Search Results (36,575)

Water buffaloes in northern Australia occupy tropical wetlands where conditions favour the proliferation of arthropod vectors and the transmission of vector-borne livestock diseases. However, their role in maintaining economically important arboviruses such as Akabane virus (AKAV), bluetongue virus (BTV), and bovine ephemeral fever virus (BEFV) remains poorly understood. These three viruses cause significant production losses in cattle and pose ongoing surveillance challenges in remote areas. To assess exposure to these viruses, a convenience sample of feral water buffaloes from the Northern Territory, Australia, was collected. Commercial enzyme-linked immunosorbent assays (ELISAs) were used to detect antibodies against AKAV, BTV, and BEFV in 119 samples stored as dried blood on filter paper. Seroprevalence was 18.5% for AKAV, 66.4% for BTV, and 15.1% for BEFV. These results are consistent with previous serological studies in northern Australian cattle, confirming the circulation of these pathogens in the region. Our findings demonstrate that water buffaloes are exposed to these economically important arboviruses and may contribute to their maintenance, highlighting the need to consider feral buffalo populations in regional arbovirus surveillance strategies and livestock disease management. Full article

This article analyses the Museo de los Desplazados (Museum of the Displaced), a collaborative platform conceived by the Left Hand Rotation collective to foster shared reflection on gentrification processes. This project takes the form of a collective and decentralised digital archive, functioning as an open, ‘in-process’ collaborative tool. Within the context of the proliferation of self-organised digital archives, this study explores how the Museum acts as a dynamic social object that articulates dispersed narratives. Drawing on Derrida’s concept of the ‘anarchive’, the research validates the hypothesis that there is a direct relationship between the profiles of autonomous collectives and their specific epistemic practices. The findings reveal that activists utilise the archive as a tool for legal defence, ‘heat-of-the-moment’ ethnography, and networking, thereby resisting ‘archival violence’ and constructing collective counter-memory. Ultimately, the Museum demonstrates that memory is not a guarded site, but a living network built through horizontal and rhizomatic collaboration. Full article

Myocarditis has been described following SARS-CoV-2 infection. The mechanisms underlying COVID-19-associated myocarditis remain incompletely understood. Peripheral blood mononuclear cells (PBMCs), IgG fractions, and myocardial biopsy tissue were obtained from a patient with COVID-19 myocarditis. Cellular responses to SARS-CoV-2 spike protein and myocardial tissue extract were assessed in vitro. PBMCs and purified IgG were passively transferred into Rag2/IL2RG-/- mice. Interferon-gamma (IFN-γ) production and cardiac IFN-γ transcript levels were measured. PBMCs from the myocarditis patient proliferated in response to spike protein and myocardial tissue extract, whereas PBMCs from a healthy control did not. PBMCs from the patient secreted higher concentrations of IFN-γ compared with the healthy control. Introduction of patient PBMCs or IgG into Rag2/IL2RG-/- mice resulted in higher cardiac IFN-γ transcript levels compared with control PBMCs or IgG. These findings demonstrate cellular reactivity to SARS-CoV-2 spike protein and myocardial tissue, increased IFN-γ production, and induction of cardiac IFN-γ expression following passive transfer of immune components. Full article

Chemokine CXCL1, also known as Gro-α and MGSA, a ligand of CXCR2, is the best-known CXC chemokine in cancer processes, after CXCL8/IL-8 and CXCL12/SDF-1. This paper is the first review on the role of CXCL1 in general molecular processes associated with cancer. It provides a comprehensive overview that allows for an in-depth understanding of the importance of CXCL1 in tumor-related processes. In this review, however, we did not address the clinical aspects of CXCL1, as these were discussed in our previous review articles. The present paper focuses on the involvement of CXCL1 in cancer processes such as proliferation, cancer stem cell (CSC) function, senescence, angiogenesis, lymphangiogenesis, migration and metastasis, and effects on tumor-associated cells such as neutrophils, tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), and cancer-associated fibroblasts (CAFs). It also describes the significance of CXCL1 in cancer-associated diseases such as cancer cachexia, cancer-associated immunodeficiency, neuroinflammatory-mediated affective-like behaviors, bone cancer pain, and acute kidney injury. We also present the effects of obesity on CXCL1-related cancer processes. Full article

