Search Results (3,510)

C. perfringens type F isolates are a leading cause of food poisoning and antibiotic-associated diarrhea. Type F isolate virulence requires production of C. perfringens enterotoxin [CPE], which acts by forming large pore complexes in host cell plasma membranes. During GI disease, CPE is produced in the intestines when type F strains undergo sporulation. The toxin is then released into the intestinal lumen when the mother cell lyses at the completion of sporulation. Once present in the lumen, CPE encounters proteases. This study examined the in vitro, ex vivo, and in vivo processing of CPE by intestinal proteases and the effects of this processing on CPE activity. Results using purified trypsin or mouse intestinal contents detected the rapid cleavage of CPE to a major band of ~32 kDa and studies with Caco-2 cells showed that this processed CPE still forms large complexes and retains cytotoxic activity. When mouse small intestinal loops were challenged with CPE, the toxin caused intestinal histologic damage, despite rapid proteolytic processing of most CPE to 32 kDa within 15 min. Intestinal large CPE complexes became more stable with longer treatment times. These results indicate that CPE processing involving trypsin occurs in the intestines and the processed toxin retains enterotoxicity. Full article

This study elucidates the adaptive mechanisms of Saccharomyces cerevisiae CZ under octanoic acid stress, revealing concentration-dependent growth inhibition (76% lethality at 800 mg/L) and notable tolerance at 600 mg/L. Initial exposure (≤6 h) showed no growth impairment, but prolonged treatment induced dose-dependent lethality, accompanied by reduced H⁺/K⁺-ATPase activity and elevated malondialdehyde (MDA) levels, indicative of oxidative damage. Transcriptomic profiling of 5665 genes highlighted the predominant downregulation of ribosomal functions (translation, ribosome biogenesis) and amino acid metabolism pathways (e.g., ARO10, ARO9). Strain-specific regulatory dynamics were observed: (1) TPO1-mediated efflux was active at 400 mg/L but absent at 600 mg/L, suggesting compensatory mechanisms under high stress; (2) HTX1-related genes exhibited bidirectional regulation (downregulated at 400 mg/L vs. upregulated at 600 mg/L), reflecting metabolic flexibility; (3) ACC1 downregulation (600 mg/L) and unaltered SFK1 expression contrasted with lipid-remodeling strategies in engineered strains; and (4) PMA2 suppression diverged from literature-reported PMA1 activation, underscoring strain-specific energy reallocation. Suppression of ergosterol biosynthesis and ribosomal genes revealed a trade-off between stress adaptation and biosynthetic processes. These findings reconcile prior contradictions by attributing discrepancies to genetic backgrounds (CZ vs. laboratory/engineered strains) and methodological variations. Unlike strains relying on phospholipid asymmetry or oleic acid overproduction, CZ’s unique tolerance stems from integrated membrane homeostasis (via lipid balance) and metabolic conservation. This work emphasizes the critical role of strain-specific regulatory networks in octanoic acid resistance and provides insights for optimizing yeast robustness through targeted engineering of membrane stability and metabolic adaptability. Future studies should employ multi-omics integration to unravel the dynamic gene regulatory logic underlying these adaptive traits. Full article

Acute pancreatitis (AP) an inflammatory condition caused by the premature activation of pancreatic proteases, leads to organ damage, systemic inflammation, and multi-organ failure. Severe acute pancreatitis (SAP) has high morbidity and mortality, affecting the liver, kidneys, and lungs. Autophagy maintains pancreatic homeostasis, with VMP1-mediated selective autophagy (zymophagy) preventing intracellular zymogen activation and acinar cell death. This study examines the protective role of VMP1 (Vacuole Membrane Protein 1)-induced autophagy using ElaI-VMP1 transgenic mice in a necrohemorrhagic SAP model (Hartwig’s model). ElaI-VMP1 mice show significantly reduced pancreatic injury, including lower necrosis, edema, and inflammation, compared to wild-type (WT) mice. Biochemical markers (lactate dehydrogenase-LDH-, amylase, and lipase) and histopathology confirm that VMP1 expression mitigates pancreatic damage. Increased zymophagy negatively correlates with acinar necrosis, reinforcing its protective role. Beyond the pancreas, ElaI-VMP1 mice exhibit preserved liver, kidney, and lung histology, indicating reduced systemic organ damage. The liver maintains normal architecture, kidneys show minimal tubular necrosis, and lung inflammation features are reduced compared to WT mice. Our results confirm that zymophagy functions as a protective pathophysiological mechanism against pancreatic and extrapancreatic tissue injury in SAP. Further studies on the mechanism of VMP1-mediated selective autophagy in AP are necessary to determine its relevance and possible modulation to prevent the severity of AP. Full article

