Search Results (111,523)

Cardiac surgery represents a cornerstone of modern cardiovascular medicine, yet it is intrinsically linked to significant systemic stress responses that can compromise remote organ function. Among postoperative complications, cardiac surgery-associated acute kidney injury (CSA-AKI) remains a significant clinical challenge characterized by high morbidity and complex pathophysiology. While hemodynamic instability and ischemia–reperfusion injury are established risk factors, renal dysfunction frequently persists despite optimal perfusion. This observation suggests the involvement of potent circulating mediators in cellular injury. Extracellular vesicles (EVs) are essential for intercellular communication and serve as central hubs for transporting bioactive lipids, proteins, and genetic material. Accumulating evidence indicates that the mechanical and oxidative stress inherent to cardiopulmonary bypass triggers substantial release of EVs from platelets, erythrocytes, and injured vascular tissues. These vesicles may function as vectors that traffic oxidized mitochondrial components and pro-inflammatory cargo to the renal parenchyma. This signaling cascade appears to disrupt renal homeostasis through a proposed “dual-hit” mechanism involving the induction of endothelial dysfunction and endothelial-to-mesenchymal transition (EndMT), followed by tubular epithelial injury via mitochondrial fragmentation, redox imbalance, and downregulation of anti-aging factors. The complexity of these EV-mediated interactions may contribute to an incomplete understanding of why specific patient phenotypes fail to recover. This narrative review examines the mechanisms of surgery-induced EV biogenesis, the molecular pathogenesis of endothelial and tubular damage, and the role of intercellular crosstalk. Additionally, we discuss future perspectives on targeting the “EV vector” through therapeutic apheresis and mitochondrial pharmacotherapy to potentially improve clinical outcomes in high-risk surgical patients. Full article

Despite the widespread use of Aloe vera extracts, their developmental toxicity in aquatic organisms remains poorly understood. This study investigated the effects of a commercial Aloe vera extract on zebrafish embryogenesis, focusing on developmental, morphological, behavioural, and oxidative stress-related endpoints. The 96 h-LC₅₀ was determined to be 0.03%. Embryos at 2 h post-fertilization (hpf) were exposed for 96 h to 0.0004% (LC₁₀) and 0.03% (LC₅₀). Exposure to 0.0004% caused no significant effects compared to controls. In contrast, exposure to 0.03% significantly increased mortality, reduced heart rate, impaired locomotion, and induced multiple malformations. Biochemical analyses revealed alterations in redox-associated biomarkers, characterized by unchanged ROS levels and mitochondrial activity, increased antioxidant enzyme activities (SOD, GPx, GR), and a decreased GSH:GSSG ratio. Lipid peroxidation levels were reduced, while a significant increase in DNA double-strand breaks (DSBs) was observed. Additionally, Nrf2 protein expression was upregulated at 0.03%. Together, these findings suggest concentration-dependent developmental toxicity correlated with alterations in redox homeostasis and genomic stability during early zebrafish development. This study provides new insight into the developmental hazard potential of a commercial Aloe vera extract in an aquatic vertebrate model. Full article

To advance the design of novel clean coal-fired boilers, this study integrates artificial intelligence with numerical simulations to optimize a 130 MW conceptual boiler based on Moderate or Intense Low-oxygen Dilution (MILD) and oxy-coal combustion technologies. First, mathematical models for pulverized-coal MILD-oxy combustion are validated using experimental data from a 0.58 MW pilot-scale boiler and then applied to the full-scale 130 MW boiler. An orthogonal experimental design with four factors and five levels is employed to generate 25 simulation cases, evaluating the effects of burner nozzle configuration and furnace geometry on boiler performance. Based on the simulation dataset, mutual information analysis is conducted to identify key influencing features, guiding nine additional simulations to refine samples in critical design areas. Finally, using the complete 34 simulation data, an optimal boiler structure is identified using support vector machine and multi-objective optimization algorithms. The results indicate that both the burner circumferential diameter and the O₂/CO₂ inlet diameter are positively correlated with nitrogen oxide (NOx) emissions, whereas the former is negatively correlated with the wall thermal non-uniformity. After optimization, the average char burnout rate increased by 1.4%, NOx emissions decreased by 4%, and wall heat non-uniformity coefficient reduced by 1.1%, demonstrating the effectiveness of the proposed approach. Full article