Obesity is characterized by abnormal adipose tissue expansion and energy metabolism imbalance. Browning of white adipose tissue (WAT), wherein white adipocytes acquire thermogenic properties similar to brown adipose tissue, represents a key mechanism for increasing energy expenditure. Although ginseng (Panax ginseng C.A. Meyer) is widely recognized as a health-promoting botanical, its role in WAT browning has not been fully elucidated. This review summarizes evidence that ginseng and its bioactive components regulate major thermogenic pathways, including β-adrenergic/cyclic adenosine monophosphate-protein kinase (cAMP-PKA) signaling, AMP-activated protein kinase (AMPK), and the peroxisome proliferator-activated receptor γ (PPARγ)/coactivator 1α (PGC-1α) axis, thereby upregulating key markers such as uncoupling protein 1 (UCP1), PR domain containing 16 (PRDM16) and type II iodothyronine deiodinase (DIO2). These effects promote mitochondrial function and fatty acid oxidation, reduce lipogenesis, alleviate inflammation, and improve insulin sensitivity, collectively fostering a microenvironment conducive to browning. Furthermore, fermentation has been found to enhance the bioactivity and thermogenic efficacy of ginseng. Recent evidence indicates that gut microbiota and their metabolites—such as short-chain fatty acids, unsaturated fatty acids, and bile acids—play a notable role in ginseng-induced thermogenesis via receptors including G-protein-coupled receptor 41/43 (GPR41/43), takeda G-protein-coupled receptor 5 (TGR5), and farnesoid X receptor (FXR). These multi-organ interaction networks involving the gut–fat, gut–liver, and gut–brain axes reflect the role of ginseng in integrating systemic metabolism. In summary, this review discusses the multi-level regulatory network through which ginseng promotes WAT browning, providing a mechanistic basis for its potential application in body weight and metabolic health management. Full article

The rapid proliferation of mobile Internet of Things (IoT) devices has introduced significant resource scheduling challenges in multi-edge computing networks, where device mobility leads to dynamic network connectivity and load imbalance, complicating task offloading and resource management. To address these issues, this paper presents a mobility-driven hierarchical optimization framework for task offloading and computation resource allocation in multi-region edge computing environments, a functionally coupled hierarchical framework that integrates mobility-aware heuristic offloading with multi-agent deep deterministic policy gradient (MADDPG)-based resource allocation. Devices are first clustered according to their mobility patterns, and offloading decisions are dynamically made based on trajectory and dwell-time characteristics. Each edge server is modeled as an autonomous agent, and an MADDPG framework is adopted to collaboratively optimize resource allocation, with the joint objective of minimizing task processing delay and system energy consumption. Experimental evaluations under diverse mobility and workload conditions show that the proposed approach achieves a 19.0% reduction in task delay compared to the Multi-Objective Gray Wolf Optimization (MOGWO) method at the largest device scale (60 devices) and maintains comparable energy efficiency. Furthermore, it exhibits stronger adaptability and scheduling performance across varying mobility group distributions. These results confirm the effectiveness of the proposed method in enhancing system performance within dynamic mobile edge computing scenarios. Full article