Dehydroabietic acid (DHA) is a secondary metabolite isolated from rosin, which has certain antifungal activity, but its inhibitory effects against Alternaria alternata are unclear. In the present study, we found that DHA inhibited the mycelial growth of A. alternata, Botrytis cinerea, Valsa mali, Pestalotiopsis neglecta, and Fusarium oxysporum in a concentration-dependent manner, with the best inhibitory effect against A. alternata. Moreover, DHA can also inhibit the spore germination of A. alternata. Then, in vivo inoculation experiments showed that the leaf lesions of Populus alba gradually decreased with the increase in DHA concentration. The disease of P. alba leaves inoculated with A. alternata was not obvious after treatment with 800 mg/L DHA. The scanning electron microscopy showed that the mycelial morphology was abnormal, with crinkles and depressions. Meanwhile, the relative conductivity, soluble protein content, malondialdehyde content and hydrogen peroxide content of A. alternata were significantly increased after DHA treatment, which affected the integrity of the cell membrane and increased the permeability of A. alternata, resulting in a large leakage of intracellular substances, exacerbating the degree of lipid peroxidation of the cell membrane of A. alternata and causing oxidative damage to cells. The enzyme activity assay showed that treatment with 56.015 mg/L (EC₅₀) DHA significantly reduced the activities of antioxidant enzymes (superoxide dismutase, catalase, peroxidase) and cell-wall-degrading enzymes (endoglucanase, polygalacturonase, pectin lyase) in A. alternata (p < 0.05), resulting in a decrease in the activity of pathogenic fungi, as well as a reduction in the ability of the A. alternata to degrade the cell wall of the host plant, which led to a decrease in the ability of the A. alternata to infest the host plant. Moreover, the decrease in the relative expression of defense-related enzyme genes (AaSOD, AaPOD, AaCAT) and pathogenicity-related enzyme genes (AaPL, AaPG) was consistent with the enzyme activity results. Thus, the present study revealed the fungicidal activity and mechanism of DHA against A. alternata and the potential of DHA to be developed as a plant-derived antifungal agent was established. Full article

3-O-Methyl-D-chiro-inositol (pinitol) has been reported to possess insulin-like effects and is known as one of the anti-diabetic agents for improving muscle and liver function. However, the beneficial effects of pinitol on human dermal microvascular endothelial cells (HDMECs) are not well understood. In this study, we investigated whether pinitol could protect HDMECs from damage induced by lipopolysaccharides (LPSs), which cause various cell defects. We observed that pinitol enhanced wound healing for LPS-damaged HDMECs. We found that pinitol significantly downregulated the LPS-induced upregulation of reactive oxygen species (ROS). Pinitol also significantly restored the mitochondrial membrane potential in these cells. Immunofluorescence analysis revealed that pinitol notably reduced the nuclear localization of NF-κB in LPS-damaged HDMECs. Furthermore, we demonstrated that pinitol decreased the phosphorylation levels of the MAPK family in LPS-damaged HDMECs. Interestingly, we observed that pinitol improved tube formation in LPS-damaged HDMECs. Taken together, we suggest that pinitol exerts several beneficial effects on LPS-damaged HDMECs and may be a promising therapeutic agent for improving vascular-related skin diseases. Full article

Due to their negligible cytoplasm and composition of the sperm plasmalemma, spermatozoa are particularly vulnerable to lipid peroxidative damage induced by reactive oxygen species (ROS). Most ROS are referred to as free radicals because they have unpaired electrons, causing them to scavenge electrons from atoms within tissues, resulting in oxidative damage to cellular components including cell membranes, intracellular organelles, and DNA. The potential consequences of oxidative stress include impaired sperm function, DNA fragmentation, and apoptosis. Understanding the mechanisms that mediate sperm damage during cryopreservation is key to the development of improved sperm freezing media formulations and methodology to mitigate its occurrence. Historically, elucidation of those mechanisms has proven largely elusive and is complicated by the positive role that ROS also play as messengers in redox signaling and the different pathways that mediate sperm DNA damage and apoptosis. More recently, oxidative stress has been revealed as the most likely suspect in cryopreservation-induced sperm DNA damage. This narrative review was intended to provide an in-depth analysis of the mechanisms involved and offer insight into possible improvements in sperm cryopreservation. Full article

