Search Results (9,852)

Chronic Obstructive Pulmonary Disease (COPD) is a multifactorial condition associated with significant systemic complications such as cardiovascular disease (CVD), metabolic disorders, muscle wasting, and sarcopenia. While Body Mass Index (BMI) is a well-established indicator of obesity and has prognostic value in COPD, its role in predicting disease outcomes is complex. Muscle wasting is prevalent in COPD patients and exacerbates disease severity, contributing to poor physical performance, reduced quality of life, and increased mortality. Additionally, COPD is linked to metabolic disorders, such as dyslipidemia and diabetes, which contribute to systemic inflammation and worse prognosis and, therefore, should be treated. The systemic inflammatory response plays a central role in the development of sarcopenia. In this review, we highlight the mixed efficacy of statins in managing dyslipidemia in COPD, considering side effects, including muscle toxicity in such a frail population. Alternative lipid-lowering therapies and nutraceuticals, in addition to standard treatment, have the potential to target hypercholesterolemia, which is a coexisting condition present in more than 50% of all COPD patients, without worsening muscle wasting. The interference between adipose tissue and lung, and particularly the potential protective role of adiponectin, an adipocytokine with anti-inflammatory properties, is also reviewed. Respiratory, metabolic and muscular health in COPD is comprehensively assessed. Identifying and managing dyslipidemia and paying attention to other relevant COPD comorbidities, such as sarcopenia and muscle wasting, is important to improve the quality of life and to reduce the clinical burden of COPD patients. Future research should focus on understanding the relationships between these intimate mechanisms to facilitate specific treatment for systemic involvement of COPD. Full article

Air pollution acts as a pervasive oxidative stressor, disrupting global crop production and ecosystem health through the overproduction of reactive oxygen species (ROS). Hazardous pollutants impair critical physiological processes—photosynthesis, respiration, and nutrient uptake—triggering oxidative damage and yield losses. This review synthesizes current knowledge on plant defense mechanisms, emphasizing the integration of enzymatic (SOD, POD, CAT, APX, GPX, GR) and non-enzymatic (polyphenols, glutathione, ascorbate, phytochelatins) antioxidant systems to scavenge ROS and maintain redox homeostasis. We highlight the pivotal roles of transcription factors (MYB, WRKY, NAC) in orchestrating stress-responsive gene networks, alongside MAPK and phytohormone signaling (salicylic acid, jasmonic acid, ethylene), in mitigating oxidative stress. Secondary metabolites (flavonoids, lignin, terpenoids) are examined as biochemical shields against ROS and pollutant toxicity, with evidence from transcriptomic and metabolomic studies revealing their biosynthetic regulation. Furthermore, we explore biotechnological strategies to enhance antioxidant capacity, including overexpression of ROS-scavenging genes (e.g., TaCAT3) and engineering of phenolic pathways. By addressing gaps in understanding combined stress responses, this review provides a roadmap for developing resilient crops through antioxidant-focused interventions, ensuring sustainability in polluted environments. Full article

Background: Exposure to per- and polyfluoroalkyl substances (PFAS, including 7H-Perfluoro-4-methyl-3,6-dioxaoctanesulfonic acid (PFESA-BP2), perfluorooctanoic acid (PFOA), and hexafluoropropylene oxide (GenX), has been associated with liver dysfunction. While previous research has characterized PFAS-induced hepatic lipid alterations, their downstream effects on energy metabolism remain unclear. This study investigates metabolic alterations in the liver following PFAS exposure to identify mechanisms leading to hepatoxicity. Methods: We analyzed RNA sequencing datasets of mouse liver tissues exposed to PFAS to identify metabolic pathways influenced by the chemical toxicant. We integrated the transcriptome data with a mouse genome-scale metabolic model to perform in silico flux analysis and investigated reactions and genes associated with lipid and energy metabolism. Results: PFESA-BP2 exposure caused dose- and sex-dependent changes, including upregulation of fatty acid metabolism, β-oxidation, and cholesterol biosynthesis. On the contrary, triglycerides, sphingolipids, and glycerophospholipids metabolism were suppressed. Simulations from the integrated genome-scale metabolic models confirmed increased flux for mevalonate and lanosterol metabolism, supporting potential cholesterol accumulation. GenX and PFOA triggered strong PPARα-dependent responses, especially in β-oxidation and lipolysis, which were attenuated in PPARα^−/− mice. Mitochondrial fatty acid transport and acylcarnitine turnover were also disrupted, suggesting impaired mitochondrial dysfunction. Additional PFAS effects included perturbations in the tricarboxylic acid (TCA) cycle, oxidative phosphorylation, and blood–brain barrier (BBB) function, pointing to broader systemic toxicity. Conclusions: Our findings highlight key metabolic signatures and suggest PFAS-mediated disruption of hepatic and possibly neurological functions. This study underscores the utility of genome-scale metabolic modeling as a powerful tool to interpret transcriptomic data and predict systemic metabolic outcomes of toxicant exposure. Full article