Coronary artery disease (CAD), including acute coronary syndromes, frequently co-occurs with depression and is associated with adverse outcomes. Trace elements may influence shared biological pathways, including oxidative stress, inflammation, and neurovascular signaling. This study evaluated the association between trace element status and depressive symptoms in CAD. A systematic review was conducted in accordance with PRISMA 2020 guidelines and prospectively registered in PROSPERO (CRD420251231129). PubMed, Scopus, and the Cochrane Library were searched from inception to 2 December 2025. Studies assessing trace element concentrations in adults with CAD and depressive symptoms were eligible. Due to limited direct evidence, partially aligned and indirect studies were also included. Data were synthesized narratively. Of 699 records, four studies were included. No studies fulfilled Tier 1 criteria. The available evidence consisted of partially aligned (Tier 2) and indirect (Tier 3) studies. Lower zinc and magnesium levels and higher copper concentrations were suggested to be associated, based exclusively on Tier 2–3, low-certainty, predominantly indirect evidence. Interventional studies reported modest improvements following zinc or combined magnesium and zinc supplementation, although not in CAD-specific populations. Evidence directly addressing trace elements and depression in CAD is extremely limited and largely indirect. Current data do not support causal inference or clinical recommendations. Findings should be considered exploratory and hypothesis-generating. Full article

Delayed cerebral ischemia (DCI) is a major complication of aneurysmal subarachnoid hemorrhage (aSAH), strongly associated with neurological deterioration and poor outcomes. Its pathophysiology remains incompletely understood and involves multiple interacting processes. Increasing evidence highlights the role of redox imbalance triggered by hemoglobin breakdown and the subsequent generation of reactive species, leading to vascular dysfunction, impaired nitric oxide signaling, and inflammatory activation This review aims to summarize current knowledge on redox-related mechanisms involved in DCI and to explore the potential role of the peroxiredoxin (PRDX) family in this setting. A narrative review of experimental and preclinical studies was performed, focusing on molecular pathways associated with vascular regulation, cellular injury, and antioxidant defense. Particular attention was given to the distribution and biological functions of PRDX isoforms within the central nervous system. This work addresses a topic not previously systematically discussed, the potential involvement of PRDX proteins in aSAH-related complications. By integrating available data, it provides a conceptual framework linking PRDX to mechanisms relevant for DCI. The manuscript serves as a starting point for future research, particularly translational and clinical studies in humans, which are necessary to verify the relevance of these findings and to better understand their potential clinical implications. Full article

An on-site investigation was conducted to analyze the causes of excessive trihalomethane (THM) formation in Plant A and to mitigate the health risks associated with THM exposure in drinking water. Adjacent Plant B was used as a reference plant. Both water treatment plants used the same source water but employed different pre-oxidants. Systematic stage-specific sampling and analysis of historical monitoring data were conducted to identify the key contributing stage for THM formation. The investigation revealed that 85% of the trichloromethane in Plant A’s finished water originated from the sodium hypochlorite pre-oxidation step, identifying this stage as the key contributing stage. THM concentrations were generally higher at Plant A than at Plant B. A multi-pathway health risk assessment of THM in drinking water indicates that non-carcinogenic risks are negligible, but lifetime carcinogenic risks warrant attention. The findings demonstrate that pre-oxidant selection is a significant governing factor of finished water disinfection by-product (DBP) levels. Following these findings, Plant A implemented measures, including enhanced chlorination management, reduced pre-chlorination, and upgraded sedimentation and V-shaped filters, which substantially reduced chlorinated DBPs in the finished water. Full article

Printed biosensors have attracted increasing attention as platforms for rapid, low-cost, and portable diagnostics because they can be fabricated on flexible or rigid substrates using scalable printing techniques. Their performance is strongly influenced by both the printing process and the materials employed, since factors such as ink rheology, particle dispersion, interfacial behavior, and post-processing conditions directly affect device architecture, sensing performance, and manufacturing reliability. This review summarizes recent advances in printed biosensors from the combined perspectives of printing technologies and functional materials. Commonly employed printing techniques, including inkjet, screen, aerosol jet, and roll-to-roll gravure printing, are discussed with emphasis on their processing characteristics and material requirements. The review also examines key material platforms used in printed biosensors, including carbon-based nanomaterials, metal oxides, metal nanoparticles, conductive polymers, dielectric materials, and hybrid composites, highlighting their roles in electrical conductivity, catalytic activity, biomolecule immobilization, mechanical flexibility, and overall analytical performance. Finally, current challenges and emerging research directions are outlined with respect to ink stability, post-processing strategies, sensor reliability, manufacturability, and practical translation. Overall, this review emphasizes that the development of high-performance printed biosensors depends on the synergistic integration of rational material design with optimized printing strategies. Full article

