Search Results (3,971)

This paper reviews and analyzes three types of vertical-axis wind rotors: the classic Savonius, spiral Savonius, and Darrieus designs. Using numerical modeling methods, including computational fluid dynamics (CFD), their aerodynamic characteristics, power output, and efficiency under different operating conditions are examined. Key parameters such as lift, drag, torque, and power coefficient are compared to identify the strengths and weaknesses of each rotor. Results highlight that the Darrieus rotor demonstrates the highest efficiency at higher wind speeds due to lift-based operation, while the spiral Savonius offers improved stability, smoother torque characteristics, and adaptability in turbulent or low-wind environments. The classic Savonius, though less efficient, remains simple, cost-effective, and suitable for small-scale urban applications where reliability is prioritized over high performance. In addition, the study outlines the importance of blade geometry, tip speed ratio, and advanced materials in enhancing rotor durability and efficiency. The integration of modern optimization approaches, such as CFD-based design improvements and machine learning techniques, is emphasized as a promising pathway for developing more reliable and sustainable vertical-axis wind turbines. Although the primary analysis relies on numerical simulations, the observed performance trends are consistent with findings reported in experimental studies, indicating that the results are practically meaningful for design screening, technology selection, and siting decisions. Unlike prior studies that analyze Savonius and Darrieus rotors in isolation or under heterogeneous setups, this work (i) establishes a harmonized, fully specified CFD configuration (common domain, BCs, turbulence/near-wall treatment, time-stepping) enabling like-for-like comparison; (ii) couples the transient aerodynamic loads p(θ,t) into a dynamic FEA + fatigue pipeline (rainflow + Miner with mean-stress correction), going beyond static loading proxies; (iii) quantifies a prototype-stage materials choice rationale (aluminum) with a validated migration path to orthotropic composites; and (iv) reports reproducible wake/torque metrics that are cross-checked against mature models (DMST/actuator-cylinder), providing design-ready envelopes for small/medium VAWTs. Overall, the work provides recommendations for selecting rotor types under different wind conditions and operational scenarios to maximize energy conversion performance and long-term reliability. Full article

During water flooding processes, the high viscosity of heavy oil and significant reservoir heterogeneity often lead to severe water channeling and low sweep efficiency. Addressing the limitations of traditional hydrophobically associating polymer-based profile-control agents—such as significant adsorption loss, mechanical degradation during reservoir migration, resulting in a limited effective radius and short functional duration—this study developed a polymeric graded profile-control agent suitable for highly heterogeneous conditions. The physicochemical properties of the system were comprehensively evaluated through systematic testing of its apparent viscosity, salt tolerance, and anti-aging performance. The microscopic oil displacement mechanisms in porous media were elucidated by combining CT scanning and microfluidic visual displacement experiments. Experimental results indicate that the agent exhibits significant hydrophobic association behavior, with a critical association concentration of 1370 mg·L⁻¹, and demonstrates a “low viscosity at low temperature, high viscosity at high temperature” rheological characteristic. At a concentration of 3000 mg·L⁻¹, the apparent viscosity of the solution is 348 mPa·s at 30 °C, rising significantly to 1221 mPa·s at 70 °C. It possesses a salinity tolerance of up to 50,000 mg·L⁻¹, and a viscosity retention rate of 95.4% after 90 days of high-temperature aging, indicating good injectivity, reservoir compatibility, and thermal stability. Furthermore, within a concentration range of 500–3000 mg·L⁻¹, the agent can effectively emulsify Gudao heavy oil, forming O/W emulsion droplets with sizes ranging from 40 to 80 μm, enabling effective plugging of pore throats of corresponding sizes. CT scanning and microfluidic displacement experiments further reveal that the agent possesses a graded control function: in the near-wellbore high-concentration zone, it primarily relies on its aqueous phase viscosity-increasing capability to control the mobility ratio; upon entering the deep reservoir low-concentration zone, it utilizes “emulsion plugging” to achieve fluid diversion, thereby expanding the sweep volume and extending the effective treatment period. This research outcome provides a new technical pathway for the efficient development of highly heterogeneous heavy oil reservoirs. Full article

