A gridded thermionic cathode electron gun was developed for the linear accelerator of the High Energy Photon Source(HEPS).An electron gun should provide a large maximum bunch charge with a wide adjustable range.To sat...A gridded thermionic cathode electron gun was developed for the linear accelerator of the High Energy Photon Source(HEPS).An electron gun should provide a large maximum bunch charge with a wide adjustable range.To satisfy these requirements,the shape of the electrode was optimized using a multi-objective genetic algorithm.A large bunch charge with an adjustable range was achieved using the grid-limited gun,the flow of which was analyzed using 3-D simulations.The electron gun has been manufactured and tested,and the measured data of the grid-limited current and simulation results are compared and discussed in this study.展开更多
Behaviour-based approach plays a key role for mobile robots to operate safely in unknown or dynamically changing environments. We have developed a hybrid control architecture for our autonomous robotic fish that consi...Behaviour-based approach plays a key role for mobile robots to operate safely in unknown or dynamically changing environments. We have developed a hybrid control architecture for our autonomous robotic fish that consists of three layers： cognitive, behaviour and swim pattern. In this paper, we describe some main design issues of the behaviour layer, which is the centre of the layered control architecture of our robotic fish. Fuzzy logic control （FLC） is adopted here to design individual behaviours. Simulation and real experiments are presented to show the feasibility and the performance of the designed behaviour layer.展开更多
Background： It is well documented that sevoflurane postconditioning （SP） has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigate...Background： It is well documented that sevoflurane postconditioning （SP） has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigated the hypothesis that the Pim-1 kinase played a key role in SP-induced cardioprotection by regulating dynamics-related protein 1 （Drpl）. Methods： A Langendorff model was used in this study. Seventy-two rats were randomly assigned into six groups as follows： CON group, ischemia reperfusion （I/R） group, SP group, SP＋proto-oncogene serine/threonine-protein kinase 1 （Pim-1） inhibitor II group, SP＋dimethylsufoxide group, and Pim- 1 inhibitor II group （n = 12, each）. Hemodynamic parameters and infarct size were measured to reflect the extent of myocardial 1/R injury. The expressions ofPim-1, B-cell leukemia/lymphoma 2 （Bcl-2） and cytochrome C （Cyt C） in cytoplasm and mitochondria, the Drp 1 in mitochondria, and the total Drp I and p-Drp I^sor637 were measured by Western blotting. In addition, transmission electron microscope was used to observe mitochondrial morphology. The experiment began in October 2014 and continued until July 2016. Results： SP improved myocardial I/R injury-induced hemodynamic parametric changes, cardiac function, and preserved mitochondrial phenotype and decreased myocardial infarct size （24.49 ± 1.72% in Sev group compared with 41.98 ± 4.37% in I/R group; P 〈 0.05）. However, Pim-1 inhibitor II significantly （P 〈 0.05） abolished the protective effect of SP. Western blotting analysis demonstrated that, compared with I/R group, the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria as well as the total p-Drplset637 in Sev group （P 〈 0.05） were upregulated. Meanwhile, SP inhibited Drp 1 compartmentalization to the mitochondria followed by a reduction in the release ofCyt C. Pretreatment with Pim- 1 inhibitor II significantly （P 〈 0.05） abolished SP-induced Pim- 1/p-Drp 1^ser637 signaling activation. Conclusions： These findings suggested that SP could attenuate myocardial ischemia-reperfusion injury by increasing the expression of the Pim-1 kinase. Upregulation of Pim-1 might phosphorylate Drpl and prevent extensive mitochondrial fission through Drpl cytosolic sequestration.展开更多
Background： Sevoflurane preconditioning （SP） has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understoo...Background： Sevoflurane preconditioning （SP） has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Writ/glycogen synthase kinase 3β（GSK3β）/β-catenin signaling pathway. Methods： Two models were established： A Langendorffperfused rat heart model and the H9C2 cell hypoxia/reoxygenation model. Both rats and H9C2 cells were randomly divided into 6 groups as follows： S group, ischemia-reperfusion （I/R） group, DMSO group, IWP group, SP group, and SP ＋ IWP group. Hemodynamic parameters, lactate dehydrogenase （LDH） activity in coronary effluent and cell culture supernatant, and the infarct size were measured to evaluate myocardial ischemia-reperfusion injuries. To determine the activity of Wnt/GSK3β/β-catenin signaling pathway, the expressions of Wnt3a, phospho-GSK3β, and β-catenin were measured by Western blotting. Results： SP improved cardiac function recovery, reduced infarct size （18 ±2% in the SP group compared with 35 ± 4% in the 1/R group; P 〈 0.05）, decreased LDH activity in coronary effluent, and culture supematant. IWP-2, an inhibitor of Wnt, abolished the cardioprotection by SR In addition, Western blotting analysis demonstrated that the expressions of Wnt3a, phospho-GSK3β, and β-catenin significantly （P 〈 0.05） increased in the I/R group, compared with the S group; and compared to I/R group, SP significantly （P 〈 0.05） increased Wnt3a, phospho-GSK3 β, and β-catenin expressions. Pretreatment with IWP-2 significantly （P 〈 0.05） abolished SP-induced Wnt/GSK3β/β-catenin signaling activation. Conclusions： The results showed for the first time that cardioprotection afforded by SP may be mediated partly via the Wnt/GSK3β/β-catenin signaling pathway.展开更多
文摘A gridded thermionic cathode electron gun was developed for the linear accelerator of the High Energy Photon Source(HEPS).An electron gun should provide a large maximum bunch charge with a wide adjustable range.To satisfy these requirements,the shape of the electrode was optimized using a multi-objective genetic algorithm.A large bunch charge with an adjustable range was achieved using the grid-limited gun,the flow of which was analyzed using 3-D simulations.The electron gun has been manufactured and tested,and the measured data of the grid-limited current and simulation results are compared and discussed in this study.