Cashmere goats produce high-value fine fibers derived from secondary hair follicles; however, the molecular mechanisms underlying this trait remain incompletely understood. In this study, comparative transcriptome sequencing was performed on skin tissues from Inner Mongolian cashmere goats and normal goats to characterize gene expression differences associated with cashmere fiber production. High-quality RNA-seq data with strong mapping efficiency and reproducibility were obtained across all samples. Differential expression analysis identified 1543 significantly differentially expressed genes (DEGs) between cashmere and normal goats, including genes involved in hair follicle morphogenesis, epidermal differentiation, cell proliferation, and extracellular matrix organization. Multivariate analyses showed a clear transcriptomic separation between fleece types, indicating that fleece phenotype is the primary driver of variation in global gene expression. Functional enrichment revealed significant involvement of the Wnt, MAPK, and PI3K–Akt signaling pathways, and several biologically relevant regulators of hair follicle development and hair cycle control, including FGF5, SOX9, LHX2, and VDR, were differentially expressed. Gene fusion events were rare and showed no group specific patterns, whereas alternative splicing was widespread, with exon skipping as the predominant splicing event in goat skin. Overall, these results provide quantitative transcriptomic evidence linking signaling regulation, follicle development, and structural differentiation to secondary hair follicle activity and cashmere fiber formation, offering candidate genes and molecular pathways for functional validation and molecular breeding in cashmere goats. Full article

Developing potential skincare formulations capable of simultaneously managing infection and promoting tissue repair remains a critical challenge in dermatological care. This study engineered bioactive oleogels using sunflower wax (SFW), rice bran wax (RBW), and 12-hydroxystearic acid (HSA) to deliver a synergistic essential oil blend (ginger, cinnamon, tea tree, geranium). A D-optimal mixture design optimized formulations to match the textural profile of a commercial benchmark. Crucially, the fatty acid architecture of the carrier oil emerged as a primary determinant of network integrity; the high oleic acid content in camellia oil facilitated robust RBW crystallization by minimizing steric hindrance, whereas the polyunsaturated, kinked structure of linoleic acid in almond oil disrupted SFW networks, resulting in lower stiffness. Thermal characterization (DSC) established a distinct stability hierarchy with RBW exhibiting the highest melting point (Tp = 60.1 °C) and enthalpy (ΔHm = 7.79 ± 0.74 J/g). Thermogravimetric analysis (TGA) confirmed high thermal resistance for wax-based systems (Tdeg ≈ 357 °C), whereas HSA displayed a biphasic degradation starting at ~206 °C. FTIR spectroscopy verified the stable physical entrapment of bioactives, with the lipid vehicle dominating the spectral fingerprint. Rheological profiling revealed that RBW oleogels, structured in high-oleic camellia oil, formed rigid networks (G′ ≈ 5.7 × 104 Pa) with high yield stress (20.91 Pa), offering superior retention. In contrast, HSA oleogels displayed “smart” thixotropic recovery with lower stiffness (G′ ≈ 2.1 × 104 Pa) and a distinct melting peak at 22.5 °C, compared to 60.1 °C for RBW. All formulations achieved a >2 Log₁₀ reduction (99%) in Staphylococcus aureus and Pseudomonas aeruginosa viability after 12 h. Furthermore, in vitro keratinocyte assays identified a hormetic therapeutic window at 1–5 μg/mL (essential oil blend equivalent); specifically, SFW oleogels at 5 μg/mL stimulated proliferation to 158.07% relative to controls. These findings confirm that optimizing the lipid vehicle–bioactive interface creates dual-action scaffolds capable of simultaneously managing infection and stimulating in vitro keratinocyte proliferation. Full article

The sodium–hydrogen exchanger-1 (NHE1) is a ubiquitously expressed transmembrane transporter that plays a central role in maintaining intracellular pH homeostasis and supporting normal cellular function. In cancer, NHE1 is overexpressed in many tumor types and has been associated with increased cancer cell metastasis and proliferation. Beyond these established roles, emerging evidence implicates NHE1 as a regulator of cancer cell metabolism. By driving intracellular alkalinization and shaping the tumor microenvironment, NHE1 influences metabolic pathway activity, mitochondrial function, redox balance, and cellular stress responses. In this review, we synthesize current evidence linking NHE1 dysregulation to metabolic reprogramming in cancer, with a focus on mitochondrial metabolism, glycolytic flux, lysosomal biology, and reactive oxygen species-associated stress pathways. We further evaluate pharmacological strategies targeting NHE1, emphasizing their metabolic consequences, translational potential, and the challenges that have limited clinical application to date. Collectively, this review highlights NHE1 as a potential integrator of ion transport and metabolic control in cancer and discusses how targeting NHE1-driven metabolic programs may support the development of novel therapeutic strategies. Full article

