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- 저자 : Mei-xia Qu (검색결과 4 건)
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Xue, Xia,Yu, Jin-Long,Sun, De-Qing,Kong, Feng,Qu, Xian-Jun,Zou, Wen,Wu, Jing,Wang, Rong-Mei Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.9
Curcumin, a polyphenol compound derived from the rhizome of the plant Curcuma longa L. has been verified as an anticancer compound against several types of cancer. However, understanding of the molecular mechanisms by which it induces apoptosis is limited. In this study, the anticancer efficacy of curcumin was investigated in human gastric adenocarcinoma SGC-7901 cells. The results demonstrated that curcumin induced morphological changes and decreased cell viability. Apoptosis triggered by curcumin was visualized using Annexin V-FITC/7-AAD staining. Curcumin-induced apoptosis of SGC-7901 cells was associated with the dissipation of mitochondrial membrane potential (MMP) and the release of cytochrome c into the cytosol. Furthermore, the down-regulation of Bcl-2 and up-regulation of Bax that led to the cleavage of caspase-3 and increased cleaved PARP was observed in SGC-7901 cells treated with curcumin. Therefore, curcumin-induced apoptosis of SGC-7901 cells might be mediated through the mitochondria pathway, which gives the rationale for in vivo studies on the utilization of curcumin as a potential cancer therapeutic compound.
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Zhu, Hong-Lin,Wei, Xing,Qu, Shun-Lin,Zhang, Chi,Zuo, Xiao-Xia,Feng, Yan-Sheng,Luo, Qi,Chen, Guang-Wen,Liu, Mei-Dong,Jiang, Lei,Xiao, Xian-Zhong,Wang, Kang-Kai Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.8
Cardiomyocytes can resist ischemia/reperfusion(I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an $in$ $vivo$ open chest rat coronary artery occlusion model and an $in$ $vitro$ model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the $in$ $vitro$ model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.
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SEL-RefineMask: A Seal Segmentation and Recognition Neural Network with SEL-FPN
Ze-dong Dun,Jian-yu Chen,Mei-xia Qu,Bin Jiang 한국정보처리학회 2022 Journal of information processing systems Vol.18 No.3
Digging historical and cultural information from seals in ancient books is of great significance. However,ancient Chinese seal samples are scarce and carving methods are diverse, and traditional digital imageprocessing methods based on greyscale have difficulty achieving superior segmentation and recognitionperformance. Recently, some deep learning algorithms have been proposed to address this problem; however,current neural networks are difficult to train owing to the lack of datasets. To solve the afore-mentionedproblems, we proposed an SEL-RefineMask which combines selector of feature pyramid network (SEL-FPN)with RefineMask to segment and recognize seals. We designed an SEL-FPN to intelligently select a specificlayer which represents different scales in the FPN and reduces the number of anchor frames. We performedexperiments on some instance segmentation networks as the baseline method, and the top-1 segmentation result of 64.93% is 5.73% higher than that of humans. The top-1 result of the SEL-RefineMask network reached67.96% which surpassed the baseline results. After segmentation, a vision transformer was used to recognizethe segmentation output, and the accuracy reached 91%. Furthermore, a dataset of seals in ancient Chinesebooks (SACB) for segmentation and small seal font (SSF) for recognition were established which are publiclyavailable on the website.
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Hong-Lin Zhu,Kang-Kai Wang,Xing Wei,Shun-Lin Qu,Chi Zhang,Xiao-Xia Zuo,Yan-Sheng Feng,Qi Luo,Guang-Wen Chen,Mei-Dong Liu,Lei Jiang,Xian-Zhong Xiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8
Cardiomyocytes can resist ischemia/reperfusion (I/R)injury through ischemic postconditioning (IPoC)which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models,an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration)followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion,MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.
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