisms. The relevance of such materials has been underscored by recent global viral outbreaks. Overall, this work aims to provide a materials science perspective on emerging textile functionalization strategies and to facilitate the transition of these technologies from laboratory-scale research to practical engineering applications. Full article

Background/Objectives: Healthcare systems increasingly rely on standardized diagnostic information to support clinical decision-making, reimbursement, and public health governance. Although accreditation of medical laboratories underpins trust in diagnostic services, in practice, it is encountered primarily through the way in which accredited status is communicated in routine healthcare documentation. This study examines national rules that govern the communication of accreditation-related information and their relevance for healthcare management and policy. Methods: A descriptive, document-based comparative analysis was conducted across all 42 national accreditation bodies participating in the European Co-operation for Accreditation Multilateral Agreement (EA-MLA). Official regulations and policies governing the use of accreditation symbols and references in medical laboratory documentation were analyzed. Only documents confirmed as valid and in force as of January 2026 were included. The analysis focused on report-level identification, differentiation of accredited and non-accredited results, use beyond reports, and consequences of misuse. Results: Across countries, accreditation communication rules define how laboratory results are recognized, reimbursed, and operationally used within healthcare systems. While regulatory detail varies, common requirements exist regarding clear identification of accredited results and safeguards against misinterpretation, which directly influence administrative processes and financing mechanisms. For example, in some healthcare systems, accredited reporting determines eligibility for public reimbursement, while in others, it constitutes a legal prerequisite for providing laboratory services. Conclusions: Accreditation-related communication functions as an element of healthcare information governance rather than a purely technical marker. National variations reflect healthcare policy and management priorities, with implications for efficiency, transparency, and access to care. Full article

Meat quality characteristics are important economic traits of ducks. To identify the molecular bases of these traits, we performed an integrated multi-omics analysis (metabolomics, transcriptomics, and miRNAomics) that compared the breast muscle of 300-day-old Liancheng white duck (LD), which is a lean-type breed prized for its soup flavor, and traditional meat duck Cherry Valley duck (CD), which is a fast-growing fat-type breed used for roasting. The results show that LD had higher levels of amino and bile acids, while CD had higher levels of carbohydrates. Integration analysis revealed key breed-specific molecular signatures. In LD, upregulation of the amino acid transporters SLC7A6 and SLC6A9 related to amino acid transport was consistent with elevated intramuscular amino acids. For carbohydrate metabolism, SOCS3—a well-established negative regulator of glucose uptake in mammalian skeletal muscle—was significantly upregulated in LD, consistent with their lower intramuscular carbohydrate levels. SLC6A9 and SOCS3 were predicted to be negatively regulated by oan-miR-1386. In LD, upregulation of the bile acid biosynthesis gene CH25H paralleled the higher bile acid content, suggesting complex, tissue-specific regulation of these pathways. This integrated analysis provides a resource for candidate genes, miRNAs, and metabolic pathways underlying breed-specific meat quality traits in ducks. The findings generate testable hypotheses for future functional studies and offer potential molecular targets for breeding strategies aimed at improving poultry meat quality. Full article

Background/Objectives: Lung cancer remains a major global health burden, largely driven by cigarette use. Although electronic cigarettes (e-cigarettes) are viewed as safer alternatives due to their reduced chemical load, growing evidence shows their vapor can disrupt cellular transcriptomes, including long noncoding RNAs (lncRNAs). In this study, we examined the regulation and function of vape-associated lncRNA transcript 1 (VALT1), a novel transcript upregulated in the oral transcriptomes of e-cigarette users and similarly elevated in non-small-cell lung cancer (NSCLC) tumors. Methods: Publicly available RNA-seq datasets were analyzed, and VALT1 was identified as an e-cigarette-responsive lncRNA. Its dose-dependent induction by e-cigarette smoke extract (eCSE) and cytoplasmic localization were confirmed via RT-qPCR. Its effects on cancer-associated phenotypes including proliferation, ROS detoxification, resistance to apoptosis, migration, cytoskeletal disorganization, and nuclear remodeling were assessed through overexpression and siRNA-mediated knockdown in A549 and BEAS-2B cells. Results: Acute eCSE exposure induced a biphasic, dose-dependent increase in VALT1 expression, accompanied by enhanced proliferation, ROS detoxification, apoptosis resistance, migration, cytoskeletal disorganization, and nuclear remodeling in A549 cells. VALT1 overexpression reproduced these phenotypes in both cell lines without eCSE treatment, whereas knockdown attenuated them. VALT1 promoted survival under cytotoxic stress in A549 but not BEAS-2B cells. Conclusions: These findings support an active role for VALT1 as an e-cigarette vapor-upregulated transcript that contributes to its phenotypic readout and enhances cellular survival under extracellular chemical stress—thereby aggravating tumorigenic phenotypes even in the absence of mutations that contribute to malignant transformation. Full article