Studies have consistently shown that long-wave ultraviolet A (UVA) radiation triggers skin photoaging, which is evident as reduced elasticity, a loss of firmness, and signs of aging. There is an urgent need to investigate photoaging mechanisms to devise protective strategies against UVA. The present study aimed to explore the effects of recombinant type XVII collagen on UVA-induced skin aging and uncover its molecular mechanisms, thereby laying a solid theoretical foundation for precise treatments and prevention. We therefore modeled photoaging damage in HaCaT cells and evaluated collagen-related protein and gene expression levels via western blot analysis and real-time quantitative polymerase chain reaction analysis. Immunofluorescent staining was also used to assess collagen secretion and basement membrane protein expression. Recombinant type XVII collagen significantly boosted type IV and type XVII collagen, laminin alpha 5, and integrin β1 production, thus counteracting UVA-induced collagen decline. The polymerase chain reaction analysis revealed matrix metalloproteinase (MMP) downregulation and tissue inhibitor of metalloproteinase (TIMP) upregulation. Modulating the transforming growth factor (TGF)-β/Smad and epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) pathways suppressed photoaging. Together, our findings suggest that recombinant type XVII collagen ameliorates UVA-induced damage by reversing MMP and TIMP gene expression, thereby preventing collagen degradation and enhancing basement membrane secretion. These results offer a theoretical basis for potent anti-photoaging products, thus paving the way for innovative solutions against UVA-induced skin aging. Full article

Laboratory evolution is an effective means of understanding microbial adaptation to the environment. We previously isolated four thermoadapted Zymomonas mobilis mutants, which showed a 2 °C rise in the critical high temperature (CHT), by performing multiple-parallel adaptation experiments. In the present study, the individual mutations in these mutants were intensively analyzed. Two mutations in each adapted mutant were found to primarily contribute to the increase in the upper temperature limit. RNA sequencing (RNA-seq) analysis revealed that the two mutations led to the upregulation of 79–185 genes and the downregulation of 242–311 genes. The findings from transcriptomic and physiological experiments suggest two common and primary mechanisms for thermal resistance: a decrease in the activity of diacylglycerol kinase, which may change the structure of lipopolysaccharide (LPS) probably to strengthen the membrane structure, and an increase in the expression of genes for GroEL/GroES or cell wall hydrolase to repair the protein or membrane damage that occurs at such critical temperatures. Additionally, transporters including efflux pumps may contribute to intracellular homeostasis by expelling toxic compounds such as ethanol and acetate or by maintaining the K⁺ concentration. The results of this study on four independently thermoadapted mutants led to the conclusion that the mutants have almost the same thermal adaptation strategies and thus their molecular diversity is limited. Full article

With the continuous and rapid development of global industries, issues such as offshore oil spills, leakage of organic chemicals, and the direct discharge of industrial oily sewage have caused serious damage to the ecological environment and water resources. Efficient oil–water separation is widely recognized as the solution. However, there is an urgent need to address the difficulties in treating thin oil films on the water surface and the low separation efficiency of existing oil–water separation materials. In view of this, this study aims to investigate high-efficiency oil–water separation materials for thin oil films. Four types of oil–water separation materials with different materials are designed to treat thin oil films on the water surface. The effects of factors such as oil film thickness, pressure, and temperature on the oil–water separation performance of these materials are studied. The viscosities of kerosene and diesel oil are tested, and the adsorption and separation effects of the oil–water separation materials on different oil products and oily organic solvents are examined. In addition, the long-term stability of the movable and portable oil–water separation components is verified. The results show that the oil-absorbing sponge-based oil–water separation membrane has an excellent microporous structure and surface roughness, endowing the membrane surface with excellent hydrophobicity and lipophilicity, and exhibiting good oil–water separation performance. The filtration flux of oil increases with the increase in pressure and temperature. It has good adsorption and separation performance for different oil products and oily organic solvents. Moreover, it maintains stable operation performance during the 12-month long-term oil–water separation process for kerosene and diesel oil. Full article