Per- and polyfluoroalkyl substances (PFASs) have attracted global attention due to their persistence and biological toxicity, becoming critical emerging contaminants in river and lake environments worldwide. Building upon existing studies, this work aims to comprehensively understand the pollution patterns, environmental behaviors, and potential risks of PFASs in freshwater systems, thereby providing scientific evidence and technical support for precise pollution control, risk prevention, and the protection of aquatic ecosystems and human health. Based on publications from 2002 to 2025 indexed in the Web of Science (WoS), bibliometric analysis was used to explore the temporal evolution and research hotspots of PFASs, and to systematically review their input pathways, pollution characteristics, environmental behaviors, influencing factors, and ecological and health risks in river and lake environments. Results show that PFAS inputs originate from both direct and indirect pathways. Direct emissions mainly stem from industrial production, consumer product use, and waste disposal, while indirect emissions arise from precursor transformation, secondary releases from wastewater treatment plants (WWTPs), and long-range atmospheric transport (LRAT). Affected by source distribution, physicochemical properties, and environmental conditions, PFASs display pronounced spatial variability among environmental media. Their partitioning, degradation, and migration are jointly controlled by molecular properties, aquatic physicochemical conditions, and interactions with dissolved organic matter (DOM). Current risk assessments indicate that PFASs generally pose low risks in non-industrial areas, yet elevated ecological and health risks persist in industrial clusters and regions with intensive aqueous film-forming foam (AFFF) use. Quantitative evaluation of mixture toxicity and chronic low-dose exposure risks remains insufficient and warrants further investigation. This study reveals the complex, dynamic environmental behaviors of PFASs in river and lake systems. Considering the interactions between PFASs and coexisting components, future research should emphasize mechanisms, key influencing factors, and synergistic control strategies under multi-media co-pollution. Developing quantitative risk assessment frameworks capable of characterizing integrated mixture toxicity will provide a scientific basis for the precise identification and effective management of PFAS pollution in aquatic environments. Full article

Ras gene mutations are frequently observed in many types of cancers. However, there are currently no effective anticancer drugs against Ras-induced cancers. Therefore, identifying the downstream effectors of the Ras signaling pathway can facilitate the development of promising novel therapeutic approaches. We previously showed that oncogenic Ras induces the expression of the receptor tyrosine kinase c-Mer proto-oncogene tyrosine kinase (MerTK) in an interleukin-1 family member NF-HEV/IL-33-dependent manner and that IL-33 and MerTK contribute to oncogenic Ras-induced cell migration. In the present study, we purified the MerTK complex from NIH-3T3 cells transformed by the expression of oncogenic Ras, H-Ras (G12V). Mass spectrometric analysis identified STK38 (also known as NDR1) as a candidate binding partner for MerTK. STK38 is a serine/threonine protein kinase that plays diverse roles in normal and cancerous cells. In addition to MerTK knockdown, STK38 knockdown effectively attenuated the H-Ras (G12V)-induced migration of NIH-3T3 cells. STK38 kinase activity is required for oncogenic Ras-induced cell migration and MerTK tyrosine phosphorylation. Furthermore, MerTK or STK38 knockdown attenuated the activation of Rac1 and Cdc42. Taken together, these results revealed a novel role for STK38 in oncogenic Ras-induced enhanced cell migration, which may be useful for developing novel therapeutic strategies targeting Ras-mutated cells. Full article

