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김기호,홍성필,포미량일 대한금속재료학회(대한금속학회) 1999 대한금속·재료학회지 Vol.37 No.1
Ion-nitriding for S45C using Al, Cr and Ti subsidiary cathodes was carried out at 823K for 3hours in an atmosphere of 30%N₂-X%H₂-Y%Ar mixing gas at 665Pa. The nitriding layers formed on S45C were characterized by XRD, XPS, microscopic observation and microhardness profile. The surface hardness of S45C was increased with Ar contents up to 20% while N₂ was maintained at 30%. Iron nitride phases of ε-Fe₂-₃N and γ'-Fe₄N were found on the surface of S45C ion-nitrided with each subsidiary cathode. From the results of XPS analysis, Al was found as a combined form with nitrogen in the nitrided layer. Using Al, Cr and Ti subsidiary cathodes, the surface hardness and thickness of compound layer became higher and thicker than the unused layer one. The surface hardness of S45C ion-nitrided without the subsidiary cathodes was about Hv521. On the contrary, the surface hardness of S45C ion-nitrided with Al, Cr and Ti subsidiary cathodes were Hv890, Hv734 and Hv667, respectively. These may be due to the sputtered atoms, which diffused into the iron nitrides and then increased lattice strain.
Injury-Mediated Vascular Regeneration Requires Endothelial ER71/ETV2
Park, Changwon,Lee, Tae-Jin,Bhang, Suk Ho,Liu, Fang,Nakamura, Rei,Oladipupo, Sunday S.,Pitha-Rowe, Ian,Capoccia, Benjamin,Choi, Hong Seo,Kim, Tae Min,Urao, Norifumi,Ushio-Fukai, Masuko,Lee, Dongjun,Mi American Heart Association, Inc. 2016 Arteriosclerosis, thrombosis, and vascular biology Vol.36 No.1
<P>Objective Comprehensive understanding of the mechanisms regulating angiogenesis might provide new strategies for angiogenic therapies for treating diverse physiological and pathological ischemic conditions. The E-twenty six (ETS) factor Ets variant 2 (ETV2; aka Ets-related protein 71) is essential for the formation of hematopoietic and vascular systems. Despite its indispensable function in vessel development, ETV2 role in adult angiogenesis has not yet been addressed. We have therefore investigated the role of ETV2 in vascular regeneration. Approach and Results We used endothelial Etv2 conditional knockout mice and ischemic injury models to assess the role of ETV2 in vascular regeneration. Although Etv2 expression was not detectable under steady-state conditions, its expression was readily observed in endothelial cells after injury. Mice lacking endothelial Etv2 displayed impaired neovascularization in response to eye injury, wounding, or hindlimb ischemic injury. Lentiviral Etv2 expression in ischemic hindlimbs led to improved recovery of blood perfusion with enhanced vessel formation. After injury, fetal liver kinase 1 (Flk1), aka VEGFR2, expression and neovascularization were significantly upregulated by Etv2, whereas Flk1 expression and vascular endothelial growth factor response were significantly blunted in Etv2-deficient endothelial cells. Conversely, enforced Etv2 expression enhanced vascular endothelial growth factor-mediated endothelial sprouting from embryoid bodies. Lentiviral Flk1 expression rescued angiogenesis defects in endothelial Etv2 conditional knockout mice after hindlimb ischemic injury. Furthermore, Etv2(+/-); Flk1(+/-) double heterozygous mice displayed a more severe hindlimb ischemic injury response compared with Etv2(+/-) or Flk1(+/-) heterozygous mice, revealing an epistatic interaction between ETV2 and FLK1 in vascular regeneration. Conclusions Our study demonstrates a novel obligatory role for the ETV2 in postnatal vascular repair and regeneration.</P>