http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Shun Kai Zhang (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Bin Yang Wu,Qiang Zhang,Shun Kai Zhang,Xiao Kun Nie,Yu Han Li,Wanhua Su 한국자동차공학회 2018 International journal of automotive technology Vol.19 No.4
Experiments and simulations were used to investigate the effect of a range of engine operating parameters and fuel characteristics on the particle size and particle number (PN) concentration at low speed and idle speed condition. The occurrence, size, and concentration of particles were tested against a range of parameters including start of injection (SOI), common rail pressure, exhaust gas recirculation (EGR) ratio and load. The results showed that the homogeneity of the mixture had the greatest impact on particle size and number concentration. The performance of particle is different at different levels of load. The particle were of nucleation mode at idle condition, and the cold idle particles had a slightly larger diameter than those produced at hot idle. By using the diesel and under high load, at EGR ratios of less than 20 %, most particles were of nucleation mode. At EGR ratios exceeding 20 %, nucleation-mode particles were gradually replaced by accumulation-mode particles. At EGR ratios above 30 %, most particles were of the accumulation mode. Under the same load, gasoline compression ignition produced particles of smaller size and reduced particulate mass (PM). The use of gasoline extended ignition delay, as the high volatility and octane number of the fuel improved the homogeneity of the mixture. Finally, a linear relationship was found between PM and PN. The relative contribution of the different factors to the formation of nucleationor accumulation-mode particles was investigated.
-
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.
-
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.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