Clinical application of ex vivo lung perfusion (EVLP) has increased marginal donor lung utilization. It has been developed as a platform for donor lung reconditioning. However, many of the current repair strategies are limited by a maximum reliable EVLP circuit duration of 12 h. Past studies have successfully extended EVLP through nutrient supplementation, but the exact components and respective mechanisms by which EVLP is extended remains unknown. As such, the focus of this study was to systematically evaluate the effects of nutritional supplements in EVLP perfusates on cell apoptosis, viability, confluence, and migration. To test this, we developed a high-throughput human lung endothelial cell culture platform where experimental perfusates with various combinations of GlutaMAX (a glutamine dipeptide), Travasol (amino acids), Intralipid (lipids), Multi-12 (vitamins), cysteine, and glycine were tested using the Incucyte Live imaging system. GlutaMAX supplementation alone significantly reduced apoptosis, improved viability and cell migration beyond all other supplements and further outperformed standard endothelial cell culture medium. Travasol offered short-term benefits, while Intralipid offered minimal functional support. Multi-12 improved viability and apoptosis independently and in combination with other supplements. The best experimental perfusate targeted the glutathione synthesis pathway, combining GlutaMAX, cysteine and glycine and further reduced apoptosis compared with GlutaMAX alone. Collectively, these results suggest that nutrient selection during EVLP is critical and highlights the need to systematically evaluate perfusate modifications as opposed to broad-spectrum nutrient delivery. This in vitro model provides a cost-effective platform for preclinical screening of perfusate modifications to enhance organ viability during EVLP. Full article

Background: Diabetic wound healing has always been a clinical challenge with minimal response or efficacy to standard treatment. This study aims to assess the therapeutic potential of hypoxia-induced extracellular vesicles (hy-EVs) produced by human umbilical cord mesenchymal stem cells (HUCMSCs) to treat diabetic wounds. Methods: HUCMSCs were isolated from umbilical cord tissue, cultured under hypoxic conditions to induce the release of extracellular vesicles (EVs) and compared with normoxia-induced extracellular vesicles (n-EVs). We assessed the functions of hy-EVs on human skin fibroblasts (HSFs) and human umbilical vein endothelial cells (HUVECs) in vitro. Simultaneously, we analyzed the pro-angiogenic effects of hy-EVs, their effects on macrophage polarization, and their ability to scavenge endogenous reactive oxygen species (ROS). In addition, a diabetic wound model was established to assess the curative effect of hy-EVs in diabetic wound healing. Results: We found by in vitro study that hy-EVs markedly improved the functional activities of HSFs, thus significantly promoting wound repair. Remarkably, it was determined that hy-EVs greatly enhanced the proliferation and migration ability as well as the angiogenic ability of HUVECs, while promoting the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial-generation-associated factor A (VEGFA), and platelet endothelial adhesion molecule (CD31), which suggested that hy-EVs can effectively activate the HIF-1α pathway to promote angiogenesis. Above all, we found that hy-EVs promoted the expression of CD206 while decreasing the expression of CD86, suggesting that hy-EVs could induce macrophages to shift from M1-type (pro-inflammatory) to M2-type (anti-inflammatory), thereby modulating the inflammatory response. Additionally, hy-EVs inhibited ROS production in both HSFs and HUVECs to reduce oxidative stress. In vivo results showed that hy-EVs enhanced collagen deposition and angiogenesis, modulated macrophage polarization, and inhibited immune response at the wound spot, which significantly enhanced diabetic wound healing. Conclusions: Our study shows that hy-EVs significantly promote angiogenesis through activation of the HIF-1α pathway, modulate macrophage polarization and attenuate cellular oxidative stress, possibly through delivery of specific miRNAs and proteins. Our discoveries offer a key theoretical basis and potential application to develop novel therapeutic strategies against diabetes-related tissue injury. Full article

While immune escape and physical invasion are two key pathways in tumor development, traditional methods for analyzing their exosomal markers are often complex and face identification bias. Microfluidic technology offers significant advantages for non-invasive liquid biopsy, particularly in the analysis of tumor progression markers carried by exosomes. Here, we developed an integrated microfluidic system for the sensitive, accurate, totally on-chip exosome isolation and automatic quantification of tumor progression markers PD-L1 and MMP9. This platform leverages microfluidic design principles for efficient sample mixing and monodisperses microbeads for precise analysis, allowing for complete processing within 40 min. The system’s high efficiency and precision are further enhanced by a lightweight YOLOv5-based positional migration strategy that automates fluorescence quantification. Validation using four different cell lines demonstrated distinct exosomal protein signatures with a low detection limit of 12.58 particles/μL. This innovative microfluidic chip provides a sensitive and easy-to-handle tool for exosomal marker analysis, holding great potential for cancer identification and personalized therapy guidance in the era of point-of-care testing (POCT). Full article