Cholestasis in children is characterized by impaired bile flow that disrupts hepatic metabolism, nutrient homeostasis, and effects trace element balance. This narrative review summarizes current evidence on the metabolism, biological functions, and clinical implications of key trace elements—zinc, selenium, copper, and manganese—in pediatric cholestatic liver disease. The liver regulates trace element absorption, intracellular trafficking, storage, and biliary excretion; cholestasis alters these processes, leading to deficiencies or toxic accumulation. Zinc and selenium deficiencies are common and contribute to impaired growth, immune dysfunction, oxidative stress, and delayed hepatic regeneration. Conversely, reduced biliary excretion promotes copper and manganese accumulation, potentially exacerbating liver injury and causing manganese-related neurotoxicity. Recent advances in understanding metal-specific hepatic transporters and trafficking pathways have provided mechanistic insight into these alterations. Management strategies emphasize individualized supplementation, monitoring during enteral and parenteral nutrition, and prevention of deficiency and toxicity. Precision-based nutritional approaches may improve outcomes in pediatric cholestatic liver disease. Full article

(1) Background: Swine hepatitis E (SHE) is an emerging zoonotic disease caused by the swine hepatitis E virus (SHEV). The open reading frame 3 (ORF3) protein is a recognized virulence factor of SHEV. Jaundice, the typical clinical sign of SHE, primarily results from disruptions in bile production, secretion, and excretion. However, the mechanism by which SHEV ORF3 influences bile metabolism remains unclear. (2) Methods: Building on our previous work involving adenovirus-mediated overexpression of genotype IV SHEV ORF3 in HepG2 cells and subsequent high-throughput lncRNA/transcriptome sequencing, this study performed KEGG enrichment analysis on differentially expressed lncRNAs. Candidate lncRNAs were validated via qRT-PCR. Cis-regulated target genes were predicted by integrating differentially expressed mRNA data. Furthermore, AlphaFold 3.0 was employed to analyze the molecular binding sites between lncRNA UBC (MSTRG.6881.4) and its target, UBC protein. (3) Results: We identified three lncRNAs associated with the bile secretion pathway (ko 04976) in HepG2 cells expressing genotype IV SHEV ORF3, which were further confirmed by qRT-PCR: lncRNA UBC (MSTRG.6881.4), lncRNA UBC (MSTRG.6881.9), and lncRNA UBC (MSTRG.6881.12). Bioinformatics prediction suggested six lncRNA-mRNA regulatory networks involved these lncRNAs and two downregulated UBC mRNA transcripts (ENST00000540700 and ENST00000536769). Molecular docking indicated that nucleotides 395U and 41C of lncRNA UBC (MSTRG.6881.4) could potentially bind to residues 82Lys, 88Thr, and 90Thr of the UBC protein, with predicted binding energies ranging from −4.73 to −0.75 kcal/mol. (4) Conclusions: The successful identification of bile secretion-related lncRNAs, coupled with the prediction of their regulatory networks and molecular interaction sites, has advanced our understanding of SHEV ORF3 function and the pathogenesis of SHEV infection. Full article

The technological promise of nonlinear optical (NLO) compounds has stimulated intense interest in optoelectronic devices, data storage, photonics, and anticancer therapy. Thiosemicarbazone ruthenium materials are of growing interest because of their tunable ligand framework and coordination sphere, allowing fine control over geometry, electronics, and functional properties. Here, we report an N-substituted salicylaldehyde thiosemicarbazone ligand and a series of octahedral Ru(III) complexes bearing triphenylphosphine or triphenylarsine and halide (Cl, Br) co-ligands. The complexes were characterized by elemental analysis, FT-IR, UV–Vis, EPR, mass spectrometry, and magnetic susceptibility measurements, which together confirm NS-chelation to a low-spin Ru(III) center in a distorted octahedral environment. Their photophysical and NLO responses were assessed by UV–Vis spectroscopy and powder second-harmonic generation measurements (Kurtz–Perry method), revealing promising NLO behavior. In parallel, antioxidant activity and in vitro anticancer effects against HeLa cells were evaluated by 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical-scavenging and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cytotoxicity assays. These results provide insight into ligand-controlled structure–activity relationships, in which the halide (Cl/Br) and ancillary triarylphosphine co-ligands regulate electronic interactions and lipophilicity and ultimately increase biological performance, underscoring the dual materials and medicinal potential of these Ru(III) complexes. Full article

