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Fu Rong Cao,Guo Qiang Xue,Bi Jin Zhou,Shun Cheng Wang 대한금속·재료학회 2019 METALS AND MATERIALS International Vol.25 No.3
To explore the ductility, a novel Mg–8.41Li–1.80Al–1.77Zn (designated as LAZ822) alloy was fabricated by casting,hot rolling and friction stir processing. The maximum elongation to failure of 489.5% was demonstrated in a fine-grainedLAZ822 alloy at a temperature of 573 K and an initial strain rate of 1.67 × 10−4 s−1. The true stress exponent of 2, the grainsize exponent of 2 and the activation energy of 89.44–121.14 kJ/mol confirm that grain boundary sliding controlled by latticediffusion governs the rate-controlling deformation process at the temperatures of 523 and 573 K. The viscous resistancemodels of dual phases were newly established. At 573 K, the lattice viscous resistance of the α-Mg phase is 2644 times aslarge as that of the β-Li phase, whereas the grain boundary viscous resistance of the α-Mg phase is 3.3 times as large as thatof the β-Li phase. Some α-Mg grains remain in an equiaxed state while the other α-Mg grains become connected at elevatedtemperatures. This experimental evidence corroborates the existence of dynamic grain connection growth. Cavity growthmechanism maps were constructed. The maps reveal that power-law cavity growth or strain controlled cavity growth is thepredominant cavity growth mechanism.
Metastasis associated genomic aberrations in stage II rectal cancer
Hong Zhao,Zhi-Zhou Shi,Rui Jiang,Dong-Bing Zhao,Hai-Tao Zhou,Jian-Wei Liang,Xin-Yu Bi,Jian-Jun Zhao,Zhi-Yu Li,Jian-Guo Zhou,Zhen Huang,Ye-Fan Zhang,Jian Wang,Xin Xu,Yan Cai,Ming-Rong Wang,Yu Zhang 한국유전학회 2016 Genes & Genomics Vol.38 No.11
Genomic aberrations of rectal carcinoma, especially DNA copy number changes associated with metastasis were largely unclear. We aim to identify the metastasis associated biomarkers in stage II rectal cancer. Formalin-fixed, paraffin-embedded primary tumor tissues of stage II rectal carcinoma were analyzed by array-based comparative genomic hybridization, and genomic aberrations were identified by Genomic Workbench and SAM software. Copy number changes and mRNA expressions were validated by Real-time PCR in an independent rectal cancer samples. The results showed that the most frequent gains in stage II rectal cancer were at 1q21.2-q23.1, 3p21.31, 11q12.2-q23.3, 12q24.11-q24.31, 12q13.11-q14.1 and losses in 18q11.2-q23, 17q21.33-q22, 13q31.1-q31.3, 21q21.1-q21.3, 8p23.3-p23.1 and 4q22.1-q23. Twenty-two amplifications and five homozygous deletions were also identified. We further found that S100A1 (1q21.3-q23.1), MCM7 (7q22.1) and JUND (19p13.11) were amplified and overexpressed in stage II rectal cancer. Interestingly, the genomic aberrations affected 14 signaling pathways including VEGF signaling pathway and fatty acid metabolism. Most importantly, loss of 13q31.1-q34 and gain of 1q44 were associated with distant metastasis. Our results indicated that these metastasis associated genomic changes may be useful to reveal the pathogenesis of rectal cancer metastasis and identify candidate biomarkers.
Zhang, Qing-Mei,Shen, Ning,Xie, Sha,Bi, Shui-Qing,Luo, Bin,Lin, Yong-Da,Fu, Jun,Zhou, Su-Fang,Luo, Guo-Rong,Xie, Xiao-Xun,Xiao, Shao-Wen Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8
Melanoma-associated antigen (MAGE) family genes have been considered as potentially promising targets for anticancer immunotherapy. MAGED4 was originally identified as a glioma-specific antigen. Current knowledge about MAGED4 expression in glioma is only based on mRNA analysis and MAGED4 protein expression has not been elucidated. In the present study, we investigated this point and found that MAGED4 mRNA and protein were absent or very lowly expressed in various normal tissues and glioma cell line SHG44, but overexpressed in glioma cell lines A172,U251,U87-MG as well as glioma tissues, with significant heterogeneity. Furthermore, MAGED4 protein expression was positively correlated with the glioma type and grade. We also found that the expression of MAGED4 inversely correlated with the overall methylation status of the MAGED4 promoter CpG island. Furthermore, when SHG44 and A172 with higher methylation were treated with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZA-CdR) reactivation of MAGED4 mRNA was mediated by significant demethylation in SHG44 instead of A172. However, 5-AZA-CdR treatment had no effect on MAGED4 protein in both SHG44 and A172 cells. In conclusion, MAGED4 is frequently and highly expressed in glioma and is partly regulated by DNA methylation. The results suggest that MAGED4 might be a promising target for glioma immunotherapy combined with 5-AZA-CdR to enhance its expression and eliminate intratumor heterogeneity.
Zhan-qing Zhang,Yan-bing Wang,,Wei Lu,,Dan-ping Liu,,Bi-sheng Shi,,Xiao-nan Zhang,,Dan Huang,,Xiu-fen Li,,Xin-lan Zhou,,Rong-rong Ding, 대한진단검사의학회 2019 Annals of Laboratory Medicine Vol.39 No.1
Background: We examined changes in hepatitis B core-related antigen (HBcrAg) during the four sequential phases of chronic hepatitis B virus (HBV) infection: hepatitis B e antigen (HBeAg)-positive chronic infection (EPCI) and hepatitis (EPCH), followed by HBeAg-negative chronic infection (ENCI) and hepatitis (ENCH). We compared the performance of serum HBcrAg, hepatitis B surface antigen (HBsAg), and HBV DNA in predicting EPCH and ENCH.