Search Results (2,170)

Foam cell formation of macrophages is a core pathological event in the progression of atherosclerosis. Investigating the changes in active molecules during macrophage foaming is critical for the early warning and mechanistic research of atherosclerosis. Superoxide anion (O₂^•−) and nitric oxide (NO) are two typical representatives of these active species; evaluating the fluctuations of O₂^•− and NO during macrophage foaming is vital for understanding the early diagnosis and pathological mechanisms of atherosclerosis. Herein, we report a fluorescent probe for the detection of O₂^•− and NO concentration changes based on the quenching effect of the urea bond and trifluoromethanesulfonate group on the fluorophore. MB-ROS features favorable sensitivity, selectivity and biocompatibility, enabling imaging of O₂^•− and NO fluctuations in macrophages. It was further validated in ox-LDL-stimulated foam cell models to visually track abnormal ROS/RNS changes during foam formation. This work offers a reliable chemical imaging tool to uncover redox imbalance underlying early atherosclerotic macrophage foaming. Full article

Coral reefs are increasingly threatened by elevated seawater temperatures associated with heatwaves and El Niño events. These phenomena challenge conventional management practices, highlighting an urgent need for innovative interventions to enhance reef resilience. Investigating the role of oxidative stress—one of the main explanations for coral bleaching—is central to these efforts, as excessive production of reactive oxygen species can impair coral physiology, disrupt the coral–algal symbiosis, and ultimately lead to mortality. Here, we investigated an antioxidant-rich food web approach by feeding the reef-building coral Stylophora pistillata with Artemia that had been pre-fed with (i) low-cost and in-house-produced pellets containing curcumin, fucoxanthin, astaxanthin, vitamins C or E, or (ii) the phytoplankton species Pavlova lutheri, Symbiodinium sp., Nannochloropsis sp., Dunaliella salina or Synechococcus sp. Curcumin and the microalga P. lutheri offered the best protection to corals against oxidative stress, and represent the best candidates for potential scalable coral conservation interventions involving targeted feeding of antioxidants. Curcumin pellets offer a streamlined alternative to P. lutheri by eliminating the need for multi-stage microalgal culturing. Direct enrichment of Artemia with antioxidant-rich pellets simplifies production and may provide a cost-effective, scalable strategy to enhance coral resilience to oxidative stress, bleaching and potential mortality. Full article

Gout is a crystal-induced inflammatory arthritis driven by hyperuricemia and monosodium urate (MSU) crystal deposition, yet urate burden alone does not explain why only a subset of hyperuricemic individuals develops clinical disease, why acute flares are usually self-limited, or why gout clusters with renal and cardiometabolic comorbidity. This structured narrative review uses a gout-specific redox-switch framework, defined as a context-dependent shift in uric acid biology according to concentration, compartment, crystallization state, xanthine oxidoreductase (XOR) activity, inflammatory priming, and disease stage rather than as a binary molecular event. We integrate evidence on XOR-derived reactive oxygen species (ROS), mitochondrial stress, NLRP3 inflammasome signaling, neutrophil oxidative responses, neutrophil extracellular traps (NETs), lipid peroxidation, and potential ferroptosis-related mechanisms. Evidence is classified into five categories: established, mechanistically supported, human-associative, conceptual, and emerging/unvalidated. The available human data support lipid-peroxidation and ferroptosis-associated molecular signatures, but do not yet establish ferroptotic cell death as a driver of gout. Therapeutic implications are therefore framed conservatively: urate-lowering therapy remains foundational, whereas redox-directed approaches require pathway specificity, disease-stage definition, and biomarker validation. The redox-switch concept is proposed as an organizing framework for mechanistic and translational research, not as a validated clinical algorithm. Full article

High-sensitivity cardiac troponin has made the diagnosis of myocardial infarction (MI) faster and more precise, but it does not measure the broader biological vulnerability that often determines the outcome after an acute coronary syndrome (ACS). Growth differentiation factor-15 (GDF-15) is induced by ischemic stress, inflammation, oxidative injury, renal dysfunction, metabolic disease, and ageing. This biology explains its appeal in ACS, but also its diagnostic limitation: GDF-15 is not cardiac-specific and should not be used as an alternative to electrocardiography and high-sensitivity troponin algorithms for early MI diagnosis. Its better supported role is prognostic. Across emergency department chest pain cohorts, non-ST elevation MI, ST elevation MI, post-ACS trial populations, and serial biomarker studies, higher GDF-15 concentrations are most consistently associated with all-cause mortality, cardiovascular mortality, heart failure, and major bleeding, while associations with recurrent ischemic events alone are less specific. The key unresolved issue is incremental clinical value. GDF-15 may improve discrimination and reclassification beyond clinical predictors, troponin, natriuretic peptides, renal function and GRACE or GRACE 2.0 in selected settings, but statistical association is not equivalent to clinical utility. Its possible role in bleeding risk estimation and antithrombotic benefit–risk assessment is clinically important, especially after the PLATO biomarker analyses, yet routine GDF-15-guided dual antiplatelet therapy decisions remain unsupported. Future implementation requires validated thresholds, calibration, decision curve evidence, health economic evaluation, and trials in which GDF-15-guided management changes care and improves outcomes. Full article