Background: During aging, skeletal muscle mass constantly diminishes and myogenic potential declines. At the cellular level, a decline in mitochondrial function is a hallmark of the aging process and the deficiency of the mitochondrial network contributes to a progressive reduction in muscle mass. Autophagic clearance of mitochondria through the process of mitophagy is required to remove impaired or damaged mitochondria, while mitophagy is a key regulator of muscle maintenance. Dysfunctional degradation of mitochondria is increasingly associated with aging (mitophaging), while mechanical stimuli have been shown to ameliorate the aging-induced impaired muscle mass and function; however, less is known about the potential effects of mechanical loading on mitophaging. The aim of the present study was to investigate the effect of mechanical stretching on mitophagy in aged myoblasts, in vitro. Methods: Cell senescence was replicated using a multiple cell division model of C2C12 myoblasts. The control and aged cells were cultured on elastic membranes and underwent passive stretching using a mechanical loading protocol of 15% elongation for 12 h at a frequency of 1 Hz. Cell signaling and gene expression responses of mitophagy-associated and myogenic regulatory factors (MRFs) were assessed through immunoblotting and qRT-PCR of the cell lysates derived from stretched and non-stretched control and aged myoblasts. Results: Mitophagy factor AMP-activated protein kinase (AMPK), mitochondrial biogenesis stimulator peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1a), and mitophagy/mitochondrial biogenesis factor Parkin were downregulated in control stretched myoblasts compared to non-stretched cells, while the specific mechanical loading protocol used also reduced the phosphorylation of unc-51-like autophagy-activating kinase 1 (p-ULK1) (p < 0.05), as well as the expression of myogenic factor 5 (Myf5) and myogenic factor 4 (myogenin) (p < 0.001). Interestingly, this mechanical loading resulted in increased PGC-1a and Parkin expression (p < 0.05) and induced the previously undetected BCL2 interacting protein 3-like (BNIP3L/NIX) and AMPK expression and p-ULK1 activation in the aged myoblasts. In addition, mechanical stretching differentially affected the expression of MRFs in aged cells, upregulating the early differentiation factor, Myf5 (p < 0.01), while downregulating the late differentiation factor myogenin (p < 0.001). Conclusions: These findings suggest the beneficial effects of mechanical loading on the impaired mitophagy and early differentiation in aged myoblasts, as indicated by the mitophagy initiation and the promotion of mitochondrial biogenesis in these cells. The mechanical loading-induced downregulation of mitophagy and myogenesis in the control myoblasts might indicate their loading-specific differential responses compared to the aged cells. Full article

Background and Objectives: Polyethylene (PE) mulching enhances crop productivity through microclimate optimization but introduces synthetic polymer-derived compounds into agricultural soils. Despite widespread use, biochemical and microbial impacts of PE mulch emissions remain poorly understood. This study investigated the impact of PE mulch emissions on soil metabolomes and microbial communities during field pea (Pisum sativum L.) cultivation. Methods: A 75-day field experiment compared PE-mulched and non-mulched soils across five temporal sampling points (T0–T4). Headspace solid-phase microextraction coupled with gas chromatography–mass spectrometry was used to identify PE-derived organic compounds in mulched soils. Microbial community structure was assessed through the phospholipids derived fatty acids (PLFA) approach, whereas mass spectrometric untargeted metabolomics was used to characterize the soil biochemical profiles. Results: Analysis identified 18 PE-derived organic compounds (n-alkanes, phthalates, and additives) in the mulched soils. PE mulching significantly increased bacterial abundance (anaerobic bacteria, actinomycetes, and aerobic bacteria) but suppressed all functional fungal guilds, particularly saprotrophic fungi (30% reduction) and arbuscular mycorrhizal symbionts. PE-derived organic compounds were associated primarily with the first RDA axis (RDA1), which alone explained 44.6% of the metabolome variance. These compounds presented strong positive correlations with organic nitrogen compounds and lipids and negative correlations with benzenoids and nucleotides. Pathway analysis revealed perturbations in energy metabolism, lipid metabolism, and xenobiotic degradation pathways. Conclusions: PE mulch emissions differentially shift soil microbial communities and metabolic networks, with bacterial proliferation contrasting with fungal suppression. These findings highlight the complex trade-offs between agronomic benefits and soil biological impacts, emphasizing the need for sustainable mulching alternatives. Full article