The discovery of novel marine natural products and their sustainable application continue to be vital focuses in marine biological research. The aim of this study is to investigate the inhibitory effect of the compound 5Z-7-Oxozeaenol isolated from the fungus Curvularia sp. MDCW-1060 on the proliferation of MDA-MB-231 cells and its molecular mechanism. A series of functional assays, including 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, Transwell migration, and colony formation, were employed to evaluate the effects of 5Z-7-Oxozeaenol on cellular viability, apoptosis, migration, and clonogenicity. The RNA sequencing (RNA-seq) coupled with bioinformatic analysis was conducted to identify affected differentiated gene expression and signaling pathways. The molecular docking was performed to predict potential protein targets, and Western blot was used to validate expression and phosphorylation levels of key signaling molecules. The results demonstrated that 5Z-7-Oxozeaenol significantly suppressed proliferation and migration while promoting apoptosis in MDA-MB-231 cells. The transcriptomic analysis indicated enrichment in pathways related to cancer, cytokine–cytokine receptor interaction, MAPK and PI3K-Akt signaling, and cell adhesion molecules. The molecular docking suggested a high binding affinity between 5Z-7-Oxozeaenol and PTPRN. While Western blot analysis confirmed the downregulation of phosphorylated FAK, PI3K, Akt, and MAPK, along with reduced cyclin D1 expression. Additionally, 5Z-7-Oxozeaenol upregulated the pro-apoptotic proteins p53 and cleaved caspase-3. In conclusion, 5Z-7-Oxozeaenol exerts potent antitumor effects on MDA-MB-231 cells through multi-pathway inhibition and induction of apoptosis, highlighting its potential as a marine-derived therapeutic candidate for breast cancer treatment. Full article

Microplastics (MPs) are emerging airborne pollutants that can migrate through various environmental pathways, with air representing one of the most critical exposure routes. Their occurrence within suspended particulate matter (PM)—a major atmospheric pollutant associated with respiratory, cardiovascular, and neurological diseases—further amplifies the risks posed by air pollution. The main sources of airborne MPs include tire and road wear, degradation of larger plastic debris, and wind-driven resuspension from soil and landfills. This review provides a comprehensive synthesis of current knowledge on airborne MPs, integrating methodological and toxicological perspectives. It summarizes sampling and separation procedures (filtration, chemical digestion, density separation) and analytical techniques for qualitative and quantitative identification. Particular emphasis is placed on the toxicological implications of MPs, including oxidative stress, inflammatory responses, and potential carcinogenicity, as revealed by in vitro and mechanistic studies. In light of the absence of standardized methodologies, this work highlights the urgent need for harmonized protocols linking environmental monitoring with biological toxicity assessment. By combining information on analytical workflows and cellular responses, this review serves as a key reference for developing environmentally relevant experimental designs and evaluating health risks associated with airborne microplastics. It therefore bridges the gap between environmental analysis and toxicological research, outlining future priorities for methodological standardization and risk assessment. Full article

Cholangiocarcinoma (CCA), an aggressive biliary tract cancer whose prevalence is rising, particularly in Thailand, is marked by elevated oxidative stress driven by chronic inflammation, parasitic infections, and dysregulated redox signaling. This study investigates the anticancer potential of tiliacorinine using a silico approach, including drug-likeness, ADMET, network pharmacology, molecular docking, and dynamics simulations. Tiliacorinine and 216 predicted targets were identified, with 79 overlapping CCA-related genes from GeneCards. GO and KEGG analyses revealed involvement in cell migration, membrane structure, kinase activity, and cancer-associated pathways. Network and PPI analyses identified ten key targets, including SRC, HIF1A, HSP90AA1, NFKB1, MTOR, MMP9, MMP2, PIK3CA, ICAM1, and MAPK1. Tiliacorinine showed the strongest affinity for MTOR (−10.78 kcal/mol, K_i = 12.62 nM), binding at the same site as known inhibitors with superior energy and specificity, supported by hydrogen bonding at ASP950 and hydrophobic interactions. Tiliacorinine also demonstrated strong binding to SRC, MMP9, and MAPK1. Molecular dynamics simulations revealed stable binding of tiliacorinine to MTOR, particularly at residues ASP950, TRP1086, and PHE1087. Comparative analysis with the MTOR–GDC-0980 complex confirmed consistent interaction patterns, reinforcing the structural stability and specificity of tiliacorinine. These results highlight its strong pharmacological potential and support its candidacy as a promising lead compound for cholangiocarcinoma therapy. Full article