Neurodegenerative diseases represent a significant clinical challenge. Understanding the pathogenic mechanisms is essential for developing more effective therapies, and mitochondria appear to play a key role in these processes. Since current treatments are limited to symptom management, natural strategies capable of preserving mitochondrial function could represent a promising preventive and therapeutic approach in neurodegeneration. This study aims at investigating the molecular mechanisms underlying the neuroprotective potential of an anthocyanin-rich extract from Callistemon citrinus flower (Cce) in differentiated SH-SY5Y cells exposed to 6-hydroxydopamine (6-OHDA). Exposure of cells to 6-OHDA inhibited cell viability and caused cell death, events hindered by the pre-treatment with Cce. Furthermore, it restored normal cell cycle distribution, as well as hampered 6-OHDA-induced apoptosis. Given the pro-oxidant effect of 6-OHDA, we observed that Cce reduced reactive oxygen species in stressed SH-SY5Y cells, along with recovering their antioxidant protection system. Focusing on mitochondria, Cce was able to protect their membranes from 6-OHDA, as suggested by the restoration of mitochondrial membrane potential. This led to a reduction in release of cytochrome c and the consequent activation of caspases 9 and 3, characteristic of the intrinsic apoptotic pathway, supporting our initial findings. Our results indicate that Cce prevents SH-SY5Y cell death induced by 6-OHDA via the preservation of mitochondrial integrity mainly through to its antioxidant properties, encouraging further studies to support its exploitation in the management of neurodegeneration. Full article

Carbon nanotubes (CNTs) have become one of the most widely investigated nanomaterials for gas sensing because their nearly one-dimensional geometry, large surface-to-volume ratio, hollow structure, and tunable metallic or semiconducting character allow trace adsorption events to be transduced into measurable electrical signals at or near room temperature. This review summarizes CNT-based gas sensors from a system-oriented perspective, linking four interconnected topics: (i) CNT structure, synthesis, and film/device fabrication; (ii) sensing mechanisms, including charge transfer, Schottky-barrier modulation, carrier-lifetime effects, and field-enhanced ionization; (iii) functional interfaces based on noble metals, metal oxides, conducting polymers, and graphene derivatives; and (iv) gas-specific and flexible/wearable device performance. Particular attention is given to recent room-temperature and mechanically compliant CNT-film sensors fabricated on polymer, cellulose, paper, textile, and mask substrates. Rather than cataloguing only individual response values, this review compares representative devices in terms of target gas, operating condition, sensitivity, recovery strategy, selectivity, humidity tolerance, and wearable relevance. The review concludes by discussing remaining challenges in reproducibility, selectivity, humidity compensation, recovery, power consumption, and standardization, and by outlining future directions toward robust, scalable, and intelligent CNT-enabled sensing systems. Full article

Despite their introduction two decades ago as cessation tools, vaping devices and electronic cigarettes (ECs) have surged dramatically among adolescents and adults worldwide. The widespread misconception that ECs are harmless has raised substantial concern about their potential contribution to chronic diseases associated with oxidative stress (OS) pathways. To map this rapidly growing field, we combined a bibliometric analysis of human research on vaping-associated OS over the past decade with a narrative review of EC component toxicology and regulatory updates. The bibliometric analysis of 189 human studies identified four keyword clusters reflecting clinico-epidemiological, biological/mechanistic, methodological, and acute-event research themes. The results of this bibliometric analysis structure the narrative synthesis, which evaluates the chemical constituents of ECs, including e-liquid constituents, device-derived contaminants, and their aerosol by-products, and links them to pathways associated with OS development. Oxidative stress was the most frequent bridging keyword, reflecting predominant academic trends as research shifted from acute-focused investigations toward mechanistic chronic disease research. No prior review has integrated EC component toxicology with bibliometric evidence to map this landscape. This combined approach provides researchers, clinicians, and policymakers with an integrated evidence base and identifies priority areas for future investigation, including long-term exposure thresholds, age- and sex-specific outcomes, and the urgent need for harmonized global regulation. Full article