文摘Behaviour-based approach plays a key role for mobile robots to operate safely in unknown or dynamically changing environments. We have developed a hybrid control architecture for our autonomous robotic fish that consists of three layers： cognitive, behaviour and swim pattern. In this paper, we describe some main design issues of the behaviour layer, which is the centre of the layered control architecture of our robotic fish. Fuzzy logic control （FLC） is adopted here to design individual behaviours. Simulation and real experiments are presented to show the feasibility and the performance of the designed behaviour layer.
文摘Background： It is well documented that sevoflurane postconditioning （SP） has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigated the hypothesis that the Pim-1 kinase played a key role in SP-induced cardioprotection by regulating dynamics-related protein 1 （Drpl）. Methods： A Langendorff model was used in this study. Seventy-two rats were randomly assigned into six groups as follows： CON group, ischemia reperfusion （I/R） group, SP group, SP＋proto-oncogene serine/threonine-protein kinase 1 （Pim-1） inhibitor II group, SP＋dimethylsufoxide group, and Pim- 1 inhibitor II group （n = 12, each）. Hemodynamic parameters and infarct size were measured to reflect the extent of myocardial 1/R injury. The expressions ofPim-1, B-cell leukemia/lymphoma 2 （Bcl-2） and cytochrome C （Cyt C） in cytoplasm and mitochondria, the Drp 1 in mitochondria, and the total Drp I and p-Drp I^sor637 were measured by Western blotting. In addition, transmission electron microscope was used to observe mitochondrial morphology. The experiment began in October 2014 and continued until July 2016. Results： SP improved myocardial I/R injury-induced hemodynamic parametric changes, cardiac function, and preserved mitochondrial phenotype and decreased myocardial infarct size （24.49 ± 1.72% in Sev group compared with 41.98 ± 4.37% in I/R group; P 〈 0.05）. However, Pim-1 inhibitor II significantly （P 〈 0.05） abolished the protective effect of SP. Western blotting analysis demonstrated that, compared with I/R group, the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria as well as the total p-Drplset637 in Sev group （P 〈 0.05） were upregulated. Meanwhile, SP inhibited Drp 1 compartmentalization to the mitochondria followed by a reduction in the release ofCyt C. Pretreatment with Pim- 1 inhibitor II significantly （P 〈 0.05） abolished SP-induced Pim- 1/p-Drp 1^ser637 signaling activation. Conclusions： These findings suggested that SP could attenuate myocardial ischemia-reperfusion injury by increasing the expression of the Pim-1 kinase. Upregulation of Pim-1 might phosphorylate Drpl and prevent extensive mitochondrial fission through Drpl cytosolic sequestration.
文摘Background： Sevoflurane preconditioning （SP） has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Writ/glycogen synthase kinase 3β（GSK3β）/β-catenin signaling pathway. Methods： Two models were established： A Langendorffperfused rat heart model and the H9C2 cell hypoxia/reoxygenation model. Both rats and H9C2 cells were randomly divided into 6 groups as follows： S group, ischemia-reperfusion （I/R） group, DMSO group, IWP group, SP group, and SP ＋ IWP group. Hemodynamic parameters, lactate dehydrogenase （LDH） activity in coronary effluent and cell culture supernatant, and the infarct size were measured to evaluate myocardial ischemia-reperfusion injuries. To determine the activity of Wnt/GSK3β/β-catenin signaling pathway, the expressions of Wnt3a, phospho-GSK3β, and β-catenin were measured by Western blotting. Results： SP improved cardiac function recovery, reduced infarct size （18 ±2% in the SP group compared with 35 ± 4% in the 1/R group; P 〈 0.05）, decreased LDH activity in coronary effluent, and culture supematant. IWP-2, an inhibitor of Wnt, abolished the cardioprotection by SR In addition, Western blotting analysis demonstrated that the expressions of Wnt3a, phospho-GSK3β, and β-catenin significantly （P 〈 0.05） increased in the I/R group, compared with the S group; and compared to I/R group, SP significantly （P 〈 0.05） increased Wnt3a, phospho-GSK3 β, and β-catenin expressions. Pretreatment with IWP-2 significantly （P 〈 0.05） abolished SP-induced Wnt/GSK3β/β-catenin signaling activation. Conclusions： The results showed for the first time that cardioprotection afforded by SP may be mediated partly via the Wnt/GSK3β/β-catenin signaling pathway.