The marine plant Undaria pinnatifida belongs to the large group of brown macroalgae (Ochrophyta) and is valued both as a nutritious food and a source of pharmaceutical compounds. It has been widely consumed in East Asia as part of the traditional diet and is generally regarded as a “healthy longevity food.” Consequently, it represents one of the most promising natural sources of biomedicinal and bioactive products. This review aims to synthesize current scientific evidence on the pharmacologically active compounds of U. pinnatifida, emphasizing their mechanisms of action and therapeutic potential in neurodegenerative and chronic diseases. This narrative review is based on a comprehensive literature search of peer-reviewed articles from scientific databases, focusing on studies addressing the pharmacological properties of U. pinnatifida and its major bioactive constituents. Recent research highlights that compounds such as fucoxanthin (a carotenoid), fucosterol (a sterol), fucoidan (a polysaccharide), alginate, and dietary fiber found in U. pinnatifida possess significant potential for developing treatments for conditions including goitre, urinary diseases, scrofula, dropsy, stomach ailments, and hemorrhoids. Moreover, these compounds exhibit remarkable pharmacological properties, including immunomodulation, antitumor, antiviral, antioxidant, antidiabetic, anti-inflammatory, anticoagulant, antithrombotic, and antibacterial activities, all with low toxicity and minimal side effects. Additionally, U. pinnatifida shows promise in the treatment or prevention of neurodegenerative diseases such as Alzheimer’s and Parkinson’s, as well as neuropsychiatric conditions like depression, supported by its antioxidant effects against oxidative stress and neuroprotective activities. Numerous in vitro and in vivo studies have confirmed that U. pinnatifida polysaccharides (UPPs), particularly fucoidans, exhibit significant biological activities. Thus, accumulating evidence positions UPPs as promising therapeutic agents for a variety of diseases. Full article

This study investigates the effect of the surface functionalization of tungsten disulfide (WS₂) nanoparticles with aminoacetic acid (glycine) on the structure, curing behavior, and mechanical performance of epoxy nanocomposites. Aminoacetic acid, as a non-toxic, bio-based modifier, enables a sustainable approach to producing more efficient nanofillers. Functionalization, as confirmed by FTIR, EDS, and XRD analyses, led to elevated surface polarity and greater chemical affinity between WS₂ and the epoxy matrix, thereby promoting uniform nanoparticle dispersion. The strengthened interfacial bonding resulted in a notable decrease in the curing onset temperature—from 51 °C (for pristine WS₂) to 43 °C—accompanied by an increase in polymerization enthalpy from 566 J/g to 639 J/g, which reflects more extensive crosslinking. The SEM examination of fracture surfaces revealed tortuous crack paths and localized plastic deformation zones, indicating superior fracture resistance. Mechanical testing showed marked improvements in flexural and tensile strength, modulus, and impact toughness at the optimal WS₂ loading of 0.5 phr and a 7.5 wt% aminoacetic acid concentration. The surface-modified WS₂ nanoparticles, which perform dual functions, not only reinforce interfacial adhesion and structural uniformity but also accelerate the curing process through chemical interaction with epoxy groups. These findings support the development of high-performance, environmentally sustainable epoxy nanocomposites utilizing amino acid-modified 2D nanofillers. Full article

Microorganisms serve as a vital source of natural anticancer agents, with many of their secondary metabolites already employed in clinical oncology. In recent years, salt-adapted microbes, including halophilic and halotolerant species from marine, salt lake, and other high-salinity environments, have gained significant attention. Their unique adaptation mechanisms and diverse secondary metabolites offer promising potential for novel anticancer drug discovery. This review consolidated two decades of research alongside current global cancer statistics to evaluate the therapeutic potential of salt-adapted microorganisms. Halophilic and halotolerant species demonstrate significant promise, with their bioactive metabolites exhibiting potent inhibitory effects against major cancer cell lines, particularly in lung and breast cancer. Evidence reveals structurally unique secondary metabolites displaying enhanced cytotoxicity compared to conventional anticancer drugs. Collectively, salt-adapted microorganisms represent an underexplored yet high-value resource for novel anticancer agents, offering potential solutions to chemotherapy resistance and treatment-related toxicity. Full article

