In the discharge of EAST tokamak, it is observed that （2, 1） neoclassical tearing mode （NTM） is triggered by mode coupling with a （1, 1） internal mode. Using singular value decomposition （SVD） method for soft ...In the discharge of EAST tokamak, it is observed that （2, 1） neoclassical tearing mode （NTM） is triggered by mode coupling with a （1, 1） internal mode. Using singular value decomposition （SVD） method for soft X-ray emission and for electron cyclotron emission （ECE）, the coupling spatial structures and coupling process between these two modes are analyzed in detail. The results of SVD for ECE reveal that the phase difference between these two modes equals to zero. This is consistent with the perfect coupling condition. Finally, performing statistical analysis of r1/1, ξ1/1 and w2/1, we find that r1/1 more accurately represents the coupling strength than ξ1/1, and r1/1 is also strongly related to the （2, 1） NTM triggering, where r1/1 is the width of （1, 1） internal mode, ξ1/1 is the perturbed amplitude of （1, 1） internal mode, and w2/1 denotes the magnetic island width of （2, 1） NTM.展开更多
Cardiac dysfunction is a well-known consequence of diabetes,with sustained hyperglycaemia leading to the development of a cardiomyopathy that is independent of cardiovascular disease or hypertension.Animal models of d...Cardiac dysfunction is a well-known consequence of diabetes,with sustained hyperglycaemia leading to the development of a cardiomyopathy that is independent of cardiovascular disease or hypertension.Animal models of diabetes are commonly used to study the pathophysiology of diabetic cardiomyopathy,with the hope that increased knowledge will lead ultimately to better therapeutic strategies being developed.At physiological temperature,left ventricular trabeculae isolated from the streptozotocin rat model of type 1 diabetes showed decreased stress and prolonged relaxation,but with no evidence that decreased contractility was a result of altered myocardial Ca2+handling.Although sarcoplasmic reticulum(SR)Ca2+reuptake appeared slower in diabetic trabeculae,it was offset by an increase in actionpotential duration,thereby maintaining SR Ca2+content and favouring increased contraction force.Frequency analysis of t-tubule distribution by confocal imaging of ventricular tissue labeled with wheat germ agglutinin or ryanodine receptor antibodies showed a reduced T-power for diabetic tissue,but the differences were minor in comparison to other models of heart failure.The contractile dysfunction appeared to be the result of disrupted F-actin in conjunction with the increased typeⅠcollagen,with decreased myofilament Ca2+sensitivity contributing to the slowed relaxation.展开更多
Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early...Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction （LVEF）. This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure. Methods： Twenty-six patients with Stage B heart failure （SBHF） and 31 healthy controls （CONs） were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging （TDI） combined with electrocardiography （ECG） was used to measure cardiac electromechanical coupling time. Results： There was no significant difference in LVEF between SBHF patients and CONs （64.23 ± 8.91% vs. 64.52 ± 5.90%; P= 0.886）. However, all four electromechanical coupling time courses （Qsb： onset of Q wave on ECG to beginning of S wave on TDI, Qst： onset of Q wave on ECG to top of S wave on TDI, Rsb： top of R wave on ECG to beginning orS wave on TDI, and Rst： top of R wave on ECG to top orS wave on TDI） of SBHF patients were significantly longer than those of CONs （Qsb： 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P 〈 0.001 ; Qst： 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb： 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P 〈 0.001; and Rst： 122.37 ± 36.66 ins vs. 93.25 ± 16.72 ms, P = 0.001 ）, and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF （Rst： P =0.032; Rsb： P = 0.003; and Qsb： P = 0.004）. Conclusions： The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.展开更多
Calcium is a crucial element for striated muscle function. As such, myoplasmic free Ca2+ concentration is delicately regulated through the concerted action of multiple Ca2+ pathways that relay excitation of the plasma...Calcium is a crucial element for striated muscle function. As such, myoplasmic free Ca2+ concentration is delicately regulated through the concerted action of multiple Ca2+ pathways that relay excitation of the plasma membrane to the intracellular contractile machinery. In skeletal muscle, one of these major Ca2+ pathways is Ca2+ release from intracellular Ca2+ stores through type-1 ryanodine receptor/Ca2+ release channels (RyR1), which positions RyR1 in a strategic cross point to regulate Ca2+ homeostasis. This major Ca2+ traff ic point appears to be highly sensitive to the intracellular environment, which senses through a plethora of chemical and protein-protein interactions. Among these modulators, perhaps one of the most elusive is Triadin, a musclespecif ic protein that is involved in many crucial aspect of muscle function. This family of proteins mediates complex interactions with various Ca2+ modulators and seems poised to be a relevant modulator of Ca2+ signaling in cardiac and skeletal muscles. The purpose of this review is to examine the most recent evidence and current understanding of the role of Triadin in muscle function, in general, with particular emphasis on its contribution to Ca2+ homeostasis.展开更多