C1q/TNF-related protein 6 (CTRP6) is emerging as a critical regulator of cancer biology with direct implications for clinical outcomes. Across a wide spectrum of malignancies, CTRP6 plays a central role in coordinating key oncogenic processes and linking metabolic, inflammatory, and signaling pathways that drive tumor progression. While CTRP6 generally promotes oncogenic behavior in cancers such as hepatocellular carcinoma, lung cancer, and clear cell renal cell carcinoma, conflicting findings have been reported in gastric cancer and oral or head and neck squamous cell carcinoma, where its tumor-promoting versus tumor-suppressive roles remain unresolved. CTRP6 has been shown to modulate fundamental processes including angiogenesis, ferroptosis, proliferation, apoptosis, migration, invasion, and inflammation. These effects are primarily mediated through activation of the PI3K/AKT and MEK/ERK signaling pathways, which are central to tumor growth, metastasis, and therapeutic resistance. Beyond its mechanistic roles, CTRP6 demonstrates potential as a diagnostic and prognostic biomarker, with altered expression patterns linked to cancer initiation, progression, and patient survival. Inhibition of CTRP6 in preclinical models enhances ferroptotic cell death and suppresses tumor progression, highlighting its promise as a therapeutic target. By consolidating current evidence from multiple cancer models, this review provides a comprehensive overview of CTRP6’s contributions to oncogenesis and underscores its dual potential as both a biomarker and a therapeutic target. Advancing a deeper understanding of CTRP6 in specific tumor contexts will be critical for unlocking its clinical utility and may open new opportunities to improve diagnosis, optimize therapeutic strategies, and ultimately enhance patient outcomes. Full article

Fibroblasts determine repair quality during skin-wound healing. Our previous study found that Activin B promotes keratinocyte proliferation and migration, facilitating re-epithelialization. However, specific mechanisms governing fibroblast function during wound healing remain unclear. Here, we aimed to elucidate the mechanism by which Activin B regulates fibroblast activity during skin-wound healing. Using a murine skin-wound model, we performed hematoxylin-eosin, immunohistochemical, and Masson’s trichrome staining to evaluate Activin B’s effects on granulation tissue formation, angiogenesis, and collagen fiber synthesis. We assessed Activin B’s effects on fibroblast proliferation, migration, and collagen protein synthesis and investigated signaling pathway mechanisms in vitro. Animal experiments showed that Activin B accelerated wound healing by promoting granulation tissue regeneration and angiogenesis without affecting collagen fibers and Type I collagen synthesis. In vitro experiments demonstrated that Activin B modulates fibroblast proliferation and migration by activating JNK and ERK signaling pathways. Activin B may enhance angiogenesis by stimulating fibroblasts to secrete vascular endothelial growth factor, which induces dermal microvascular endothelial cell proliferation, promoting angiogenesis. Thus, we elucidated the dual regulatory paradigm of Activin B in fibroblasts; Activin B drives proliferation and migration via JNK/ERK signaling but does not directly regulate collagen synthesis. Full article