Melanoma is a highly malignant neoplasm of the skin with early metastatic spread and increasing incidence worldwide. Although there are significant therapeutic advances in immunotherapy, especially with the checkpoint inhibitors targeting PD-1 and CTLA-4, challenges such as treatment-related toxicities, a heterogeneous response to therapy, and drug resistance continue to exist. There are unmet needs for novel therapeutic strategies and/or approaches to complement the existing treatment options. Potential targets for future melanoma treatment are the gap junction proteins, connexins, which show an altered pattern of regulation during melanoma progression. In this review, we highlight the regulation of gap junctions during melanoma progression and the characterization of gap junctions as tumor suppressors during early-stage tumor development and then the reversion to enhancers of tumor metastasis during late-stage melanoma progression. We provide a comprehensive overview of gap junctions in the skin and how the connexin proteins, which comprise gap junctions, are alternatively regulated in melanoma progression. Connexins are protein channels in the human body that consist of 21 isoforms. These isoforms form gap junctions that provide important intercellular signaling and permeability channels. Each connexin protein consists of four transmembrane domains and a C-terminal tail, which is an important part of its function and regulation. Permeants of gap junctions include signaling molecules such as cyclic AMP and inositol triphosphate which are linked to key cellular behaviors such as proliferation and migration, making them essential for several tumor-related processes. At least ten connexin isoforms are found in normal skin. Connexin 43 (Cx43) is classified as the most prevalent isoform while Connexin 26 (Cx26) has been reported to be more specialized with restricted expression patterns. Cx43 and Cx26 regulate the growth, differentiation, and repair of the epidermis after injury. Evidence suggests that connexins have a stage-related function in melanoma. Loss of connexin expression and gap junctional intercellular communication is linked to tumor suppression and loss of differentiation in early-stage melanoma, while re-expression or overexpression of specific connexins, notably Cx43, may promote metastasis through enhanced tumor–stromal interactions and increased motility in late-stage melanoma. Such opposing actions of connexins support their candidacy as biomarkers and therapeutic targets. Understanding the dual-stage related functions of connexins in melanoma development and progression may lead to less cytotoxic and more efficient future therapeutic approaches. Full article

Sodium–glucose cotransporter 2 inhibitors (SGLT2is) have revolutionized the treatment of heart failure and are now established as disease-modifying therapies across the spectrum of left ventricular ejection fraction. More recently, these agents have been evaluated in the early post-acute myocardial infarction (AMI) setting, raising interest in their potential role beyond heart failure prevention. Evidence from post-AMI randomized trials and contemporary meta-analyses consistently shows neutral effects on ischemic coronary outcomes, despite favorable effects on heart failure-related endpoints, ventricular remodeling, and cardiometabolic parameters. At the same time, data from experimental and translational research provide a biological framework in which SGLT2i exert anti-atherogenic effects through multiple complementary mechanisms, including improvement of cardiometabolic risk factors, attenuation of vascular and systemic inflammation, modulation of endothelial function, regulation of vascular smooth muscle cell behavior, macrophage inflammatory polarization, inhibition of inflammasome signaling, and modulation of the perivascular adipose tissue–vascular interface. Taken together, the available evidence highlights a dissociation between clinical trial outcomes in the early post-AMI phase and the underlying vascular biology associated with SGLT2 inhibition. While the dominant early clinical effects of SGLT2i appear to relate to hemodynamic and heart failure-preventive mechanisms, their potential impact on atherosclerotic disease may be more gradual and context-dependent. This review summarizes current clinical and mechanistic evidence supporting this interpretation and discusses the implications for understanding the role of SGLT2i in patients after AMI. Full article

