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RISS 인기검색어
- 검색키워드
- 저자 : Zhu Minmin (검색결과 2 건)
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Tay, Roland Yingjie,Park, Hyo Ju,Lin, Jinjun,Ng, Zhi Kai,Jing, Lin,Li, Hongling,Zhu, Minmin,Tsang, Siu Hon,Lee, Zonghoon,Teo, Edwin Hang Tong American Chemical Society 2018 Chemistry of materials Vol.30 No.19
<P>Spiral growth of various nanomaterials including some two-dimensional (2D) transition metal dichalcogenides had recently been experimentally realized using chemical vapor deposition (CVD). However, such growth that is driven by screw dislocation remained elusive for graphene and is rarely discussed because of the use of metal catalysts. In this work, we show that formation of few-layer graphene (FLG) with a spiral structure driven by screw dislocation can be obtained alongside FLG having a concentric layered structure formed by interfacial nucleation (nucleation at the graphene/Cu interface) using Cu-catalyzed ambient pressure CVD. Unlike commonly reported FLG grown by interfacial nucleation where the second layer is grown independently beneath the first, the growth of a spiral structure adopts a top growth mechanism where the top layers are an extension from the initial monolayer which spirals around an axial dislocation in self-perpetuating steps. Since the same atomic orientation is preserved, the subsequent spiraling layers are stacked in an oriented AB-stacked configuration. This contrasts with FLG formed by interfacial nucleation where turbostratic stacking of the entire adlayer may exist. In both growth scenarios, the second layer (either top or bottom) can grow across the grain boundaries of the initial monolayer domains, forming partial regions with turbostratic stacking configuration due to weak interlayer van der Waals interactions. The unique interlayer coupling of FLG spirals, which enable superior conductivity along the normal of the 2D crystal with spiraling trajectories, are expected to have new and interesting nanoscale applications.</P> [FIG OMISSION]</BR>
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Shen Xuefang,Chen Xiangyuan,Wang Jing,Liu Jing,Wang Zhiyao,Hua Qing,Wu Qichao,Su Yanguang,He Huanzhong,Hu Yuqin,Meng Zhipeng,Xiong Wanxia,Zhu Minmin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-
Hyperglycemia-mediated endothelial inflammation participates in the pathogenesis of cardiovascular complications in subjects with diabetes. Previous studies reported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) and SET8 participate in high glucose-mediated endothelial inflammation. In this study, we hypothesize that SET8 regulates PTEN expression, thus contributing to high glucose-mediated vascular endothelial inflammation. Our data indicated that plasma soluble intercellular adhesion molecule-1 (sICAM-1) and endothelial selectin (e-selectin) were increased in patients with diabetes and diabetic rats. PTEN expression was augmented in the peripheral blood mononuclear cells of patients with diabetes and in the aortic tissues of diabetic rats. Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose led to endothelial inflammation via upregulation of PTEN. Furthermore, high glucose inhibited SET8 expression and histone H4 lysine 20 methylation (H4K20me1), a downstream target of SET8. SET8 overexpression reversed the effects of high-glucose treatment. shSET8-mediated endothelial inflammation was counteracted by siPTEN. Furthermore, SET8 was found to interact with FOXO1. siFOXO1 attenuated high glucose-mediated endothelial inflammation. FOXO1 overexpression-mediated endothelial inflammation was counteracted by siPTEN. H4K20me1 and FOXO1 were enriched in the PTEN promoter region. shSET8 increased PTEN promoter activity and augmented the positive effect of FOXO1 overexpression on PTEN promoter activity. Our in vivo study indicated that SET8 was downregulated and FOXO1 was upregulated in the peripheral blood mononuclear cells of patients with diabetes and the aortic tissues of diabetic rats. In conclusion, SET8 interacted with FOXO1 to modulate PTEN expression in vascular endothelial cells, thus contributing to hyperglycemia-mediated endothelial inflammation.
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