Triple-negative breast cancer (TNBC) lacks effective targeted therapies, and the mechanisms by which developmental endothelial locus-1 (EDIL3/Del-1) promotes TNBC remain incompletely defined. We profiled Del-1 and AMPK subunits in TNBC cell lines by RT-PCR and immunoblotting, performed functional assays in CRISPR/Cas9 Del-1 knockout and AMPKβ-manipulated cells, and evaluated AMPKβ in early-stage TNBC tumors using tissue microarrays (TMA) (immunohistochemistry; n = 100) and AMPKβ2 mRNA quantification. Del-1 and AMPKβ were enriched in TNBC cells, most prominently in the mesenchymal stem-like subtype, whereas AMPKα levels were relatively stable. Increased Del-1 and activated AMPKβ enhanced proliferation and invasion, while Del-1 deletion reduced AMPKβ expression and suppressed tumor-promoting phenotypes. Mechanistically, Del-1 increased AMPKβ phosphorylation at serine 108, and a phospho-mimetic AMPKβ mutant further amplified oncogenic effects. In the pilot TMA study, high AMPKβ protein expression showed a trend toward poorer DFS in Kaplan–Meier analysis, while multivariate analysis identified high AMPKβ protein expression as an independent factor associated with poorer DFS in patients with early TNBC. These data support AMPKβ as a key mediator of Del-1-driven signaling and suggest AMPKβ could be a therapeutic target in aggressive TNBC subsets. Full article

The proliferation of generative artificial intelligence (AI) as an autonomous recommendation agent fundamentally challenges traditional paradigms of marketing communication. As AI systems increasingly mediate consumer–brand relationships, understanding how artificial agents construct persuasive discourse—distinct from human communicators—becomes critical for developing effective dual-channel marketing strategies. Grounded in Source Credibility Theory and the Computers Are Social Actors (CASA) paradigm, this study investigates the semantic and structural divergence between AI-generated product recommendations and human influencer marketing messages in social commerce contexts. Employing a mixed-methods computational approach integrating term frequency analysis, TF-IDF weighting, Latent Dirichlet Allocation (LDA) topic modeling, and BERT-based contextualized semantic embedding analysis (KR-SBERT), we examined 330 Instagram influencer posts and 541 AI-generated responses concerning inner beauty enzyme products—a hybrid category combining functional health claims with hedonic beauty appeals—in the Korean social commerce market. AI-generated responses were collected through a systematically designed query protocol with empirically grounded prompts derived from actual consumer search behaviors, and analytical robustness was verified through sensitivity analyses across multiple parameter thresholds. Our findings reveal a fundamental divergence in persuasive architecture: human influencers construct experiential narratives exhibiting message characteristics typically associated with peripheral-route cues (sensory descriptions, emotional testimonials, social context), while AI recommendations employ systematic, evidence-based discourse exhibiting message characteristics typically associated with central-route argumentation (functional mechanisms, ingredient specifications, objective criteria). Topic modeling identified four distinct thematic clusters for each source type: human discourse centers on embodied experience and relational consumption, whereas AI discourse organizes around informational utility and rational decision support. Jensen–Shannon Divergence analysis (JSD = 0.213 bits) confirmed moderate distributional divergence, while chi-square testing (χ² = 847.23, p < 0.001) and Cramér’s V (0.312, indicating a medium-to-large effect) demonstrated statistically significant and substantively meaningful differences. These findings extend CASA theory by demonstrating that AI recommendation agents develop a characteristic “AI communication signature” distinguishable from human persuasion patterns. We propose an integrated Dual-Agent Persuasion Proposition—synthesizing CASA, ELM, and Source Credibility perspectives—suggesting that AI and human recommenders serve complementary functions across different stages of the consumer decision journey—a proposition whose predictions regarding sequential persuasive effectiveness and consumer processing routes await experimental validation. These findings carry implications for AI content strategy optimization, platform design, and emerging regulatory frameworks for AI-generated content labeling. Full article