Acidic chitinase (Chia) degrades chitin, a structural polysaccharide in insect exoskeletons, and plays important roles in omnivorous and insectivorous mammals and birds. In birds, gene duplications have generated multiple Chia paralogs with functional divergence, but the molecular basis for this diversification remains unclear. Here, we characterized three chicken Chia paralogs (Chia1–3) and identified distinct pH-dependent enzymatic profiles. Chia1 is enzymatically inactive but was captured by chitin-affinity resin despite lacking a canonical chitin-binding domain, suggesting residual substrate interaction through the catalytic domain or a non-catalytic role. Chia2 exhibits maximal activity at pH 2.0, whereas Chia3 peaks at pH 5.0 and displays broader activity. Exon swapping and site-directed mutagenesis identified residues 104 (Ala in Chia2, Asp in Chia3) and 269 (His vs. Asn) as key contributors to pH-dependent activity differences. Reciprocal substitutions shifted pH profiles accordingly. Structural modeling and computational pKa predictions suggested that D213 and residue 269 may function as a pKa-regulating module influencing catalytic ionization. Comparative sequence analysis revealed lineage-specific conservation of these residues, consistent with adaptive divergence. Our findings show that limited amino acid substitutions can markedly modify pH-dependent enzymatic activity, providing mechanistic insight into how local residue variation contributes to the functional diversification of duplicated genes. Full article

Sports performance in aquatic environments is governed by biomechanical, physiological, neuromuscular and perceptual–mental constraints that differ fundamentally from those encountered on land. As a result, athletes with comparable general physiological or motor capacities may achieve markedly different performance outcomes in aquatic sports. Within functional kinesiology and sport science, aquatic performance is still frequently interpreted through isolated physiological, biomechanical, or technical variables, which limits both explanatory depth and applied relevance. This Perspective article introduces aquaticity as an integrated latent construct representing a multidimensional determinant of sports performance specific to the aquatic environment. Aquaticity is conceptualized as a functional framework that modulates how general physiological and motor capacities are expressed under aquatic constraints, integrating key domains of exercise physiology, sport biomechanics, neuromuscular control, energetic regulation, and perceptual–mental stability. The relative contribution of these domains is considered discipline-specific and dependent on task and environmental demands. Breath-hold diving is presented as a particularly suitable model for examining aquaticity, as apnea and hypoxic–hypercapnic stress amplify interactions between physiological regulation, neuromuscular control, and biomechanical efficiency. Training and diagnostic tasks performed in real aquatic settings are interpreted as manifest indicators of aquaticity, enabling ecologically valid athlete monitoring and performance assessment. Within this framework, energetic aquaticity is highlighted as a central functional sub-construct linking metabolic regulation, movement efficiency, and neural control during performance under respiratory constraints. The proposed conceptual framework has important implications for functional kinesiology, sport biomechanics, exercise physiology, and applied athlete monitoring in aquatic sports. Aquaticity is advanced not merely as a descriptive concept, but as a unifying framework that can guide future experimental research, discipline-specific diagnostics, individualized training design, and safety-oriented performance assessment in aquatic environments. Full article

Salt stress severely constrains wheat growth and yield by inducing osmotic imbalance, ion toxicity, and excessive accumulation of reactive oxygen species (ROS). Although salt-tolerant cultivars can adapt through rapid signaling transduction and maintenance of cellular homeostasis, the underlying dynamic regulatory networks remain insufficiently characterized. In this study, we reanalyzed publicly available time-series RNA-seq data (0, 1, 3, 6, 12, and 24 h) from the salt-tolerant wheat cultivar Xiaoyan22 under salt stress and constructed a time-series-based co-expression network using weighted gene co-expression network analysis (WGCNA). Multiple gene modules were identified, among which the black module showed significant positive correlations with both salt treatment (treatment_bin) and stress duration (time_h). This module displayed a progressively increasing eigengene expression pattern throughout the stress period. Gene significance (GS) was positively correlated with module membership (MM), facilitating the identification of highly connected hub genes within this module. Functional enrichment analysis indicated that genes in the black module were primarily associated with DNA replication and genome stability maintenance, RNA metabolic regulation, phenylpropanoid metabolism, and cuticle/suberin/wax biosynthesis. Physiological analysis further revealed enhanced activities of superoxide (SOD), peroxide (POD), and catalase (CAT), enhanced accumulation of proline and soluble sugars, and a time-dependent increase in MDA under salt stress. qRT-PCR confirmed significant induction of candidate genes, including a ZAR1-like receptor kinase, Remorin, and NETWORKED 1D. Collectively, these findings integrate co-expression network inference with physiological and molecular validation, providing candidate regulators and pathways for understanding salt tolerance and supporting future molecular breeding efforts. Full article

