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Effect of the Liquid Density Difference on Interface Shape of Double-Liquid Lens
Meimei Kong,Lingfeng Zhu,Dan Chen,Zhongcheng Liang,Rui Zhao,Enming Xu 한국광학회 2016 Current Optics and Photonics Vol.20 No.3
The effect of the liquid density difference on interface shape of a double-liquid lens is analyzed indetail. The expressions of interface shape of two liquids with liquid density difference are analyzed andfitted with “even asphere”. The imaging analysis of the aspheric interface shape of a double-liquid lensis presented. The results show that the density difference of two liquids can cause the interface to bean aspheric surface, which can improve the image quality of a double-liquid lens. The result providesa new selection for the related further research and a wider application field for liquid lenses.
Shenghan Su,Qingrui Zhao,Lingfeng Dan,Yuqing Lin,Xuebei Li,Yunjin Zhang,Chunxiao Yang,Yimeng Dong,Xiaohan Li,Romano Regazzi,Changhao Sun,Xia Chu,Huimin Lu 대한내분비학회 2022 Endocrinology and metabolism Vol.37 No.6
Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR-8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion: These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a-5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.