One of the most persistent and damaging diseases in olive trees is olive knot disease. This disease is caused by an infection by the Gram-negative phytopathogenic bacterium Pseudomonas savastanoi pv. savastanoi that is notoriously difficult to control. The increasing demand for eco-friendly and sustainable agricultural solutions has driven research into plant-based agents. This study investigated the antibacterial properties of essential oils (EOs) and their constituents, olive mill wastewater (OMWW), the phenolic compound hydroxytyrosol (HTyr), and algae and garlic extracts, as well as copper-based and plant-stimulating commercial products against P. savastanoi pv. savastanoi, a significant olive tree pathogen. Antibacterial activity was determined using the Kirby–Bauer disc diffusion and broth microdilution methods. The EOs derived from Thymus vulgaris (thyme) and Origanum compactum (oregano), and their key components thymol and carvacrol, exhibited the strongest antibacterial efficacy. Conversely, the OMWW, plant-stimulating products, and algae and garlic extracts showed limited to no antibacterial activity in vitro, with their antibacterial properties determined using the disc diffusion method. While the EOs were highly effective in vitro, regardless of the testing method, their efficacy in bacterial growth inhibition was strain- and concentration-dependent, possibly highlighting some metabolic or genetic variability in the target pathogen, even though the MIC values against all tested strains of P. savastanoi pv. savastanoi were equal. Bacterial membrane disruption and the consequent leakage of metabolites were determined as the modes of action of carvacrol and oregano EO. Carvacrol also promoted plant growth in lettuce without significant phytotoxic effects, although minor necrotic lesions were observed in young olive leaves at higher concentrations, presenting these agents as potential next-generation green bactericides. Full article

The broad use of (stainless steel) SS 316 L bipolar plates (BPs) in proton exchange membrane fuel cells relies (PEMFC) on high conductivity and corrosion resistance. To enhance the properties of stainless steel, this study applies ion implantation and heat treatment to form a non-homogeneous modified layer on SS 316 L. The injection of C and Mo ions on the SS 316 L surface caused irradiation damage, producing holes. But with the heat treatment of the ion-implanted samples, the irradiation-damaged surface will be repaired to a certain extent. The corrosion current density (I_corr) of the 600 °C sample in the kinetic potential test (5.32 × 10⁻⁴ A/cm²) was 54% lower than that of the naked SS 316 L (1.17 × 10⁻³ A/cm²). In the electrostatic potential test, the corrosion current of the 600 °C sample stabilized at a low value (about 0.26 μA/cm²), with the lowest concentration of dissolved metal ions (Fe²⁺ 2.908 mg/L). After anodic electrostatic potential polarization, the interfacial contact resistance (ICR) of (Mo+C)_600-1 was much lower than that of the untreated SS 316 L. Heat treatment experiments show that samples treated at 600 °C for 1 h exhibit significantly higher conductivity and anodic corrosion resistance than naked SS 316 L. This improvement is mainly due to the heat treatment under these conditions, which facilitated the formation of Mo carbides from the implanted C and Mo elements. Ion implantation and heat treatment enhance stainless steel surface conductivity and passive film corrosion resistance. These findings are useful in altering stainless steel BPs. Full article

Pathogenic fungi represent a growing concern for human health, necessitating a deeper understanding of their molecular mechanisms of virulence to formulate effective antifungal strategies. Recent research has increasingly highlighted the role of phospholipid components in fungal cell membranes, which are not only vital for maintaining cellular integrity but also significantly influence fungal pathogenicity. This review focuses on the impact of membrane phospholipid composition on fungal growth, morphogenesis, stress responses, and interactions with host cells. To be specific, membrane phospholipid composition critically influences fungal virulence by modulating growth dynamics and morphogenesis, such as the transition from yeast to hyphal forms, which enhances tissue invasion. Additionally, phospholipids mediate stress adaptation, enabling fungi to withstand host-derived oxidative and osmotic stresses, crucial for survival within hostile host environments. Phospholipid asymmetry also impacts interactions with host cells, including adhesion, phagocytosis evasion, and the secretion of virulence factors like hydrolytic enzymes. These adaptations collectively enhance fungal pathogenicity by promoting colonization, immune evasion, and damage to host tissues, directly linking membrane architecture to infection outcomes. By elucidating the molecular mechanisms involved, we aim to underscore the potential of targeting phospholipid metabolic pathways as a promising avenue for antifungal therapy. A comprehensive understanding of how membrane phospholipid composition regulates the virulence of pathogenic fungi can provide valuable insights for developing novel antifungal strategies. Full article

