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- 저자 : Han Shasha (검색결과 3 건)
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Dongheng Xu,Han Wang,Xuewei Tao,Zhengjun Yao,Shasha Zhang,Moliar Oleksander 대한금속·재료학회 2021 METALS AND MATERIALS International Vol.27 No.5
The Inconel 718 (IN718) alloy coatings were successfully fabricated using electron beam wire-feeding deposition technology.The macrostructure, microstructure and elemental analysis of the deposited coatings were characterized by OM, SEMand EDS. Moreover, the hardness and wear resistance were also investigated experimentally. The results showed that thecross section of the deposited coatings can be divided into three different regions: clad zone (CZ), fusion zone (FZ) and heataffected zone. Equiaxed dendrites appeared in the CZ while columnar dendrites occurred in the FZ, and discrete fine Lavesphase particles were formed under low beam current while continuous coarse Laves phase particles were found under highbeam current. The EDS results showed that the degree of Nb segregation in FZ is higher than that in CZ. More importantly,the microstructure coarsened and the degree of Nb segregation increased with the increase of beam current. The depositedcoating under the lowest beam current (10 mA) has the highest hardness (263 HV0.2) and the minimum specific wear rate(3.95391 × 10−15 m3/Nm), which is corresponding to the fine microstructure, discrete Laves phase particles and low degreeof Nb segregation under low beam current.
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Sun Junxia,Han Shasha,Chen Ping 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.1
Background Posterior capsule opacification (PCO), also known as after-cataract, is a special condition in which the cortex of the cataract remains in the pupil area or the formation of a fibrogenic membrane after surgical cataract extraction. Objective To explore the effect of lncRNA X inactivation-specific transcript (XIST) on PCO. Results First, we proved that XIST was up-regulated in TGF-β2-treated SRA01/04 cells. Inhibition of XIST significantly reduced the proliferation and migration of SRA01/04 cells, and affected the expression of EMT markers. Further research data illustrated that miR-98-5p and COL5A2 were targets of XIST. Besides, pathway enrichment analysis showed that the PI3K/Akt/FOXO1 signaling pathway was associated with XIST. Conclusion In the study, we demonstrated that lncRNA XIST contributed to EMT in PCO via regulating miR-98-5p/COL5A2 and PI3K/Akt/FOXO1 pathway, which provided a new treatment strategy for PCO.
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Xuehua Liu,Mengmeng Li,Yuzhu Peng,Xiaoshan Hu,Jing Xu,Shasha Zhu,Zhangbin Yu,Shuping Han 생화학분자생물학회 2016 Experimental and molecular medicine Vol.48 No.-
MicroRNAs (miRNAs) are small, non-coding single-stranded RNAs that suppress protein expression by binding to the 3′ untranslated regions of their target genes. Many studies have shown that miRNAs have important roles in congenital heart diseases (CHDs) by regulating gene expression and signaling pathways. We previously found that miR-30c was highly expressed in the heart tissues of aborted embryos with ventricular septal defects. Therefore, this study aimed to explore the effects of miR-30c in CHDs. miR-30c was overexpressed or knocked down in P19 cells, a myocardial cell model that is widely used to study cardiogenesis. We found that miR-30c overexpression not only increased cell proliferation by promoting cell entry into S phase but also suppressed cell apoptosis. In addition, we found that miR-30c inhibited dimethyl sulfoxide-induced differentiation of P19 cells. miR-30c knockdown, in contrast, inhibited cell proliferation and increased apoptosis and differentiation. The Sonic hedgehog (Shh) signaling pathway is essential for normal embryonic development. Western blotting and luciferase assays revealed that Gli2, a transcriptional factor that has essential roles in the Shh signaling pathway, was a potential target gene of miR-30c. Ptch1, another important player in the Shh signaling pathway and a transcriptional target of Gli2, was downregulated by miR-30c overexpression and upregulated by miR-30c knockdown. Collectively, our study revealed that miR-30c suppressed P19 cell differentiation by inhibiting the Shh signaling pathway and altered the balance between cell proliferation and apoptosis, which may result in embryonic cardiac malfunctions.
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