Eggplant (Solanum melongena L.), the world’s fifth most important vegetable crop, is highly sensitive to waterlogging (WL), which limits its productivity under climate-driven flooding events. This study evaluated whether humic acid (HA) and fulvic acid (FA) alleviate WL-induced stress by improving nutrient acquisition and antioxidant defense. Eggplant seedlings were subjected to WL stress for 10 days with and without bio-stimulant treatments, under controlled conditions using a simple, completely randomized design. Waterlogging deteriorated soil properties, reducing pH from 7.7 to 5.4, organic matter by ~75%, soil nutrients 73%, resulting in a decline in plant growth (61%), nutrients (23–74%), chlorophyll concentrations (25–45%), and increased oxidative stress indicators (33–314%). Both HA and FA significantly mitigated these stress effects, restoring plant growth by 11–43%, increasing chlorophyll by ~42%, and enhancing nutrients by 10–17-fold. However, HA and FA differentially modulated stress responses. HA reduced H₂O₂ and MDA by 40–75% and normalized antioxidant enzyme activities, indicating redox homeostasis, while FA maintained relatively higher H₂O₂ levels (133.7 mmol kg⁻¹) while improving growth and chlorophyll (~32–67%), suggesting a stress priming rather than stress suppression mechanism. Overall, HA conferred WL tolerance by limiting oxidative damage, whereas FA promoted growth through reactive oxygen species signaling, supporting the potential of humic substances as sustainable bio-stimulants for climate-resilient crop production. Full article

The RING-type E3 ubiquitin ligase plays a significant role in plant responses and adaptations to abiotic stresses such as drought. However, few studies have explored the role of E3 ubiquitin ligases in potato drought stress, especially DRIP1. In this study, 172 StHCa genes were identified across the potato genome. These genes were unevenly distributed on twelve chromosomes and divided into six subclades (group I–VI). The molecular weight of potato HCa proteins ranges from 5445.38 to 143,293.69 Da. More than half of them are acidic proteins and most are unstable. There are 161 hydrophilic proteins, and the subcellular localization analysis indicated that they were mainly located in the nucleus. The co-linearity analysis of StHCa genes showed that 172 genes underwent 40 tandem duplications and 28 segmental duplication events. Potato and tomato share a recent common ancestor and exhibit highly similar evolutionary trajectories. Promoter sequence analysis of the StHCa family identified abundant cis-acting elements associated with light signal transduction, hormone responses, plant growth and development, and abiotic stress responses. These results suggest that the StHCa genes may play important regulatory roles in different environmental signals and developmental stages. Expression profiling revealed that StDRIP1 exhibited higher transcript levels in potato roots than in stems and leaves, and its expression was significantly induced by drought stress. Physiological phenotyping demonstrated that StDRIP1-overexpressing (OE) plants displayed reduced root growth compared with wild-type (WT) plants, with decreases in root length, total root area, total root volume, and root vitality. Under 20% PEG-6000-simulated drought stress, the root expression level of StDRIP1 was higher in OE lines than in WT plants. Furthermore, StDRIP1 overexpression suppressed the activities of antioxidant enzymes (POD, CAT, and SOD) and weakened their osmotic adjustment ability by reducing proline (Pro) accumulation. At the late stage of stress treatment (9 h), the SOD, POD, and CAT activities of OE plants were 5.0%, 19.9%, and 25.1% lower than those of WT plants, respectively. These physiological alterations exacerbated oxidative damage, as evidenced by increased malondialdehyde (MDA) content and elevated electrolyte leakage in OE plants. In summary, this study comprehensively characterized the StHCa gene family in potato, providing a valuable theoretical basis for elucidating the functional mechanism of StDRIP1 in modulating drought stress responses. Collectively, StDRIP1 acts as a negative regulator of potato drought tolerance through two primary mechanisms: (1) repressing root growth and weakening root vitality, thereby reducing the water absorption capacity of roots; and (2) diminishing antioxidant enzyme activities and impairing osmotic homeostasis, which further exacerbates oxidative damage under drought stress. Full article