Background: Magnetic Particle Imaging (MPI) is an emerging biomedical imaging modality that detects superparamagnetic iron oxide nanoparticles (SPIONs), providing high contrast, sensitivity, and quantification capabilities without ionizing radiation, making it particularly suitable for cancer diagnostics. Considerable engineering efforts are underway to translate MPI technology to clinical settings. Most of these MPI scanners feature a cylindrical bore geometry similar to that of other clinical imaging modalities, which limits their potential application primarily to head scanning. Methods: We have developed a single-sided MPI scanner designed to expand the modality’s applicability to other regions of the human body through a unique hardware design developed in our previous work. Imaging experiments were performed on an anatomical breast phantom containing implanted SPION point sources placed at anatomically plausible locations for breast tumors. These point sources served as artificial tumors for evaluating the system’s suitability for breast imaging applications. Results: The scanner successfully detected and clearly resolved the implanted SPION tumors in two orthogonal imaging planes. Tumor positioning was independently validated by ultrasound imaging, confirming MPI’s accurate localization. In addition, sensitivity measurements demonstrated a detection limit of 4.0 $\mathsf{\mu }\mathrm{g}$ of iron, below the estimated 4.8 $\mathsf{\mu }\mathrm{g}$ sensitivity threshold required for breast tumor detection with electronic depth scanning up to 3.5 cm deep. Conclusions: Together, these results demonstrate the capability of a single-sided MPI geometry for breast imaging applications. Imaging an anatomical breast-shaped volume presents significant challenges for MPI due to the size and accessibility constraints of conventional hardware. The results presented highlight the advantages of this approach and support its potential to extend MPI from small-animal imaging to clinically relevant applications. Full article

With the rapid development of electronic devices and wireless communication systems, electromagnetic interference pollution has become a critical concern, driving the urgent demand for high-performance, lightweight, and flexible electromagnetic interference (EMI) shielding materials. To endow fabrics with excellent electromagnetic shielding, a Fe₃O₄/Ag/RGO ternary nanocomposite-coated cotton fabric for electrical conductivity and EMI shielding application was developed. The cotton fabric pretreated with dopamine was coated with graphene oxide (GO), followed by silver nanoparticles (Ag) via a microwave-assisted chemical reduction method, and Ag/reduced graphene oxide (RGO)-coated cotton. Subsequently, nano-ferroferric oxide was deposited on Ag/RGO-coated cotton fabric using a coprecipitation method. The results show that the surface resistance of Fe₃O₄/Ag/RGO-coated cotton fabric arrives at 1.68 Ω/sq, demonstrating excellent electrically conductive performance. Fe₃O₄/Ag/RGO-coated cotton fabric demonstrates outstanding electromagnetic shielding performance, with SE values exceeding 45 dB across the entire 1–18 GHz range. The flexibility and superior electromagnetic shielding performance of Fe₃O₄/Ag/RGO-coated cotton fabric render it a promising candidate for applications in wearable electronics, aerospace, advanced protective systems, and military protective clothing. Full article

Background: Spasmolytic polypeptide-expressing metaplasia (SPEM) is an injury-induced gastric epithelial reprogramming state with limited therapeutic options. Although mitochondrial dysfunction has been implicated in epithelial stress responses, its contribution to SPEM development remains incompletely understood. Traditional herbal decoctions have shown potential in alleviating gastric epithelial injury, yet their underlying mechanisms remain largely unclear. Purpose: This study aimed to investigate whether refined Jianpi Huayu Jiedu Decoction attenuates tamoxifen (TAM)-induced SPEM, with a focus on LCN2-associated mitochondrial dysfunction. Methods: TAM-induced SPEM models were established in mice and gastric epithelial cells. Histological, molecular, and mitochondrial analyses were performed to evaluate SPEM features and epithelial stress responses. UPLC–MS/MS-based chemical profiling, network pharmacology, transcriptomic analysis, and LCN2 knockdown experiments were integrated to explore the underlying regulatory mechanisms. Results: Refined Jianpi Huayu Jiedu Decoction significantly alleviated TAM-induced gastric mucosal injury and suppressed the expression of SPEM-associated markers in vivo and in vitro. JHJD treatment improved mitochondrial function, reduced oxidative stress, and normalized mitochondrial dynamics, accompanied by downregulation of LCN2 expression. Chemical profiling identified multiple bioactive components of JHJD, and integrative analyses combining transcriptomics, network pharmacology, and molecular docking suggested that these components are associated with LCN2-related epithelial stress and mitochondrial regulatory networks. Functional validation further demonstrated that LCN2 knockdown partially recapitulated the protective effects of JHJD on mitochondrial homeostasis and epithelial reprogramming. Conclusions: These findings indicate that refined Jianpi Huayu Jiedu Decoction attenuates TAM-induced SPEM in association with restoration of mitochondrial homeostasis and suppression of LCN2-related stress signaling, providing mechanistic insight into early gastric epithelial reprogramming. Full article

