Modeling techniques for active shape and vibration control of macro-fiber composite laminated structures

Shun-Qi Zhang,Min Chen,Guo-Zhong Zhao,Zhan-Xi Wang,Rüdiger Schmidt,Xian-Sheng Qin 국제구조공학회 2017 Smart Structures and Systems, An International Jou Vol.19 No.6

The complexity of macro-fiber composite (MFC) materials increasing the difficulty in simulation and analysis of MFC integrated structures. To give an accurate prediction of MFC bonded smart structures for the simulation of shape and vibration control, the paper develops a linear electro-mechanically coupled static and dynamic finite element (FE) models based on the first-order shear deformation (FOSD) hypothesis. Two different types of MFCs are modeled and analyzed, namely MFC-d31 and MFC-d33, in which the former one is dominated by the d31 effect, while the latter one by the d33 effect. The present model is first applied to an MFC-d33 bonded composite plate, and then is used to analyze both active shape and vibration control for MFC-d31/-d33 bonded plate with various piezoelectric fiber orientations.

Secondary Aerosol Sampling and Measurement by Using State-of-the-Art Analytical Equipment

Shun-cheng Lee,Yan Tan,Qi Yuan,Haiwei Li,Zhuozhi Zhang 한국분석과학회 2019 학술대회논문집 Vol.2019 No.11

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

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.

Strength failure behavior of granite containing two holes under Brazilian test

Huang, Yan-Hua,Yang, Sheng-Qi,Zhang, Chun-Shun Techno-Press 2017 Geomechanics & engineering Vol.12 No.6

A series of Brazilian tests under diameter compression for disc specimens was carried out to investigate the strength and failure behavior by using acoustic emission (AE) and photography monitoring technique. On the basis of experimental results, load-displacement curves, AE counts, real-time crack evolution process, failure modes and strength property of granite specimens containing two pre-existing holes were analyzed in detail. Two typical types of load-displacement curves are identified, i.e., sudden instability (type I) and progressive failure (type II). In accordance with the two types of load-displacement curves, the AE events also have different responses. The present experiments on disc specimens containing two pre-existing holes under Brazilian test reveal four distinct failure modes, including diametrical splitting failure mode (mode I), one crack coalescence failure mode (mode II), two crack coalescences failure mode (mode III) and no crack coalescence failure mode (mode IV). Compared with intact granite specimen, the disc specimen containing two holes fails with lower strength, which is closely related to the bridge angle. The failure strength of pre-holed specimen first decreases and then increases with the bridge angle. Finally, a preliminary interpretation was proposed to explain the strength evolution law of granite specimen containing two holes based on the microscopic observation of fracture plane.

Prediction of postoperative pancreatic fistula using a nomogram based on the updated definition

Cheng-Xiang Guo,Yi-Nan Shen,Qi Zhang,Xiao-Zhen Zhang,Jun-Li Wang,Shun-Liang Gao,Jian-Ying Lou,Ri-Sheng Que,Tao Ma,Ting-Bo Liang,Xue-Li Bai 대한외과학회 2020 Annals of Surgical Treatment and Research(ASRT) Vol.98 No.2

Purpose: The International Study Group on Pancreatic Fistula’s definition of postoperative pancreatic fistula (POPF) has recently been updated. This study aimed to identify risk factors for POPF in patients having pancreaticoduodenectomy (PD) and to generate a nomogram to predict POPF. Methods: Data on 298 patients who underwent PD from March 2012 to October 2017 was retrospectively reviewed and POPF statuses were redefined. A nomogram was constructed using data from 220 patients and validated using the remaining 78 patients. Independent risk factors for POPF were identified using univariate and multivariate analyses. A predictive nomogram was established based on the independent risk factors and was compared with existing models. Results: Texture of the pancreas, size of the main pancreatic duct, portal vein invasion, and definitive pathology were the identified risk factors. The nomogram had a C-index of 0.793 and was internally validated. The nomogram performed better (C-index of 0.816) than the other most cited models (C-indexes of 0.728 and 0.735) in the validation cohort. In addition, the nomogram can assign patients into low- (less than 10%), intermediate- (10% to 30%), and high-risk (equal or higher than 30%) groups to facilitate personalized management. Conclusion: The nomogram accurately predicted POPF in patients having PD.

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

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.