Docetaxel is a chemotherapeutic agent widely used for breast cancer treatment; however, its efficacy is often limited by drug resistance and associated toxicity. This review examines the molecular mechanisms of docetaxel resistance in breast cancer and discusses research advances and future directions for overcoming this challenge. Key resistance mechanisms include alterations in drug targets (microtubules), increased drug efflux, suppression of apoptosis, activation of survival signalling pathways, epithelial-to-mesenchymal transition (EMT), and cancer stem cell enrichment. An evolutionary perspective distinguishes between intrinsic and acquired resistance, emphasising the need for adaptive therapeutic strategies. Recent advances in genomic profiling, non-coding RNA research, novel drug combinations, and biomarker-guided therapies have also been reviewed. Emerging approaches, such as targeting the tumour microenvironment, harnessing immunotherapy, and implementing adaptive dosing schedules, have been discussed. This review emphasises the understanding of resistance as a multifactorial phenomenon that requires multipronged interventions. Research has aimed to identify predictive biomarkers, develop targeted agents to reverse resistance, and design rational combination strategies to improve patient outcomes. Progress in deciphering and targeting docetaxel resistance mechanisms holds promise for enhancing treatment responses and extending survival in patients with breast cancer. Full article

Non-small cell lung cancer (NSCLC) is a predominant form of lung cancer that is often diagnosed at an advanced metastatic stage. The processes of cancer cell migration and invasion involve epithelial-to-mesenchymal transition (EMT), which is crucial for metastasis. Targeting cancer aggressiveness with effective plant compounds has gained attention as a potential adjuvant therapy. Eurycomanone (ECN), a bioactive quassinoid found in the root of Eurycoma longifolia Jack, has demonstrated anti-cancer activity against various carcinoma cell lines, including human NSCLC cells. This study aimed to investigate the in vitro effects of ECN on the migration and invasion of human NSCLC cells and to elucidate the mechanisms by which ECN modulates the EMT in these cells. Non-toxic doses (≤IC20) of ECN were determined using the MTT assay on two human NSCLC cell lines: A549 and Calu-1. The results from wound healing and transwell migration assays indicated that ECN significantly suppressed the migration of both TGF-β1-induced A549 and Calu-1 cells. ECN exhibited a strong anti-invasive effect, as its non-toxic doses significantly suppressed the TGF-β1-induced invasion of NSCLC cells through Matrigel and decreased the secretion of MMP-2 from these cancer cells. Furthermore, ECN could affect the TGF-β1-induced EMT process in various ways in NSCLC cells. In TGF-β1-induced A549 cells, ECN significantly restored the expression of E-cadherin by inhibiting the Akt signaling pathway. Conversely, in Calu-1, ECN reduced the aggressive phenotype by decreasing the expression of the mesenchymal protein N-cadherin and inhibiting the TGF-β1/Smad pathway. In conclusion, this study demonstrated the anti-invasive activity of eurycomanone from E. longifolia Jack in human NSCLC cells and provided insights into its mechanism of action by suppressing the effects of TGF-β1 signaling on the EMT program. These findings offer scientific evidence to support the potential of ECN as an alternative therapy for metastatic NSCLC. Full article

Micro- and Nanoplastic (MNP) pollution is an emerging challenge globally, posing a significant threat to both aquatic and terrestrial ecosystems worldwide. This review critically examines the sources, exposure routes, and impact of plastics, with particular focus on implications for the livestock sector. MNPs enter animals’ bodies primarily through ingestion of contaminated feed and water, inhalation, and dermal exposure, subsequently accumulating in various organs, disrupting physiological functions. Notably, MNPs facilitate the horizontal transfer of antimicrobial resistance genes (ARGs), exacerbating the global challenge of antimicrobial resistance (AMR). In agricultural environments, sources such as organic fertilizers, wastewater irrigation systems, surface runoff, and littering contribute to soil contamination, adversely affecting plant growth and soil health, which in turn compromises feed quality and ultimately animals’ productivity. This review synthesizes current evidence demonstrating how MNP exposure impairs animal production, reproduction, and survival, and highlights the interconnected risks to food safety and ecosystem health. The findings call for the urgent need for comprehensive research under controlled conditions to underscore the fine details regarding mechanisms of MNP toxicity and to inform effective mitigation strategies. Addressing MNP pollution is crucial for safeguarding animal health, ensuring sustainable livestock production, and promoting environmental sustainability and integrity. Full article