The simulations and potential forecasting of dust storms are of significant interest to public health and environment sciences.Dust storms have interannual variabilities and are typical disruptive events.The computing...The simulations and potential forecasting of dust storms are of significant interest to public health and environment sciences.Dust storms have interannual variabilities and are typical disruptive events.The computing platform for a dust storm forecasting operational system should support a disruptive fashion by scaling up to enable high-resolution forecasting and massive public access when dust storms come and scaling down when no dust storm events occur to save energy and costs.With the capability of providing a large,elastic,and virtualized pool of computational resources,cloud computing becomes a new and advantageous computing paradigm to resolve scientific problems traditionally requiring a large-scale and high-performance cluster.This paper examines the viability for cloud computing to support dust storm forecasting.Through a holistic study by systematically comparing cloud computing using Amazon EC2 to traditional high performance computing(HPC)cluster,we find that cloud computing is emerging as a credible solution for(1)supporting dust storm forecasting in spinning off a large group of computing resources in a few minutes to satisfy the disruptive computing requirements of dust storm forecasting,(2)performing high-resolution dust storm forecasting when required,(3)supporting concurrent computing requirements,(4)supporting real dust storm event forecasting for a large geographic domain by using recent dust storm event in Phoniex,05 July 2011 as example,and(5)reducing cost by maintaining low computing support when there is no dust storm events while invoking a large amount of computing resource to perform high-resolution forecasting and responding to large amount of concurrent public accesses.展开更多
MicroRNAs (miRNAs) play important roles in maintaining normal heart function. Abnormal expression of miR-331 has been observed in the hearts of patients with atrial fibrillation and Marfan syndrome. However, whether m...MicroRNAs (miRNAs) play important roles in maintaining normal heart function. Abnormal expression of miR-331 has been observed in the hearts of patients with atrial fibrillation and Marfan syndrome. However, whether miR-331 regulates cardiac function under physiological and pathological conditions still remains unknown. In the present study, we investigated the function and underlying mechanisms of miR-331 in a pressure overload-induced heart failure model and miR-331 transgenic rat model. First, we found that the expression of miR-331-3p exhibited a 1.7-fold increase in hypertrophy compared with that in the sham group (P<0.01), yet the expression of miR-331-5p remained unchanged. Furthermore, overexpression of miR-331 in cardiomyocytes and defective excitation-contraction (E-C) coupling efficiency were observed. Luciferase assays showed that miR-331-3p suppressed JPH2 expression by binding to the coding region of JPH2 mRNA. Finally, in the miR-331 transgenic rat model, JPH2 expression was suppressed at both the mRNA and protein levels in vivo, which resulted in impairment of both the E-C coupling efficiency of cardiomyocytes and systolic function of the heart. This finding mechanistically linked miR-331 to JPH2 downregulation and suggested an important role for the abnormal expression of miR-331 leading to the dysfunction of E-C coupling in heart failure.展开更多
基金supported by the National Magnetic Confinement Fusion Science Program of China(Nos.2014GB103000,2011GB101000 and2013GB102000)sponsored in part by National Natural Science Foundation of China(Nos.10725523,10990212 and 11205199)
文摘In the discharge of EAST tokamak, it is observed that （2, 1） neoclassical tearing mode （NTM） is triggered by mode coupling with a （1, 1） internal mode. Using singular value decomposition （SVD） method for soft X-ray emission and for electron cyclotron emission （ECE）, the coupling spatial structures and coupling process between these two modes are analyzed in detail. The results of SVD for ECE reveal that the phase difference between these two modes equals to zero. This is consistent with the perfect coupling condition. Finally, performing statistical analysis of r1/1, ξ1/1 and w2/1, we find that r1/1 more accurately represents the coupling strength than ξ1/1, and r1/1 is also strongly related to the （2, 1） NTM triggering, where r1/1 is the width of （1, 1） internal mode, ξ1/1 is the perturbed amplitude of （1, 1） internal mode, and w2/1 denotes the magnetic island width of （2, 1） NTM.
基金Supported by The Health Research Council of New Zealand
文摘Cardiac dysfunction is a well-known consequence of diabetes,with sustained hyperglycaemia leading to the development of a cardiomyopathy that is independent of cardiovascular disease or hypertension.Animal models of diabetes are commonly used to study the pathophysiology of diabetic cardiomyopathy,with the hope that increased knowledge will lead ultimately to better therapeutic strategies being developed.At physiological temperature,left ventricular trabeculae isolated from the streptozotocin rat model of type 1 diabetes showed decreased stress and prolonged relaxation,but with no evidence that decreased contractility was a result of altered myocardial Ca2+handling.Although sarcoplasmic reticulum(SR)Ca2+reuptake appeared slower in diabetic trabeculae,it was offset by an increase in actionpotential duration,thereby maintaining SR Ca2+content and favouring increased contraction force.Frequency analysis of t-tubule distribution by confocal imaging of ventricular tissue labeled with wheat germ agglutinin or ryanodine receptor antibodies showed a reduced T-power for diabetic tissue,but the differences were minor in comparison to other models of heart failure.The contractile dysfunction appeared to be the result of disrupted F-actin in conjunction with the increased typeⅠcollagen,with decreased myofilament Ca2+sensitivity contributing to the slowed relaxation.