Endocrine-disrupting pesticides (EDPs) are environmental toxicants capable of perturbing hormonal homeostasis through multiple molecular and cellular mechanisms. Growing evidence indicates that these compounds contribute to a broad spectrum of adverse health outcomes extending beyond classical endocrine dysfunction. This review critically synthesizes current knowledge on the toxicological mechanisms of EDPs and evaluates epidemiological evidence linking exposure to human disease. Mechanistically, EDPs act through modulation of nuclear hormone receptors, disruption of membrane-associated signaling pathways, interference with hormone synthesis, metabolism, and transport, induction of oxidative stress and mitochondrial dysfunction, and epigenetic reprogramming. These molecular events converge on shared biological pathways that affect multiple organ systems and life stages. Human and experimental evidence associates EDP exposure with reproductive dysfunction, endocrine-related cancers, metabolic disorders, thyroid abnormalities, and neurodevelopmental impairments. Particular concern surrounds exposure during critical windows of susceptibility, especially prenatal development and early childhood, when endocrine systems are highly vulnerable to disruption and developmental programming. Across disease endpoints, recurring mechanisms, including endocrine receptor perturbation, oxidative stress, inflammation, and epigenetic alterations, support a unifying toxicological framework linking diverse adverse outcomes. Despite substantial progress, important uncertainties remain regarding chronic low-dose exposure, non-monotonic dose–response relationships, cumulative effects of pesticide mixtures, and the translation of mechanistic findings into human risk assessment. Future research should integrate repeated biomonitoring, advanced mixture modeling, mechanistic biomarkers, and multi-omics approaches within longitudinal life-course studies. Improved integration of toxicological and epidemiological evidence will strengthen causal inference, refine hazard characterization, and support more protective regulatory strategies for reducing the human health burden associated with endocrine-disrupting pesticides worldwide. Full article

Cyanotoxin events are among the most serious consequences of cyanobacterial harmful algal blooms. Microcystins (MCs), among the most prevalent cyanotoxins, are known to adversely affect human health. Recently, respiratory exposure has emerged as an important exposure route for MCs, with potential downstream effects on the gut microbiome through the lung–gut axis. In this pilot study, we investigated acute respiratory immune responses and gut microbiome alterations following MC inhalation using female C57BL/6J mice. Mice were assigned to three dose groups: control (0 µg/kg body weight), medium (25 µg/kg), and high (50 µg/kg). MC-LR was administered intranasally once daily for 3 days. Fecal samples were collected daily for 16S rRNA sequencing, and bronchoalveolar lavage (BAL) fluids were collected following sacrifice for immune cell analysis. MC exposure resulted in significantly increased monocyte counts (p < 0.1), while neutrophil, macrophage, and total cell counts did not significantly change (p > 0.1), suggesting selective lower respiratory tract inflammation. Functional prediction analysis of gut microbiota revealed significant increases (p < 0.1) in pathways associated with host health, including heme biosynthesis, sulfur oxidation, carbon metabolism, and antibiotic resistance. These findings suggest that inhaled MCs may induce respiratory inflammation and contribute to gut microbiome dysbiosis via the lung–gut axis. Full article

Background/Objectives: Long COVID is characterised by persistent symptoms such as fatigue, pain, cognitive impairment, sleep disturbances, and reduced quality of life (QoL) following SARS-CoV-2 infection. Proposed mechanisms include persistent immune activation, chronic inflammation, oxidative stress, endothelial dysfunction, mitochondrial disturbances, and virus-induced cellular senescence. Current management is largely supportive, highlighting the need for complementary strategies targeting these pathways. Natural polyphenols such as quercetin and curcumin possess anti-inflammatory, antioxidant, immunomodulatory, and potential senolytic properties that may modulate multiple pathways implicated in Long COVID. This study aimed to explore the potential complementary effects of oral quercetin–curcumin co-supplementation, administered alongside usual symptomatic management, in adults with persistent Long COVID symptoms. Methods: This single-centre, open-label, single-arm, pragmatic exploratory study enrolled 15 adults with Long COVID in an outpatient real-life clinical practice setting. Participants received a nutraceutical formulation containing quercetin (65 mg) and Curcuma longa extract standardised to provide 42 mg curcumin (Nasafytol^®), administered as two capsules twice daily for 8 weeks in addition to standard care. The primary endpoint was change in overall symptom burden assessed using the COVID-19 Yorkshire Rehabilitation Scale (C19-YRS). Secondary outcomes included fatigue (Fatigue Severity Scale, FSS), pain (Brief Pain Inventory—Short Form, BPI-SF), cognitive function (Patient-Reported Outcomes Measurement Information System Cognitive Function Short Form 8a, PROMIS-CF-8a), mood (Hospital Anxiety and Depression Scale, HADS), sleep quality (Pittsburgh Sleep Quality Index, PSQI), autonomic symptoms (Composite Autonomic Symptom Score-31, COMPASS-31), and health-related QoL (Medical Outcomes Study 36-Item Short-Form Health Survey, SF-36). Results: After 8 weeks, overall symptom burden significantly decreased (C19-YRS median 50 to 32; q = 0.018). Significant reductions were observed in patient-reported fatigue (q = 0.006), pain severity and interference (q = 0.006), and improved physical health-related QoL (SF-36 PCS; q = 0.025). Numerically favourable changes were also observed in cognitive function, anxiety, sleep quality, and autonomic symptoms, although these did not reach statistical significance. The supplementation was generally well tolerated with no serious adverse events. Conclusions: Quercetin–curcumin co-supplementation was associated with lower patient-reported symptom burden, fatigue, and pain and better physical health-related QoL after 8 weeks of supplementation in adults with Long COVID. These observed findings represent treatment-associated changes within this uncontrolled exploratory study and should be interpreted cautiously. Further evaluation in adequately powered randomised placebo-controlled trials is warranted. Trial registration: ClinicalTrials.gov (ID NCT06974058). Full article

