目的探讨门控心肌灌注显像(GSMPI)评估冠心病心脏收缩同步性规律及与疾病进展的相关性。方法选取我院2014年6月至2018年10月收治的行GSMPI检查的人群共116例,其中冠心病心肌缺血患者76例(轻度心肌缺血30例,中度心肌缺血24例,重度心肌缺...目的探讨门控心肌灌注显像(GSMPI)评估冠心病心脏收缩同步性规律及与疾病进展的相关性。方法选取我院2014年6月至2018年10月收治的行GSMPI检查的人群共116例,其中冠心病心肌缺血患者76例(轻度心肌缺血30例,中度心肌缺血24例,重度心肌缺血22例),正常对照者40例,比较4组间相位直方图带宽(PHB)和相位标准差(PSD)水平,同时对同步性参数和心肌缺血参数间相关性进行分析。结果冠心病中重度心肌缺血患者心脏收缩同步性指标水平均显著高于正常对照者( P <0.05);冠心病中度和重度心肌缺血患者心脏收缩同步性指标水平均显著高于轻度心肌缺血患者( P <0.05);冠心病重度心肌缺血患者心脏收缩同步性指标水平均显著高于中度心肌缺血患者( P <0.05);Pearson双变量相关分析显示,收缩同步性丧失程度与心肌缺血严重程度具有正相关关系( P <0.05)。结论 GSMPI能够用于冠心病患者心肌缺血和心脏收缩同步性程度评估,有助于筛选心脏收缩同步性丧失早期患者;同时冠心病心脏收缩同步性丧失程度与心肌缺血严重程度间呈显著正相关。展开更多
In order to make the typical Montgomery’s algorithm suitable for implementation on FPGA, a modified version is proposed and then a high-performance systolic linear array architecture is designed for RSA cryptosystem ...In order to make the typical Montgomery’s algorithm suitable for implementation on FPGA, a modified version is proposed and then a high-performance systolic linear array architecture is designed for RSA cryptosystem on the basis of the optimized algorithm. The proposed systolic array architecture has dis- tinctive features, i.e. not only the computation speed is significantly fast but also the hardware overhead is drastically decreased. As a major practical result, the paper shows that it is possible to implement public-key cryptosystem at secure bit lengths on a single commercially available FPGA.展开更多
Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very hi...Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very high frequency （VHF） component of the power spectrum normalized to represent its relative value in proportion to the total power minus the very low frequency component. Methods Patients （n = 130） were divided into a study group, consisting 66 patients with decreased left ventricular systolic function, and a control group, consisting 64 patients with normal heart structure and function and without severe coronary artery stenosis （〈 50%）. Results VHFI in the study group was significantly higher than that in the control group （19.17 ± 13.35 vs 11.37 ± 10.77, P 〈 0.001）. Cardiac events occurred in 18 patients during follow-up （33.34 i 3.26 months）. Defining the positive test as VHFI =15 and negative test as VHFI 〈15, achieved a sensitivity of 57.58% and a specificity of78.13% for predicting decreased left ventricular systolic function, and achieved a sensitivity of 66.67% and a specificity of 64.29% for predicting cardiac events. Univariate Cox regression analysis showed that positive VHFI test was an independent variable in predictive cardiac events. Conclusions The results suggest that VHFI is a useful tool for quick evaluation of left ventricular systolic function and prediction of prognosis展开更多
Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart...Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart Meridian and the heart. Methods: Acute myocardial ischemia (AMI) was produced by intravenous infusion of pituitrin (40 u + 5% glucose injection 500 ml, 60 drips/min) in the rabbit. Left intraventricular pressure (LVP), maximal rising velocity of LVP (dp/dt max), isovolumetric pressure (IP) and end-diastolic pressure (EDP) of the left cardiac ventricle were used as the indexes. Three points of Heart Meridian [HM, from 'Shenmen' (HT 7) to 'Lingdao' (HT 4)] and the three points of Lung Meridian [LM, from 'Taiyuan' (LU 9) to 'Lieque' (LU 7)] were punctured with filiform needles and stimulated with hand-manipulation and electrically with ZY2-1 EA Therapeutic Apparatus. 30 rabbits anesthetized with urethane (1 g/kg) were randomly and evenly divided into control group, HM group and LM group. Result-s: The effects of EA of HM points were evidently superior to those of EA of LM points in promoting the recovery of both AMI-induced decrease of LVP and dp/dtmax, and AMI-induced increase of IP and EDP. Conclusion: Acupoints of Heart Meridian has a relatively specific connection with the heart in comparison with those of Lung Meridian; and the Heart Meridian is a functional whole.展开更多