基金This study was supported by grants from the National Natural Science Foundation of China （no. 91339105 and no. 81625001） and the Beijing Municipal Science and Technology Commission （no. Z 141100000214006）.
文摘Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction （LVEF）. This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure. Methods： Twenty-six patients with Stage B heart failure （SBHF） and 31 healthy controls （CONs） were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging （TDI） combined with electrocardiography （ECG） was used to measure cardiac electromechanical coupling time. Results： There was no significant difference in LVEF between SBHF patients and CONs （64.23 ± 8.91% vs. 64.52 ± 5.90%; P= 0.886）. However, all four electromechanical coupling time courses （Qsb： onset of Q wave on ECG to beginning of S wave on TDI, Qst： onset of Q wave on ECG to top of S wave on TDI, Rsb： top of R wave on ECG to beginning orS wave on TDI, and Rst： top of R wave on ECG to top orS wave on TDI） of SBHF patients were significantly longer than those of CONs （Qsb： 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P 〈 0.001 ; Qst： 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb： 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P 〈 0.001; and Rst： 122.37 ± 36.66 ins vs. 93.25 ± 16.72 ms, P = 0.001 ）, and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF （Rst： P =0.032; Rsb： P = 0.003; and Qsb： P = 0.004）. Conclusions： The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.
文摘Calcium is a crucial element for striated muscle function. As such, myoplasmic free Ca2+ concentration is delicately regulated through the concerted action of multiple Ca2+ pathways that relay excitation of the plasma membrane to the intracellular contractile machinery. In skeletal muscle, one of these major Ca2+ pathways is Ca2+ release from intracellular Ca2+ stores through type-1 ryanodine receptor/Ca2+ release channels (RyR1), which positions RyR1 in a strategic cross point to regulate Ca2+ homeostasis. This major Ca2+ traff ic point appears to be highly sensitive to the intracellular environment, which senses through a plethora of chemical and protein-protein interactions. Among these modulators, perhaps one of the most elusive is Triadin, a musclespecif ic protein that is involved in many crucial aspect of muscle function. This family of proteins mediates complex interactions with various Ca2+ modulators and seems poised to be a relevant modulator of Ca2+ signaling in cardiac and skeletal muscles. The purpose of this review is to examine the most recent evidence and current understanding of the role of Triadin in muscle function, in general, with particular emphasis on its contribution to Ca2+ homeostasis.
基金Research reported is supported by NSF(CSR-1117300 and IIP-1160979)NASA(NNX07AD99G)Microsoft Research.
文摘The simulations and potential forecasting of dust storms are of significant interest to public health and environment sciences.Dust storms have interannual variabilities and are typical disruptive events.The computing platform for a dust storm forecasting operational system should support a disruptive fashion by scaling up to enable high-resolution forecasting and massive public access when dust storms come and scaling down when no dust storm events occur to save energy and costs.With the capability of providing a large,elastic,and virtualized pool of computational resources,cloud computing becomes a new and advantageous computing paradigm to resolve scientific problems traditionally requiring a large-scale and high-performance cluster.This paper examines the viability for cloud computing to support dust storm forecasting.Through a holistic study by systematically comparing cloud computing using Amazon EC2 to traditional high performance computing(HPC)cluster,we find that cloud computing is emerging as a credible solution for(1)supporting dust storm forecasting in spinning off a large group of computing resources in a few minutes to satisfy the disruptive computing requirements of dust storm forecasting,(2)performing high-resolution dust storm forecasting when required,(3)supporting concurrent computing requirements,(4)supporting real dust storm event forecasting for a large geographic domain by using recent dust storm event in Phoniex,05 July 2011 as example,and(5)reducing cost by maintaining low computing support when there is no dust storm events while invoking a large amount of computing resource to perform high-resolution forecasting and responding to large amount of concurrent public accesses.
基金supported by the National Natural Science Foundation of China (81625001, 91854209, 31630035)the National Key Research & Development Program of China (2018YFC1312700, 2018YFC1312701).
文摘MicroRNAs (miRNAs) play important roles in maintaining normal heart function. Abnormal expression of miR-331 has been observed in the hearts of patients with atrial fibrillation and Marfan syndrome. However, whether miR-331 regulates cardiac function under physiological and pathological conditions still remains unknown. In the present study, we investigated the function and underlying mechanisms of miR-331 in a pressure overload-induced heart failure model and miR-331 transgenic rat model. First, we found that the expression of miR-331-3p exhibited a 1.7-fold increase in hypertrophy compared with that in the sham group (P<0.01), yet the expression of miR-331-5p remained unchanged. Furthermore, overexpression of miR-331 in cardiomyocytes and defective excitation-contraction (E-C) coupling efficiency were observed. Luciferase assays showed that miR-331-3p suppressed JPH2 expression by binding to the coding region of JPH2 mRNA. Finally, in the miR-331 transgenic rat model, JPH2 expression was suppressed at both the mRNA and protein levels in vivo, which resulted in impairment of both the E-C coupling efficiency of cardiomyocytes and systolic function of the heart. This finding mechanistically linked miR-331 to JPH2 downregulation and suggested an important role for the abnormal expression of miR-331 leading to the dysfunction of E-C coupling in heart failure.