Heavy metal pollution due to mining activities poses a significant threat to agricultural production, ecosystem health, and food security in South Africa. This review integrates current knowledge on the use of mustard spinach (Brassica juncea (L.) Czern.) for the bioremediation of polluted water and soil, focusing on enhancing phytoremediation efficiency through the use of silicon-based biostimulant treatments. Mustard spinach is known for its capacity to accumulate and tolerate high levels of toxic metals, such as Pb, Cd, and Hg, owing to its strong physiological and biochemical defense mechanisms, including metal chelation, antioxidant activity, and osmotic adjustment. However, phytoremediation potential is often constrained by the negative impact of heavy metal stress on plant growth. Recent studies have shown that silicon-based biostimulants can alleviate metal toxicity by reducing metal bioavailability, increasing metal immobilization, and improving the antioxidative capacity and growth of plants. Combining silicon amendments with mustard spinach cultivation is a promising, eco-friendly approach to the remediation of mining-impacted soils and waters, potentially restoring agricultural productivity and reducing health risks to the resident populations. This review elucidates the multifaceted mechanisms by which silicon-enhanced phytoremediation operates, including soil chemistry modification, metal sequestration, antioxidant defense, and physiological resilience, while highlighting the practical, field-applicable benefits of this combined approach. Furthermore, it identifies urgent research priorities, such as field validation and the optimization of silicon application methods. Full article

Background and Objectives: Nicotine is the most well-studied toxic substance in cigarette smoke and e-cigarette vape. However, smoke and vape are composed of other components that have a negative impact on health. The objective of this study is to investigate whether nicotine has a distinctive impact on molecular mechanisms in stem cells. Methods: The cellular impact of nicotine on the regenerative capacity of human dental pulp stem cells (DPSCs) and the microRNA (miRNA) profile was examined. Bioinformatic analysis was performed to identify miRNA-regulated cellular pathways associated with nicotine exposure. These pathways were then compared to those induced by cigarette smoke condensate (CSC). Results: Prolonged exposure to nicotine significantly impaired the regeneration of DPSCs and changed the expression of miRNAs. Nicotine upregulated the expression of hsa-miR-7977, hsa-miR-3178, and hsa-miR-10400-5p compared to vehicle control. Interestingly, nicotine did not change the expression of hsa-miR-29b-3p, hsa-miR-199b-5p, hsa-miR-26b-5p, or hsa-miR-26a-5p compared to the control. However, the expressions of these miRNAs were significantly altered when compared to CSC treatment. Further analysis revealed that nicotine was distinctively associated with certain miRNA-targeted pathways including apoptosis, ErbB, MAPK signaling, PI3K-Akt, TGF-b signaling, and Wnt signaling. Conclusions: Our work provides evidence on the distinctive miRNA signature induced by nicotine. The information will be important for identifying the unique molecular pathways downstream of nicotine from smoking and vaping in different individuals, providing a new direction for personalized disease prevention, prognosis, and treatment. Full article

Background/Objectives: In rhegmatogenous retinal detachment (RRD), vitreous cortex remnants (VCRs) may contribute to the development and progression of proliferative vitreoretinopathy (PVR). This study aimed to evaluate potential toxicity and trauma secondary to VCRs visualization and removal during pars plana vitrectomy (PPV) for RRD. Methods: Prospective study on patients with primary RRD who underwent PPV. Imaging assessment included widefield OCT (WF-OCT), ultra-WF retinography and fundus autofluorescence (FAF). During PPV, a filtered and diluted triamcinolone acetonide (TA) solution (20 mg/mL) was used to evaluate the presence and extension of VCRs, removed using an extendible diamond-dusted sweeper (EDDS). After six months, retinal and retinal pigment epithelium toxicity and retinal trauma due to VCRs removal were investigated. Results: Retinal reattachment was achieved in 21/21 cases included in the study. No signs of retinal or RPE toxicity were detected and WF-OCT performed in the areas of VCRs removal revealed an intact inner retinal architecture in the majority of eyes, with minor and localized inner retinal indentations in 4 cases. Conclusions: VCRs visualization and removal using TA and EDDS appears to be safe, with no retinal toxicity and very limited and circumscribed mechanical trauma. This approach may contribute to reducing the risk of postoperative PVR. Full article