In recent decades,a cardiomyocyte membrane scaffolding protein bridging integrator 1(BIN1) has emerged as a critical multifunctional regulator of transverse-tubule(t-tubule) function and calcium signaling in cardiomyo...In recent decades,a cardiomyocyte membrane scaffolding protein bridging integrator 1(BIN1) has emerged as a critical multifunctional regulator of transverse-tubule(t-tubule) function and calcium signaling in cardiomyocytes.Encoded by a single gene with 20 exons that are alternatively spliced,more than ten BIN1 protein isoforms are expressed with tissue and disease specificity.The recently discovered cardiac alternatively spliced isoform BIN1(cBIN1 or BIN1 +13 + 17)plays a crucial role in organizing membrane microfolds within cardiac t-tubules.These cBIN1-induced microfolds form functional dyad microdomains by trafficking L-type calcium channels(LTCC) to t-tubule membrane and recruiting ryanodine receptors(RyR) to junctional sarcoplasmic reticulum membrane.When cBIN1 is transcriptionally reduced as occurs in heart failure,cBIN1-microfolds are disrupted and fail to form LTCC and RyR couplons.As a result,impaired dyad formation limits excitation-contraction coupling thus cardiac contractility,and accumulation of orphaned leaky RyRs outside of dyads increases ventricular arrhythmias.Reduced myocardial BIN1 in heart failure is also detectable at the blood level,and plasma BIN1 level predicts heart failure progression and future arrhythmias in cardiomyopathy patients.Here we will review the recent progress in BIN1-related cardiomyocyte biology studies and discuss the diagnostic and predictive values of cBIN1 in future clinical use.展开更多
To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then ...To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then withdrawn for several days by aortic debanding,followed by subsequent myocardial exposure to ischemia/reperfusion(I/R).Following I/R injury,the myocardial infarct size and apoptosis were markedly reduced,and contractile function was significantly improved in the TAC preconditioning group compared with the control group.Mechanistically,hypertrophic preconditioning remarkably alleviated I/R-induced oxidative stress,as evidenced by the increased reduced nicotinamide adenine dinucleotide phosphate(NADPH)/nicotinamide adenine dinucleotide phosphate(NADP)ratio,increase in the reduced glutathione(GSH)/oxidized glutathione(GSSH)ratio,and reduced mitochondrial reactive oxygen species(ROS)production.Moreover,TAC preconditioning inhibited caspase-3 activation and mitigated the mitochondrial impairment by deacetylating isocitrate dehydrogenase 2(IDH2)via a sirtuin 3(SIRT3)-dependent mechanism.In addition,the expression of a genetic deacetylation mimetic IDH2 mutant(IDH2 K413R)in cardiomyocytes,which increased IDH2 enzymatic activity and decreased mitochondrial ROS production,and ameliorated I/R injury,whereas the expression of a genetic acetylation mimetic(IDH2 K413Q)in cardiomyocytes abolished these protective effects of hypertrophic preconditioning.Furthermore,both the activity and expression of the SIRT3 protein were markedly increased in preconditioned mice exposed to I/R.Treatment with an adenovirus encoding SIRT3 partially emulated the actions of hypertrophic preconditioning,whereas genetic ablation of SIRT3 in mice blocked the cardioprotective effects of hypertrophic preconditioning.The present study identifies hypertrophic preconditioning as a novel endogenous self-defensive and cardioprotective strategy for cardiac I/R injury that induces IDH2 deacetylation through a SIRT3-dependent mechanism.A therapeutic strategy targeting IDH2 may be a promising treatment for cardiac ischemic injury.展开更多