Purpose: Neuroinflammation and oxidative stress are increasingly recognized as central, interconnected drivers of neurodegeneration in the visual system. This review examines the pathogenic mechanisms shared across glaucoma, age-related macular degeneration (AMD), diabetic retinopathy (DR), and Alzheimer’s disease (AD), and evaluates the therapeutic rationale for targeting both pathways simultaneously. Methods: A narrative review of peer-reviewed literature was conducted using PubMed. Searches included the following MeSH terms: neuroinflammation, oxidative stress, retinal neurodegeneration, microglia, Müller glia, mitochondrial dysfunction, glaucoma, age-related macular degeneration, diabetic retinopathy, and Alzheimer’s disease. Priority was given to original research, systematic reviews, and high-impact publications from 2000 through 2025. However, seminal foundational works were included regardless of publication date. Studies were selected based on relevance to glial activation, mitochondrial dysfunction, reactive oxygen and nitrogen species, and disease-specific neuronal outcomes. Results: Across all four diseases, persistent microglial and Müller glial activation, mitochondrial electron transport chain dysfunction, and excess reactive oxygen species (ROS) and reactive nitrogen species (RNS) production form a self-amplifying feed-forward loop that accelerates neuronal injury. In glaucoma, these mechanisms drive intraocular pressure-independent retinal ganglion cell loss. In AMD and DR, lipid dysregulation, complement activation, and chronic hyperglycemia sustain oxidative-inflammatory injury to the retinal pigment epithelium, photoreceptors, and neurovasculature. In AD, retinal amyloid deposition and oxidative burden mirror cortical pathology, positioning the retina as a noninvasive biomarker site. Conclusions: Neuroinflammation and oxidative stress constitute unifying upstream mechanisms across major vision-threatening neurodegenerative diseases. Combination therapeutic strategies that simultaneously modulate glial activation and restore redox homeostasis may offer superior neuroprotective efficacy compared to approaches targeting isolated downstream mediators. Full article

Background: Acute lung injury (ALI) is a major complication of sepsis, driven by oxidative stress, inflammation, and apoptosis. Paeoniflorin, a monoterpenoid glycoside, has demonstrated notable antioxidant and anti-inflammatory properties, suggesting potential therapeutic value in ALI. Methods: Sepsis-induced ALI was established in mice using the cecal ligation and puncture (CLP) model. The protective effects of paeoniflorin were evaluated by measuring oxidative stress markers (SOD, GSH, and MDA) and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) using biochemical assays and RT-PCR. Histopathological examination and apoptosis assessment (Bax and Bcl-2 expression) were performed. Western blot analysis was conducted to investigate the involvement of the JAK2/STAT3 signaling pathway. Network pharmacology analysis was used to identify potential molecular targets, and molecular docking was performed to explore binding interactions. Results: CLP-induced ALI resulted in increased oxidative stress and inflammatory responses, as evidenced by elevated MDA and cytokine levels, along with reduced SOD and GSH levels. Paeoniflorin treatment significantly ameliorated these alterations. Histological damage and apoptosis were markedly reduced, accompanied by the downregulation of Bax and upregulation of Bcl-2. Additionally, paeoniflorin inhibited activation of the JAK2/STAT3 pathway. Network pharmacology identified key ALI-related targets, including IL6, TNF, IL1B, HIF1A, STAT3, NFKB1, CCL2, CYBB, CXCL8, and NOX4. Molecular docking revealed strong binding affinity of paeoniflorin toward HIF-1 and JUN, and moderate interactions with IL-1β, TNF-α, and Bax. Conclusions: Paeoniflorin exerts protective effects against sepsis-induced ALI by attenuating oxidative stress, inflammation, and apoptosis, partly through inhibition of the JAK2/STAT3 signaling pathway. These findings highlight its potential as a promising therapeutic candidate for ALI management. Full article

