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RISS 인기검색어
- 검색키워드
- 저자 : Xiaoxiang Guan (검색결과 3 건)
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Effect of grinding depth on fatigue fracture behaviors of 40Cr steel
Jianzhi Chen,Guochao Li,Ning Li,Xiaoyan Guan,Yan Wang,Zhen Xu,Xiaoxiang Bai,Honggen Zhou 대한기계학회 2023 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.37 No.4
40Cr steel specimens were ground with different grinding depth (a p ) varied from 0 μm to 35 μm, and the rotary bending fatigue behaviors of ground specimens were investigated. Fatigue results show that the fatigue life of ground specimens exhibits an increasing first and then decreasing tendency with the increment of a p , the specimen with a p of 15 μm exhibits the highest fatigue life, and the effect of a p on fatigue damage behaviors of ground specimens were analyzed from aspects of surface roughness, work hardening and compressive residual stress. Multiple crack initiation of fatigue fractured specimens was observed, the number of crack initiation sites tends to increase first and then decrease with increasing a p . The relationship model between the fatigue striation width and the a p was established, and the prediction deviation of the model is ~2.08 %. It is expected that the model may provide new clues for optimizing the grinding process of mechanical parts.
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Lai, Jing,Yang, Fang,Zhang, Wenwen,Wang, Yanru,Xu, Jing,Song, Wei,Huang, Guichun,Gu, Jun,Guan, Xiaoxiang Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.8
The p73 gene contains an extrinsic P1 promoter and an intrinsic P2 promoter, controlling the transcription of the pro-apoptotic TAp73 isoform and the anti-apoptotic ${\Delta}Np73$ isoform, respectively. The DNA methylation status of both promoters act equally in the epigenetic transcriptional regulation of their relevant isoforms. The aim of this study was to analyze the different effects of these p73 isoforms in 5-aza-2'-deoxycytidine (5-aza-dC)-induced apoptosis in breast cancer cells. We investigated the effects of the DNA demethylation agent, 5-aza-dC, on the T-47D breast cancer cell line, and evaluated the methylation status of the p73 promoters and expression of TAp73 and ${\Delta}Np73$. Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells. 5-aza-dC induced significant anti-tumor effects in T-47D cells, including inhibition of cell viability, G1 phase arrest and apoptosis. This was associated with p73 promoter demethylation and a concomitant increase in TAp73 mRNA and protein expression. In contrast, the methylation status of promoter P2 was not associated with ${\Delta}Np73$ mRNA or protein levels. Furthermore, demethylation of P2 failed to inhibit the expression of ${\Delta}Np73$ with 5-aza-dC in the p53 knockdown cell model. Our study suggests that demethylation of the P1 and P2 promoters has opposite effects on the expression of p73 isoforms, namely up-regulation of TAp73 and down-regulation of ${\Delta}Np73$. We also demonstrate that p53 likely contributes to 5-aza-dC-induced ${\Delta}Np73$ transcriptional inactivation in breast cancer cells.
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Jing Lai,Fang Yang,Wenwen Zhang,Yanru Wang,Jing Xu,Wei Song,Guichun Huang,Jun Gu,Xiaoxiang Guan 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.8
The p73 gene contains an extrinsic P1 promoter and an intrinsic P2 promoter, controlling the transcription of the pro-apoptotic TAp73 isoform and the anti-apoptotic ΔΝp73 isoform, respectively. The DNA methylation status of both promoters act equally in the epigenetic transcriptional regulation of their relevant isoforms. The aim of this study was to analyze the different effects of these p73 isoforms in 5-aza-2'-deoxycytidine (5-aza-dC)-induced apoptosis in breast cancer cells. We investigated the effects of the DNA demethylation agent, 5-aza-dC, on the T-47D breast cancer cell line, and evaluated the methylation status of the p73 promoters and expression of TAp73 and ΔNp73. Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells. 5-aza-dC induced significant anti-tumor effects in T-47D cells, including inhibition of cell viability, G1 phase arrest and apoptosis. This was associated with p73 promoter demethylation and a concomitant increase in TAp73 mRNA and protein expression. In contrast, the methylation status of promoter P2 was not associated with ΔNp73 mRNA or protein levels. Furthermore, demethylation of P2 failed to inhibit the expression of ΔNp73 with 5-aza-dC in the p53 knockdown cell model. Our study suggests that demethylation of the P1 and P2 promoters has opposite effects on the expression of p73 isoforms, namely up-regulation of TAp73 and down-regulation of ΔΝp73. We also demonstrate that p53 likely contributes to 5-aza-dC-induced ΔNp73 transcriptional inactivation in breast cancer cells.
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