Environmental exposure to per- and polyfluoroalkyl substances (PFASs) has been increasingly associated with skin disorders, including atopic dermatitis (AD); however, the underlying molecular mechanisms remain unclear. This study aimed to evaluate the effects of perfluorononanoic acid (PFNA) and perfluorooctanoic acid (PFOA)—two widely detected PFASs—on epidermal function and gene expression in Human Epithelial Keratinocyte, neonatal (HEKn). We assessed cell viability, morphology, and transcriptomic changes using in vitro assays and RNA-seq analysis from a neonatal cohort. PFASs induced dose-dependent cytotoxicity and downregulation of barrier-related genes. Ingenuity pathway analysis identified calcitriol as a suppressed upstream regulator. Functional validation revealed that calcitriol partially reversed the PFAS-induced suppression of antimicrobial peptide genes. These findings support the hypothesis that PFASs may contribute to AD-like skin pathology by impairing vitamin D receptor signaling and antimicrobial defense, and calcitriol demonstrates potential as a protective modulator. This study provides mechanistic insights into the impact of environmental toxicants on skin homeostasis and suggests a potential protective role for calcitriol in PFAS-induced skin barrier damage. Full article

Chromium slag sites pose severe environmental risks due to hexavalent chromium (Cr(VI)) contamination, characterized by high mobility and toxicity. This study focused on chromium-contaminated soil from a historical chromium slag site in North China, where long-term accumulation of chromate production residues has led to serious Cr(VI) pollution, with Cr(VI) accounting for 13–22% of total chromium and far exceeding national soil risk control standards. To elucidate Cr(VI) transformation mechanisms and elemental linkages, a combined approach of macro-scale condition experiments and micro-scale analysis was employed. Results showed that acidic conditions (pH < 7) significantly enhanced Cr(VI) reduction efficiency by promoting the conversion of CrO₄²⁻ to HCrO₄⁻/Cr₂O₇²⁻. Among reducing agents, FeSO₄ exhibited the strongest effect (reduction efficiency >30%), followed by citric acid and fulvic acid. Temperature variations (−20 °C to 30 °C) had minimal impact on Cr(VI) transformation in the 45-day experiment, while soil moisture (20–25%) indirectly facilitated Cr(VI) reduction by enhancing the reduction of agent diffusion and microbial activity, though its effect was weaker than chemical interventions. Soil grain-size composition influenced Cr(VI) distribution unevenly: larger particles (>0.2 mm) in BC-35 and BC-36-4 acted as main Cr(VI) reservoirs due to accumulated Fe-Mn oxides, whereas BC-36-3 showed increased Cr(VI) in smaller particles (<0.074 mm). μ-XRF and correlation analysis revealed strong positive correlations between Cr and Ca, Fe, Mn, Ni (Pearson coefficient > 0.7, p < 0.01), attributed to adsorption–reduction coupling on iron-manganese oxide surfaces. In contrast, Cr showed weak correlations with Mg, Al, Si, and K. This study clarifies the complex factors governing Cr(VI) behavior in chromium slag soils, providing a scientific basis for remediation strategies such as pH adjustment (4–6) combined with FeSO₄ addition to enhance Cr(VI) reduction efficiency. Full article

Background/Objectives: Gallic acid, a natural phenolic compound, was used as a crosslinking agent to achieve protein–polyphenol conjugation under alkaline conditions, presenting an innovative approach to stabilize gelatin. Methods: The formulated inks were evaluated for their rheological properties and 3D printing performance. Once the scaffolds were printed, physicochemical properties were assessed by color changes and FTIR. Additionally, three different post-processing methods were studied to avoid toxicity: incubation in PBS, incubation in NaOH followed by PBS neutralization, and incubation in HCl followed by PBS neutralization. Results: The inks exhibited shear-thinning behavior with self-supporting capacity after extrusion, indicating their suitability for use as inks in 3D printing. After printing, changes in color and in the amide I band/amide II band ratio were observed due to alkaline oxidation, confirming the gelatin crosslinking. Among the tested treatments, incubation in PBS or NaOH followed by neutralizing with PBS proved to be the most suitable for obtaining cytocompatible scaffolds. The mechanical properties demonstrated the suitability of the proposed crosslinking systems for creating scaffolds. Conclusions: This strategy confirms that gallic acid-mediated crosslinking under alkaline conditions enables the fabrication of cytocompatible and mechanically stable gelatin-based scaffolds, making them suitable for tissue engineering. Full article