Context: S-phase kinase-associated protein 2 (SKP2) is an oncogene and cell cycle regulator that mediates the ubiquitination of cell cycle regulators. Curcumol, a sesquiterpene natural product, has been reported to regulate SKP2-mediated ubiquitination degradation to overcome drug resistance in cancer cells. However, whether the cell cycle arrest effect of curcumol is related to SKP2’s function in cancer cells and its mechanisms are still unclear. Objective: To investigate the role of SKP2 in curcumol-induced cell cycle arrest and its underlying mechanisms. Materials and Methods: Transcriptomic and proteomic analyses were used to screen the ubiquitination-related factors in curcumol treated hepatocellular carcinoma cells. Lentiviral overexpression, co-immunoprecipitation assays, ubiquitination analysis, and cell-line-derived xenograft (CDX) models were used to dissect the role and mechanisms of the identified ubiquitination-related factor in the cell cycle arrest effect of curcucmol. Results: Curcumol modulated the expression of CDK4, CDK6, Cyclin D1, p27 and SKP2. SKP2 was one candidate target of curcumol selected by multi-omics. Overexpressed SKP2 partially reversed curcumol-induced growth inhibition and G1-phase arrest. The increased expression of p27 induced by curcumol was attenuated by overexpressed SKP2. Curcumol impaired the interaction between SKP2 and p27, and led to the ubiquitination and degradation of p27. In vivo, curcumol effectively reduced tumor growth, and its antitumor effect was significantly mitigated by SKP2 overexpression. Discussion and Conclusions: Curcumol reduced SKP2 expression, weakened the interaction between SKP2 and p27, inhibited degradation of p27, and then induced G1 phase cell-cycle arrest in SK-Hep-1 cells. Full article

The mitogen-activated protein kinase (MAPK) cascade constitutes a core component of signal transduction pathways in eukaryotic organisms. With its precise, efficient, and specific mechanism of action, this cascade pathway integrates, amplifies, and rapidly transmits signals. Among them, the specificity and functional diversity of the MPK3 cascade depend on the phosphorylation interaction between MKK and MPK3, as well as the specific interaction between MPK3 and its substrates. MPK3 targets an extremely diverse array of substrates, including transcription factors, RNA-binding proteins, enzymes, and transporters. The summary of the regulatory role of the MPK3 signal mainly focuses on three functional mechanisms: The most well-known regulatory mechanism is to recognize and phosphorylate substrate proteins or transcription factors, thereby affecting the stability and transcriptional activity of downstream substrates, and thus regulating the transcriptional regulatory activity and expression of downstream genes. MPK3 can also participate in downstream functional regulation by triggering the MAPKKK-MKK4/5-MPK3/6 signaling pathways or feedback mechanisms. MPK3 can exert regulatory effects independently or together with MPK6. The redundancy of the MPK3/6 function is related to the synergistic effect of the component cascade reaction, as well as the dose-dependent activation effect. This article presents a comprehensive synthesis of the latest research progress on the regulatory role of MPK3, in plant growth, development, and stress adaptation and defence. Moreover, it provides critical evaluations and forward-looking perspectives on the future investigation of the underlying molecular mechanisms governing MPK3-mediated regulation. Full article

Background: Chronic pain is a prevalent and disabling condition that affects physical health but also cognitive domains. Executive functions, including inhibitory control, cognitive flexibility, and working memory, essentials for self-regulation, treatment adherence, and coping with symptoms, are particularly compromised. Physiotherapy interventions, traditionally aimed at physical outcomes, may also influence executive functions; however, their impact remains unclear. Objective: This review aimed to synthesize current evidence regarding the effects of physiotherapy-related interventions on executive function in adults with chronic pain. Methods: The review followed the Cochrane Handbook and Preferred Reporting Items for Systematic Reviews (PRISMA) guidelines, and the protocol was registered in PROSPERO (CRD42024611800). A comprehensive search was performed. Randomized controlled trials (RCTs) included adults with chronic pain (≥3 months) whose executive function outcomes were evaluated after physiotherapy-based interventions. Results: Out of 12,391 records, 10 randomized controlled trials were included. Populations primarily had fibromyalgia, chronic low back pain, and chronic musculoskeletal pain. Interventions encompassed transcranial direct current stimulation (tDCS), transcranial magnetic stimulation (rTMS), neurofeedback, structured exercise, and multimodal physical-cognitive-mindfulness training. Intervention durations ranged from one session to 16 weeks. Executive function was assessed with diverse neuropsychological tests. tDCS improved attention, inhibitory control, cognitive flexibility, and working memory. Exercise interventions showed benefits in working memory and inhibitory control. Conclusions: Preliminary evidence suggests that physiotherapy interventions, particularly anodal tDCS and structured exercise, may improve executive functions in individuals with chronic pain. Future trials should incorporate long-term follow-up. Integrating cognitive targets into physiotherapy may enhance the multidimensional management of chronic pain. Full article