Capacitive sensors implemented in complementary metal-oxide-semiconductor (CMOS) technology are widely used in lab-on-chip (LoC), biomedical, and microfluidic systems. While most capacitive sensor interfaces are designed for high-resolution capacitance quantification, many practical applications require only binary decisions, event detection, or state discrimination. In such scenarios, conventional readout architectures introduce unnecessary circuit complexity, power consumption, latency, and data-processing overhead. This paper presents a CMOS cross-coupled-based capacitance detector (CBCD) that directly converts the imbalance between a sensing capacitance and a reference capacitance into a digital output. By exploiting regenerative positive feedback in a dynamic latch architecture, the proposed detector integrates sensing, comparison, and digitization within a single stage, eliminating the need for analog amplification, analog-to-digital conversion, frequency-based readout, and external thresholding circuitry. Circuit-level simulations show the ability to detect extremely small capacitance differences, demonstrate robust operation across a wide range of input capacitances, and achieve negligible power consumption. Process-corner, noise, and Monte Carlo analyses further verify reliable operation in the presence of device mismatch and process variations. Owing to its compact structure, digital-native output, and energy-efficient operation, the proposed CBCD is well suited for decision-driven sensing applications, including droplet presence detection, bubble monitoring, threshold-based diagnostics, event detection, and time-of-evaporation (ToE) measurements. The proposed architecture provides a scalable and low-complexity front-end solution for next-generation CMOS-integrated sensing platforms. Full article

Long-term implantable neural electrodes underpin brain–machine interfaces, deep brain stimulation, epilepsy monitoring, and closed-loop neuromodulation. Following chronic implantation, however, the foreign body response (FBR) at the electrode–tissue interface remains a major constraint on long-term performance, as reflected by increased interfacial impedance, lower signal-to-noise ratios, fewer resolvable units, and higher stimulation thresholds. This deterioration arises from interrelated events that include implantation injury, protein adsorption, blood–brain barrier disruption, complement activation, glial reactivity, oxidative stress, glial scar formation, and neuronal loss. It cannot be attributed solely to material ageing or encapsulation failure. This review examines the molecular mechanisms of neural-electrode FBR and relates them to surface-biofunctionalization strategies, including antifouling coatings, bioactive ligands, immobilized neurotrophic factors, drug-eluting electrodes, and emerging immunomodulatory interfaces. Establishing mechanistic links among molecular events, material interfaces, and functionalization strategies may guide the rational design of durable neural electrodes. Full article

Malondialdehyde (MDA) is one of the main end-products of lipid peroxidation (LPO) and represents a widely investigated marker of oxidative stress (OS) and oxidative tissue damage. Beyond its role as a measurable byproduct of polyunsaturated fatty acid peroxidation, MDA can interact with proteins and nucleic acids, generating adducts that may contribute to mutagenic, genotoxic, and cytotoxic events involved in carcinogenesis and tumor progression. This narrative review summarizes current evidence on the role of MDA in cancers, including breast, lung, head and neck, colorectal, cervical, and cutaneous tumors. Across these cancer types, increased circulating or tissue MDA levels have frequently been associated with enhanced LPO, impaired antioxidant defenses, tumor burden, advanced disease stage, aggressive histopathological features, treatment-related oxidative injury, and, in selected studies, poorer clinical outcomes. MDA-derived DNA adducts may further reflect oxidative DNA damage and provide mechanistic insight into the relationship between chronic redox imbalance, inflammation, and malignant transformation. However, MDA remains a non-specific biomarker influenced by age, smoking, diet, metabolic disorders, systemic inflammation, comorbidities, treatment exposure, and analytical methodology. Current evidence therefore supports MDA as a biologically relevant indicator of oxidative damage rather than a validated stand-alone diagnostic, prognostic, or therapeutic biomarker. Larger prospective studies using standardized and specific analytical methods are needed to clarify its clinical utility and to integrate MDA within broader redox biomarker panels. Full article