文摘目的探讨门控心肌灌注显像(GSMPI)评估冠心病心脏收缩同步性规律及与疾病进展的相关性。方法选取我院2014年6月至2018年10月收治的行GSMPI检查的人群共116例,其中冠心病心肌缺血患者76例(轻度心肌缺血30例,中度心肌缺血24例,重度心肌缺血22例),正常对照者40例,比较4组间相位直方图带宽(PHB)和相位标准差(PSD)水平,同时对同步性参数和心肌缺血参数间相关性进行分析。结果冠心病中重度心肌缺血患者心脏收缩同步性指标水平均显著高于正常对照者( P <0.05);冠心病中度和重度心肌缺血患者心脏收缩同步性指标水平均显著高于轻度心肌缺血患者( P <0.05);冠心病重度心肌缺血患者心脏收缩同步性指标水平均显著高于中度心肌缺血患者( P <0.05);Pearson双变量相关分析显示,收缩同步性丧失程度与心肌缺血严重程度具有正相关关系( P <0.05)。结论 GSMPI能够用于冠心病患者心肌缺血和心脏收缩同步性程度评估,有助于筛选心脏收缩同步性丧失早期患者;同时冠心病心脏收缩同步性丧失程度与心肌缺血严重程度间呈显著正相关。
文摘In order to make the typical Montgomery’s algorithm suitable for implementation on FPGA, a modified version is proposed and then a high-performance systolic linear array architecture is designed for RSA cryptosystem on the basis of the optimized algorithm. The proposed systolic array architecture has dis- tinctive features, i.e. not only the computation speed is significantly fast but also the hardware overhead is drastically decreased. As a major practical result, the paper shows that it is possible to implement public-key cryptosystem at secure bit lengths on a single commercially available FPGA.
文摘Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very high frequency （VHF） component of the power spectrum normalized to represent its relative value in proportion to the total power minus the very low frequency component. Methods Patients （n = 130） were divided into a study group, consisting 66 patients with decreased left ventricular systolic function, and a control group, consisting 64 patients with normal heart structure and function and without severe coronary artery stenosis （〈 50%）. Results VHFI in the study group was significantly higher than that in the control group （19.17 ± 13.35 vs 11.37 ± 10.77, P 〈 0.001）. Cardiac events occurred in 18 patients during follow-up （33.34 i 3.26 months）. Defining the positive test as VHFI =15 and negative test as VHFI 〈15, achieved a sensitivity of 57.58% and a specificity of78.13% for predicting decreased left ventricular systolic function, and achieved a sensitivity of 66.67% and a specificity of 64.29% for predicting cardiac events. Univariate Cox regression analysis showed that positive VHFI test was an independent variable in predictive cardiac events. Conclusions The results suggest that VHFI is a useful tool for quick evaluation of left ventricular systolic function and prediction of prognosis
基金grants of State Scientific-technological Scale Project
文摘Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart Meridian and the heart. Methods: Acute myocardial ischemia (AMI) was produced by intravenous infusion of pituitrin (40 u + 5% glucose injection 500 ml, 60 drips/min) in the rabbit. Left intraventricular pressure (LVP), maximal rising velocity of LVP (dp/dt max), isovolumetric pressure (IP) and end-diastolic pressure (EDP) of the left cardiac ventricle were used as the indexes. Three points of Heart Meridian [HM, from 'Shenmen' (HT 7) to 'Lingdao' (HT 4)] and the three points of Lung Meridian [LM, from 'Taiyuan' (LU 9) to 'Lieque' (LU 7)] were punctured with filiform needles and stimulated with hand-manipulation and electrically with ZY2-1 EA Therapeutic Apparatus. 30 rabbits anesthetized with urethane (1 g/kg) were randomly and evenly divided into control group, HM group and LM group. Result-s: The effects of EA of HM points were evidently superior to those of EA of LM points in promoting the recovery of both AMI-induced decrease of LVP and dp/dtmax, and AMI-induced increase of IP and EDP. Conclusion: Acupoints of Heart Meridian has a relatively specific connection with the heart in comparison with those of Lung Meridian; and the Heart Meridian is a functional whole.