Glucose-6-phosphate dehydrogenase (G6PD) deficiency impairs NADPH generation through the pentose phosphate pathway, resulting in reduced glutathione regeneration and increased vulnerability to oxidative stress. While its clinical significance is well described in hemolytic disorders, its impact on tumor biology and chemosensitivity remains poorly characterized. Cisplatin, a backbone agent in the management of nasopharyngeal carcinoma (NPC), exerts its cytotoxicity through the formation of DNA adducts and the robust induction of reactive oxygen species (ROS) activity. We report a patient with non-keratinizing NPC and a G6PD variant, a (class III) deficiency, who demonstrated a rapid and pronounced objective response to cisplatin-based induction and concurrent chemoradiotherapy. Unfortunately, the patient also exhibited signs of rapid and persistent hematologic (platelets and white cells) toxicity. Notably, no hemolytic events occurred. A narrative review of the available literature indicates that G6PD-deficient cells exhibit a reduced antioxidant reserve, increased cisplatin-induced DNA damage, and impaired activation of ROS-detoxifying pathways. A few clinical observations similarly report enhanced tumor responsiveness in G6PD-deficient individuals, although the evidence is sparse and heterogeneous. Preclinical data support the notion that diminished NADPH availability amplifies cisplatin-triggered oxidative injury, thereby increasing tumor susceptibility. This case adds to emerging evidence that G6PD deficiency may potentiate cisplatin efficacy in NPC by exploiting intrinsic redox vulnerabilities. While preliminary, these findings suggest the potential utility of metabolic phenotyping in treatment stratification. Prospective studies are needed to define the predictive value, safety, and therapeutic implications of G6PD status in cisplatin-based regimens. Full article

Epidemiological studies have demonstrated that kidney aging is a risk factor for acute kidney injury (AKI) and chronic kidney disease (CKD). Therefore, understanding the mechanisms of kidney aging is key to designing novel anti-kidney aging strategies. In this regard, animal models of kidney aging are essential tools. In this review article, we focus on D-galactose (D-gal)-induced accelerated aging in rodents. This animal aging model is a popular and widely used experimental method in the field of aging and aging-related degenerative disorders. It has been shown that the major characteristics of the D-gal-induced aging process are increased oxidative stress, decreased antioxidant enzymes, elevated cell death, increased tissue fibrosis, and accumulation of inflammatory mediators. This review focuses on D-gal-induced kidney aging in mice and rats, with discussions on both kidney aging mechanisms and anti-kidney aging regimens using this model. It is our belief that D-gal induction of accelerated kidney aging will continue to be used as a convenient platform for elucidating kidney aging mechanisms and exploring novel anti-kidney aging targets that may slow down kidney aging and retard the development of aging-related renal disorders. Full article

The secretome of ESKAPE pathogens, including Klebsiella pneumoniae, comprises a diverse array of bioactive molecules that govern virulence, antibiotic resistance, and the establishment of an immunosuppressive microenvironment. However, the high chemical complexity of the secretome impedes the identification of key metabolites mediating pathogenesis. In this study, we profiled the metabolite composition of cell-free K. pneumoniae supernatant using a combined approach of chromatographic fractionation and Raman spectroscopy. Chromatographic separation enabled the resolution of the complex secretome and revealed fractions with distinct biochemical signatures. A key finding was the identification of Fraction 3, characterized by a unique metabolic profile: it was enriched in nucleic acid fragments, peptides containing tyrosine and methionine, polysaccharides, and stress-response metabolites (e.g., citrate), while notably lacking markers of tryptophan and sterol-like lipids. These spectral signatures suggest a potential role for Fraction 3 metabolites in intercellular communication, biofilm formation, and protection against oxidative stress. The remaining fractions also exhibited distinct biochemical profiles, defined by unique profiles of lipids, nucleotides, and amino acids. Collectively, these data underscore the critical role of specific K. pneumoniae secreted metabolites to pathogen survival and host immune modulation. The combined approach effectively resolves functionally relevant secretome fractions, offering new avenues for identifying diagnostic and therapeutic targets for multidrug-resistant infections. Full article