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FeNiMo/SiO2 powder cores were prepared using the sol-gel method. Tetraethyl orthosilicate (TEOS) was added to produce an amorphous SiO2 coating outside the FeNiMo particles to form a core-shell structure. The thickness of the SiO2 layer was designed by varying the concentration of TEOS, and the optimized permeability and magnetic loss of the powder core could achieve 78.15 and 633.44 kW m-3 at 100 kHz and 100 mT, respectively. Compared with other soft magnetic composites, these FeNiMo/SiO2 powder cores have a significantly higher effective permeability and a lower core loss. Surprisingly, the high-frequency stability of permeability could be substantially enhanced through the insulation coating process in which µf/µ100 kHz could reach 98.7% at 1 MHz. In comparison with 60µ commercial products, the comprehensive soft magnetic properties of the FeNiMo/SiO2 cores were superior to most manufacturers, which would be potentially applied to high-performance inductance devices in high-frequency ranges.
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BACKGROUND: A deeper understanding of new prognostic and diagnostic biomarkers for vitiligo, an autoimmune disease, is needed. The purpose of this study is to identify the underlying long noncoding RNAs (lncRNAs) and immune infiltration related to the cause of vitiligo. METHODS: The microarray data (GSE75819) were available to be downloaded from NCBI-GEO. Eight hub genes were identified from the Protein-protein interaction (PPI) network by the dissection of differentially expressed genes (DEG), Kyoto Gene and Genomic Encyclopedia (KEGG) expansion pathway, and Gene Ontology (GO). Further analysis based on the immune infiltration as well as the correlation between DEGs and immune cells was performed. Our conclusions were verified by using the GSE534 eventually. RESULTS: According to our analysis, we obtained a total of 666 DEGs and 8 hub genes that include ECT2, CCT8, VRK1, UQCRH, EBNA1BP2, CRY2, IFIH1, and BCCIP, which may play an important role in vitiligo. Moreover, the immune infiltration profiles varied significantly between normal and vitiligo tissues. Compared with normal tissues, vitiligo tissues contained a greater proportion of mast cells (P<0.05). The analysis revealed that T cells regulatory (Tregs) have a negative correlation with the VRK1 expression (R=-0:77, P<0.001), whereas the mast cells resting have a positive correlation with the VRK1 expression (R=0:72, P<0.001) in vitiligo. CONCLUSION: The gene expression profile of vitiligo was realized by a bioinformatics method. The expressions of 8 hub genes and 22 immune cells were found, as the same as CRY2 and VRK1 have a special correlation with immune cells, which may be a significant cause of the pathogenesis of vitiligo. This provides a new idea for the diagnosis and treatment of vitiligo.
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Osteoarthritis (OA) is a multifactorial disease that affects the entire joint, often resulting in severe pain, disability, psychological distress, and a lower quality of life. Patient self-management is emphasized in OA clinical recommendations. Currently, the clinical treatment of OA mainly focuses on pain relief and the improvement of joint function, with few options for regenerating degenerative cartilage or slowing the progression of OA. Therefore, we first reviewed the current treatment of OA, and then summarized the research advances of nanotechnology in OA treatment, including nano drug delivery systems for small molecule drugs, nucleic acids and proteins, nano-scaffolds for cartilage regeneration, and nanoparticle lubricants. Finally, we discussed the opportunities and potential challenges of nanotechnology in OA treatment.
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Osteoarthritis (OA) is the most common joint disease, usually occurring in middle-aged and elderly people. However, current treatment for OA in its early stages is ineffective, and drug therapy is often ineffective in slowing the progression of the disease. In fact, a deeper understanding of the underlying molecular mechanisms of OA could help us to better develop effective therapeutic measures. N6-methyladenosine (m6A) is a methylation that occurs at the adenosine N6-position, which is the most common internal modification on eukaryotic mRNAs. The role and mechanisms of m6A in mammalian gene regulation have been extensively studied. The "Writer", "eraser", and "reader" proteins are key proteins involved in the dynamic regulation of m6A modifications. Recent studies on post-transcriptional regulation alone have shown that m6a modification has an important role in the development of OA. This paper summarizes the specific regulatory processes of M6A in disease and reviews the role of m6A in OA, describing its pathophysiological role and molecular mechanisms, as well as its future research trends and potential clinical applications in OA.
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Osteoporosis is one of the most frequent skeletal disorders and a major cause of morbidity and mortality in the expanding aging population. Evidence suggests that hesperidin may have a therapeutic impact on osteoporosis. Nevertheless, little is known about the role of hesperidin in the development of osteoporosis. Bioinformatics analyses were carried out to explore the functions and possible molecular mechanisms by which hesperidin regulates osteogenic differentiation. In the present study, we screened and harvested 12 KEGG pathways that were shared by hesperidin-targeted genes and osteoporosis. The p53 signaling pathway was considered to be a key mechanism. Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.