Uncontained Engine Rotor Failure(UERF)can cause a catastrophic failure of an aircraft,and the quantitative assessment of the hazards related to UERF is a very important part of safety analysis.However,the procedure fo...Uncontained Engine Rotor Failure(UERF)can cause a catastrophic failure of an aircraft,and the quantitative assessment of the hazards related to UERF is a very important part of safety analysis.However,the procedure for hazard quantification of UERF recommended by the Federal Aviation Administration in advisory circular AC20-128A is cumbersome,as it involves building auxiliary lines and curve projections.To improve the efficiency and general applicability of the risk angle calculation,a boundary discretization method is developed that involves discretizing the geometry of the target part/structure into node points and calculating the risk angles numerically by iterating a particular algorithm over each node point.The improved efficiency and excellent accuracy for the developed algorithm was validated through a comparison with manual solutions for the hazard quantification of the engine nacelle structures of a passenger aircraft using the guidance in AC20-128A.To further demonstrate the applicability of the boundary discretization method,the proposed algorithm was used to examine the influence of the target size and the distance between the target and rotor on the hazard probability.展开更多
Aim Leptin, a 16 ku hormone from the ob gene, has been identified as an important protein involved obesity. As a chronic metabolic disorder, Obesity is associated with a high risk of developing cardiovascular and meta...Aim Leptin, a 16 ku hormone from the ob gene, has been identified as an important protein involved obesity. As a chronic metabolic disorder, Obesity is associated with a high risk of developing cardiovascular and metabolic diseases, such as heart failure. The main aim of this paper is to probe the effects of leptin on contractile function of cardiomyocyte in adult rat. And the mechanism of the action involved of oxidative stress and autophagy were investigated. Methods Isolated adult rat cardiomyocytes were exposed to leptin （1, 10, and 100 nmol · L^-1） for 1 hour. The calcium transients and contraction in adult rat cardiomyocytes were recorded with SoftEdge MyoCam system. Using the corresponding agents such as apocynin, tempol and rapamycin, the underlying mecha- nism of leptin involved of oxidative stress and autophagy was determined. Werstern blot was employed to evaluate the expression of LC3B and Beclin-1. Results While perfusing the cardiomyocytes with leptin, peak shortening （PS） and maximal velocity of shortening/relengthening （ ± dL/dtmax） of cell shortening were markedly decreased, and prolonged time to 50% relengthening （TR50%）. As well as, baseline （bl） , peak and time to 50% baseline （TB50%） of calcium transient were markedly depressed. Leptin attenuated autophagy as evidenced by decreased LC3-Ⅱ and Beclin-1. All of the abnormalities were significantly attenuated by apocynin, tempol or rapamyein. Conclusion Leptin has depressing effects on intracellular free calcium and myocardial systolic function. Apocy-nin, tempol or rapamycin could block the effects of leptin. The mechanism involved oxidative stress and autophagy.展开更多
基金supported by the National Natural Science Foundation of China(No.51706187)。
文摘Uncontained Engine Rotor Failure(UERF)can cause a catastrophic failure of an aircraft,and the quantitative assessment of the hazards related to UERF is a very important part of safety analysis.However,the procedure for hazard quantification of UERF recommended by the Federal Aviation Administration in advisory circular AC20-128A is cumbersome,as it involves building auxiliary lines and curve projections.To improve the efficiency and general applicability of the risk angle calculation,a boundary discretization method is developed that involves discretizing the geometry of the target part/structure into node points and calculating the risk angles numerically by iterating a particular algorithm over each node point.The improved efficiency and excellent accuracy for the developed algorithm was validated through a comparison with manual solutions for the hazard quantification of the engine nacelle structures of a passenger aircraft using the guidance in AC20-128A.To further demonstrate the applicability of the boundary discretization method,the proposed algorithm was used to examine the influence of the target size and the distance between the target and rotor on the hazard probability.
文摘Aim Leptin, a 16 ku hormone from the ob gene, has been identified as an important protein involved obesity. As a chronic metabolic disorder, Obesity is associated with a high risk of developing cardiovascular and metabolic diseases, such as heart failure. The main aim of this paper is to probe the effects of leptin on contractile function of cardiomyocyte in adult rat. And the mechanism of the action involved of oxidative stress and autophagy were investigated. Methods Isolated adult rat cardiomyocytes were exposed to leptin （1, 10, and 100 nmol · L^-1） for 1 hour. The calcium transients and contraction in adult rat cardiomyocytes were recorded with SoftEdge MyoCam system. Using the corresponding agents such as apocynin, tempol and rapamycin, the underlying mecha- nism of leptin involved of oxidative stress and autophagy was determined. Werstern blot was employed to evaluate the expression of LC3B and Beclin-1. Results While perfusing the cardiomyocytes with leptin, peak shortening （PS） and maximal velocity of shortening/relengthening （ ± dL/dtmax） of cell shortening were markedly decreased, and prolonged time to 50% relengthening （TR50%）. As well as, baseline （bl） , peak and time to 50% baseline （TB50%） of calcium transient were markedly depressed. Leptin attenuated autophagy as evidenced by decreased LC3-Ⅱ and Beclin-1. All of the abnormalities were significantly attenuated by apocynin, tempol or rapamyein. Conclusion Leptin has depressing effects on intracellular free calcium and myocardial systolic function. Apocy-nin, tempol or rapamycin could block the effects of leptin. The mechanism involved oxidative stress and autophagy.