The Candida tropicalis (C. tropicalis) named YB-3 was isolated by the Atmospheric and room temperature plasma mutagenesis from 6.5 g/L furfural tolerance. The comprehensive transcriptomic analysis of YB-3 was performed. During the stress of furfural treatment, C. tropicalis YB-3 protected cells from oxidative stress damage by increasing the accumulation of the glutathione reductase gene and the expression of antioxidant enzymes, with the enhancement of the inositol phosphate synthase to maintain the structural integrity and transport function of the inner membrane system, thereby affecting the cells’ tolerance. Through the gene knockout and exogenous verification, it was further confirmed that the pathways involved in the three genes of sulfate adenosine transferase gene, glutathione reductase gene, and inositol phosphate synthase gene had significant effects on improving the tolerance of the strain to furfural. The deep excavation of furfural-tolerant gene components and directional modification of C. tropicalis to enhance tolerance are key steps for improving the utilization rate of biomass. Full article

The skin is continuously exposed to environmental changes, rendering it vulnerable to damage from external stressors that contribute to premature skin aging. This study aims to explore skin longevity pathways stimulated by a rose extract (RE) derived from petals. Human keratinocytes treated with RE exhibited a significant increase in NRF2 (NF-E2-related factor 2; ≈2–4% of induction) and LAMP2A (Lysosome-Associated Membrane Protein 2A; ≈6–12% of induction) levels. The presence of RE significantly mitigated the increase in carbonylation levels (≈34–37% of protection) and the number of labeled P16^INK4A cells (≈60–72% of protection), associated with proliferation arrest, both induced by exposure to BAP (Benzo[a]pyrene) coupled with UV-A (Ultraviolet A) irradiation. The beneficial effects mediated by RE were inhibited by Compound C, a specific AMPK inhibitor (AMP-activated protein kinase). The involvement of the AMPK pathway in mediating the beneficial effects of RE has been confirmed by assessing its activation through the evaluation of its phosphorylation state which was significantly elevated in the presence of RE compared to the stress condition. In conclusion, the activation of the AMPK pathway enhances antioxidant defenses and promotes autophagy. This dual action, mediated by RE, helps protect skin cells from oxidative damage and senescence while maintaining proteostasis, skin integrity, and cellular proliferation under pollution-induced stress (BAP + UV-A). These findings highlight the potential in mitigating age-related skin changes through the modulation of longevity pathways. Full article

Background/Objectives: We wished to evaluate in vitro whether vacuum plasma surface treatment of bone graft substitutes and resorbable membranes could improve the hydrophilicity and wettability of the tested materials. Methods: A total of 28 sterilized samples were considered for this research and divided into three groups. Six samples were used for the SEM-EDS analysis. The other 22 samples were randomly assigned into the test (plasma-treated, n = 11) and control (no treatment, n = 11) groups. Vacuum plasma surface treatment was performed in the test group before the SEM-EDS analysis using the ACTILINK reborn with a material holder (Plasmapp Co., Ltd., Daejeon, Republic of Korea). Plasmatreat (Plasmatreat, Steinhagen, Germany) inks were used to evaluate the differences in the hydrophilicity between the test and control groups. The outcome measures were the absorption time, wettability grade, and grade of decontamination after different time cycles. Results: After the vacuum plasma surface treatment, the absorption time of the inks statistically decreased in all of the subgroups (p < 0.05), while the wettability grade increased. The SEM-EDS analyses showed an increased reduction rate of carbon impurities after up to three vacuum plasma surface treatment cycles. Furthermore, the SEM-EDS analysis did not reveal any areas of damage caused by the multiple treatments. Conclusions: Within the limitations of this in vitro study, the vacuum plasma surface treatment increased the hydrophilicity and wettability of the tested biomaterials. Particle bone graft and bone blocks should be treated using longer time programs. Further well-conducted randomized clinical trials with sample size calculations are needed to confirm these preliminary results. Full article