Given the challenges in treating metastatic melanomas, there is a growing need for novel and effective therapeutic strategies. This study aimed to understand molecular mechanisms underlying synergistic effects of a Tempol and ML210 combination in B16F10 murine melanoma cells and to evaluate its therapeutic potential. We hypothesized that this combination would synergistically induce cell death by increasing oxidative stress and triggering ER stress. B16F10 melanoma cells were treated with Tempol and ML210 alone or in combination for 48 h. Cell viability was determined using MTT assay. Oxidative stress was evaluated by measuring Total Antioxidant Status (TAS), Total Oxidant Status (TOS), and intracellular H₂O₂ levels. Apoptotic markers (caspase-3, Bax, Bcl-2) and ER stress proteins (GRP78, GADD153, IRE1α, ATF6) were quantified by ELISA. Combination treatment significantly inhibited cell proliferation compared to monotherapies. Molecular analyses revealed that combination caused depletion of TAS and increase in TOS and intracellular H₂O₂ levels. Furthermore, combination treatment synergistically upregulated ER stress markers and pro-apoptotic proteins while significantly suppressing anti-apoptotic Bcl-2 expression. In conclusion, the combination of Tempol and ML210 synergistically induces cell death in B16F10 melanoma cells by disrupting redox balance and activating ER stress-mediated apoptosis. These findings suggest a potential strategy for melanoma treatment that warrants further in vivo investigation. Full article

Background/Objectives: Acute myeloid leukemia (AML) remains a hematologic malignancy with poor prognosis. The neddylation inhibitor MLN4924 has demonstrated potent anti-leukemic activity in preclinical models, yet its clinical translation faces significant challenges. The aim of this study was to explore combination therapy strategies that could further enhance MLN4924’s anti-leukemia potential. Methods: AML cell lines used in this study were Kasumi-1 and MOLM-13. Cell viability was assessed using CCK-8 assays. mRNA and protein expression levels were determined through RT-qPCR and Western blot, respectively. Flow cytometry was employed to analyze surface markers (SLC1A5, CD11b, CD14, CD16), mitochondrial membrane potential (JC-1), and apoptosis (Annexin V-FITC/PI). In vivo efficacy was validated using an NCG mouse xenograft model. Transcriptomic profiling was performed to explore the potential mechanism by which MLN4924 in combination with V9302 inhibits leukemia. Results: Treatment with MLN4924 significantly upregulated key glutamine metabolic proteins, GLUL and the glutamine transporter SLC1A5, in AML cells. Knockdown of SLC1A5 significantly enhanced AML cell sensitivity to MLN4924. The combination of MLN4924 and the SLC1A5 inhibitor V9302 synergistically inhibited AML cell proliferation, induced monocytic differentiation, and promoted apoptosis. Transcriptomic analysis revealed that this combination therapy prominently suppressed the tricarboxylic acid (TCA) cycle. Conclusions: Neddylation inhibition induces compensatory upregulation of glutamine metabolism in AML. Co-targeting neddylation and glutamine transporter SLC1A5 synergistically exerts anti-leukemic effects, at least in part through disruption of the TCA cycle. This combination represents a novel and effective therapeutic strategy against AML. Full article