Facile Construction of Nanostructured Cermet Anodes with Strong Metal-Oxide Interaction for Efficient and Durable Solid Oxide Fuel Cells.

Nanostructured anodes generate massive reaction sites to oxidize fuels in solid oxide fuel cells (SOFCs); however, the nonexistence of a practically viable approach for the construction of nanostructures and the retention of these nanostructures under the harsh operating conditions of SOFCs poses a significant challenge. Herein, a simple procedure is reported for the construction of a nanostructured Ni-Gd-doped CeO2 anode based on the direct assembly of pre-formed nanocomposite powder with strong metal-oxide interaction. The directly assembled anode forms heterointerfaces with the electrolyte owing to the electrochemical polarization current and exhibits excellent structural robustness against thermal ripening. An electrolyte-supported cell with the directly assembled anode produces a peak power density of 0.73 W cm-2 at 800 °C, while maintaining stability for 100 h, which is in contrast to the drastic degradation of the cermet anode prepared using the conventional method. These findings provide clarity on the design and construction of durable nanostructured anodes and other electrodes for SOFCs.

Comparative physiological and transcriptome analysis provide insights into the inhibitory effect of 6-pentyl-2H-pyran-2-one on Clarireedia jacksonii.

Clarireedia spp. is a destructive phytopathogenic fungus that causes turf dollar spot of bent-grass, leading to widespread lawn death. In this study, we explored the antifungal capability of 6-pentyl-2H-pyran-2-one (6PP), a natural metabolite volatilized by microorganisms, which plays an important role in the biological control of turfgrass dollar spot. However, the mechanisms by which 6PP inhibits Clarireedia jacksonii remain unknown. In the present study, C. jacksonii mycelial growth was inhibited by the 6PP treatment and the 6PP treatment damaged cell membrane integrity, causing an increase in relative conduc-tivity. Furthermore, physiological and biochemistry assay showed that 6PP treatment can enhance reactive oxygen species (ROS) levels, malondialdehyde (MDA) content obviously increased with 6PP exposure, increased alchohol dehydrogenase (ADH) and depleted acetalde-hyde dehydrogenase (ALDH), and activated the activities of many antioxidant enzymes in C. jacksonii. Gen Ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed that some genes in C. jacksonii after 6PP treatment related to integrity of the cell wall and membrane, and oxidative stress were significantly downregulated. It is worth mentioning that the fatty acid degradation pathway is significantly upregulated, with an increase in ATP content and ATP synthase activity, which may promote fungal cell apoptosis. Moreover, we found that the expression of ABC transporters, and glutathione metabolism encoding genes were increased to respond to external stimuli. Taken together, these findings revealed the potential antifungal mechanism of 6PP against Clarireedia spp., which also provides a theoretical basis for the commercial utilization of 6PP as a green pesticide in the future.

Morin hydrate inhibits atherosclerosis and LPS-induced endothelial cells inflammatory responses by modulating the NFκB signaling-mediated autophagy.

Atherosclerosis (AS) is a chronic inflammatory disease involving blood vessels. Inflammation affects different cells and increases the expression of adhesion molecules. Morin hydrate (MO) is a naturally occurring bioflavonoid with anti-inflammatory and anti-oxidant effects. Although the exact mechanism has not been fully elucidated, MO possibly influences autophagy pathways in immunity and inflammation. In this study, MO showed the potential to inhibit atherosclerotic and promote vascular endothelial autophagy in apolipoprotein E (ApoE)-/- mice with a high-fat diet. Then, we aimed to explore the anti-inflammatory effects of MO in human umbilical vein endothelial cells (HUVECs) and its relationship with autophagy. We found that MO inhibited lipopolysaccharide (LPS)-induced monocyte adhesion and the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase 9 (MMP-9) in HUVECs. Moreover, MO reduced the expression of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) by inhibiting the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor kappa B (NFκB) signaling pathway. MO induced autophagy by inhibiting the NFκB signaling pathway in normal HUVECs and LPS-stimulated HUVECs. When autophagy was inhibited by 3-methyladenine (3-MA) or small interfering RNA (siRNA), the anti-inflammatory effect of MO was reduced. In conclusion, MO inhibits atherosclerosis in ApoE-/- mice and LPS-induced inflammatory responses by inhibiting the activation of the PI3K/Akt1/NFκB signaling pathway in a NFκB signaling-mediated autophagy way.

Anti-inflammatory effects of Platycodin D on dextran sulfate sodium (DSS) induced colitis and E. coli Lipopolysaccharide (LPS) induced inflammation.

Platycodin D (PLD) is a saponin found in Platycodon grandiflorum, which has been reported to have anti-inflammatory effects. However, the effects of PLD on ulcerative colitis (UC) remain unknown. In this study, PLD showed the potential to reduce inflammation, ameliorate intestinal damage, and maintain intestinal integrity in DSS-induced colitis. However, the beneficial effect of PLD was reduced when macrophages were depleted, indicating the key role of macrophages in the beneficial effect of PLD in DSS-induced colitis. Meanwhile, we found that PLD inhibited the expression of M1 markers and promoted the expression of M2 markers in colon. Similarly, we found PLD significantly attenuated the levels of pro-inflammatory cytokines, increased the level of anti-inflammatory cytokine and altered macrophage proportions in LPS-stimulated RAW 264.7 cells in vitro. Moreover, treating LPS-stimulated RAW 264.7 cells with PLD increased the activation of the PI3K/Akt signaling pathway and decreased activation of NF-κB pathway. Furthermore, we found that the anti-inflammatory and macrophage polarization regulatory effects of PLD was Adenosine 5'-monophosphate-activated protein kinase (AMPK)-dependent. These results indicate that PLD attenuates DSS-induced colitis and LPS-induced inflammation, and the mechanism behind the phenomenon may be regulating macrophage polarization via activation of AMPK. Our study provides a theoretical basis for PLD to be used as a potential treatment of colitis.

Regulatory Roles of Related Long Non-coding RNAs in the Process of Atherosclerosis.

Atherosclerosis (AS) is the main cause of coronary heart disease, cerebral infarction, and peripheral vascular disease, which comprise serious hazards to human health. Atherosclerosis is characterized by the deposition of lipids on the interior walls of blood vessels, causing an inflammatory response of immune cells, endothelial cells, and smooth muscle cells, and a proliferation cascade reaction. Despite years of research, the underlying pathogenesis of AS is not fully defined. Recent advances in our understanding of the molecular mechanisms by which non-coding RNA influences the initiation and progression of AS have shown that long non-coding RNAs (lncRNAs) regulate important stages in the atherosclerotic process. In this review, we summarize current knowledge of lncRNAs, which influence the development of AS. We review the regulatory processes of lncRNAs on core stages of atherosclerotic progression, including lipid metabolism, inflammation, vascular cell proliferation, apoptosis, adhesion and migration, and angiogenesis. A growing body of evidence suggests that lncRNAs have great potential as new therapeutic targets for the treatment of vascular diseases.