Background/Objectives: Endometrial cancer (EC), a malignancy arising from the uterine lining, is a leading gynecological cancer in developed countries. Syringic acid (SA), a naturally occurring phenolic compound, possesses various bioactivities including antioxidant, anti-inflammatory, chemoprotective, and anti-angiogenic properties. This study aimed to investigate the effects of SA on the proliferation and migration of RL95-2 EC cells, its protective role in normal endometrial stromal cells (HESCs), and the underlying molecular mechanisms. Furthermore, the potential synergistic anticancer effects of SA in combination with chemotherapeutic agents against EC were evaluated. Methods: Cell viability was assessed using nuclear fluorescence staining, the MTT assay, and clonogenic survival assay. Cell migration was evaluated through wound closure and Transwell migration assays. Gene expression levels were analyzed by the RT-PCR method. Results: SA significantly inhibited the proliferation of RL95-2 EC cells, with an IC₅₀ value of 27.22 μM. Co-treatment with SA and the chemotherapeutic agent doxorubicin (Dox) demonstrated an additive inhibitory effect. Mechanistically, both SA and the SA-Dox combination induced apoptosis by upregulating the expression of caspases-3, -8, and -9, increasing the expression of pro-apoptotic genes (Bax and Bad), and downregulating anti-apoptotic genes (Bcl-XL and Bcl-2). Cell cycle analysis revealed the downregulation of cyclin D and the upregulation of tumor suppressors p21 and p27, contributing to growth arrest. In addition, both SA and the combination treatment effectively suppressed cell migration by downregulating matrix metalloproteinases (MMPs) and β-catenin. SA treatment also induced the expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activated NF-κB signaling, leading to an elevated expression of inflammatory mediators such as COX-2 and iNOS. Furthermore, SA promoted oxidative stress in RL95-2 cells by inhibiting the Nrf2 pathway and reducing the expression and activities of antioxidant enzymes including catalase, glutathione peroxidase, and superoxide dismutase, thereby enhancing reactive oxygen species (ROS) accumulation. In contrast, in lipopolysaccharide-stimulated HESC cells, SA attenuated inflammation and ROS generation, indicating its selective cytoprotective role in normal endometrial cells. Conclusions: SA may serve as a promising adjuvant candidate to enhance chemotherapeutic efficacy while protecting normal cells by mitigating inflammation and oxidative stress. Full article

Endometrial cancer is one of the most common malignancies of the female reproductive system, with incidence rising globally due to population ageing and life-style-related risk factors. Calcium (Ca²⁺) is a ubiquitous second messenger regulating diverse physiological processes, and its dysregulation has been increasingly implicated in carcinogenesis, including endometrial. Altered expression and function of Ca²⁺ channels, pumps, exchangers, and binding proteins disrupt the finely tuned balance of Ca²⁺ influx, efflux, and intracellular storage, leading to aberrant signalling that promotes tumour proliferation, migration, survival, and metastasis. This review summarises current knowledge on the molecular “Ca²⁺ toolkit” in the human uterus, highlighting the role of voltage-gated calcium channels (VGCCs), transient receptor potential (TRP) channels, store-operated calcium entry (SOCE) components, Na⁺/Ca²⁺ exchangers, purinergic receptors, P-type ATPases (SERCA, SPCA, PMCA), ryanodine (RyR) and inositol 1,4,5-trisphosphate (IP₃R) receptors, and mitochondrial Ca²⁺ uniporter (MCU) complexes in endometrial cancer progression. Multiple Ca²⁺-handling proteins, including CACNA1D, CACNA2D1, TRPV4, TRPV1, TRPM4, MCU, and RyR1, exhibit cancer-associated overexpression or functional changes, correlating with poor prognosis and aggressive disease features. Emerging evidence supports the therapeutic potential of targeting Ca²⁺ homeostasis using small-molecule inhibitors, ion channel modulators or gene-silencing strategies. These interventions may restore Ca²⁺ balance, induce apoptosis or autophagy, and suppress metastatic behaviour. While no clinical trials have yet explicitly focused on Ca²⁺ modulation in endometrial cancer, the diversity of dysregulated Ca²⁺ pathways offers a rich landscape for novel therapeutic strategies. Targeting key components of the Ca²⁺ signalling network holds promise for improving outcomes in endometrial cancer. Full article