基金supported by the United States National Institute of Health/National Heart,Lung,and Blood Institute (NIH/NHLBI,Hong R01 HL133286)American Heart Association (AHA)(IRG27780031,BGIA27770151)
文摘In recent decades,a cardiomyocyte membrane scaffolding protein bridging integrator 1(BIN1) has emerged as a critical multifunctional regulator of transverse-tubule(t-tubule) function and calcium signaling in cardiomyocytes.Encoded by a single gene with 20 exons that are alternatively spliced,more than ten BIN1 protein isoforms are expressed with tissue and disease specificity.The recently discovered cardiac alternatively spliced isoform BIN1(cBIN1 or BIN1 +13 + 17)plays a crucial role in organizing membrane microfolds within cardiac t-tubules.These cBIN1-induced microfolds form functional dyad microdomains by trafficking L-type calcium channels(LTCC) to t-tubule membrane and recruiting ryanodine receptors(RyR) to junctional sarcoplasmic reticulum membrane.When cBIN1 is transcriptionally reduced as occurs in heart failure,cBIN1-microfolds are disrupted and fail to form LTCC and RyR couplons.As a result,impaired dyad formation limits excitation-contraction coupling thus cardiac contractility,and accumulation of orphaned leaky RyRs outside of dyads increases ventricular arrhythmias.Reduced myocardial BIN1 in heart failure is also detectable at the blood level,and plasma BIN1 level predicts heart failure progression and future arrhythmias in cardiomyopathy patients.Here we will review the recent progress in BIN1-related cardiomyocyte biology studies and discuss the diagnostic and predictive values of cBIN1 in future clinical use.
基金supported by the National Natural Science Foundation of China(81870290,81521001,81800235,and 81800238)。
文摘To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then withdrawn for several days by aortic debanding,followed by subsequent myocardial exposure to ischemia/reperfusion(I/R).Following I/R injury,the myocardial infarct size and apoptosis were markedly reduced,and contractile function was significantly improved in the TAC preconditioning group compared with the control group.Mechanistically,hypertrophic preconditioning remarkably alleviated I/R-induced oxidative stress,as evidenced by the increased reduced nicotinamide adenine dinucleotide phosphate(NADPH)/nicotinamide adenine dinucleotide phosphate(NADP)ratio,increase in the reduced glutathione(GSH)/oxidized glutathione(GSSH)ratio,and reduced mitochondrial reactive oxygen species(ROS)production.Moreover,TAC preconditioning inhibited caspase-3 activation and mitigated the mitochondrial impairment by deacetylating isocitrate dehydrogenase 2(IDH2)via a sirtuin 3(SIRT3)-dependent mechanism.In addition,the expression of a genetic deacetylation mimetic IDH2 mutant(IDH2 K413R)in cardiomyocytes,which increased IDH2 enzymatic activity and decreased mitochondrial ROS production,and ameliorated I/R injury,whereas the expression of a genetic acetylation mimetic(IDH2 K413Q)in cardiomyocytes abolished these protective effects of hypertrophic preconditioning.Furthermore,both the activity and expression of the SIRT3 protein were markedly increased in preconditioned mice exposed to I/R.Treatment with an adenovirus encoding SIRT3 partially emulated the actions of hypertrophic preconditioning,whereas genetic ablation of SIRT3 in mice blocked the cardioprotective effects of hypertrophic preconditioning.The present study identifies hypertrophic preconditioning as a novel endogenous self-defensive and cardioprotective strategy for cardiac I/R injury that induces IDH2 deacetylation through a SIRT3-dependent mechanism.A therapeutic strategy targeting IDH2 may be a promising treatment for cardiac ischemic injury.
