由体表电位分布推算心脏外膜电位——心脏电活动的逆解

心脏外膜电位分布对研究心脏电活动机制和诊断心脏某些疾病有重要意义。本文介绍由体表电位估算心外膜电位的原理、方法和实验装置,并着重叙述从体表到心外膜电位传输系数的两种估算方法——几何测量法和有限元法——及它们的结果。     

心电逆问题的虚拟心脏模型参数解用于心室预激旁道定位的研究

提出了一种新的心电逆问题求解方法,即基于虚拟心脏模型的心电逆问题的模型参数解。详细研究了心室预激旁道位置与体表电位分布（ＢＳＰＭ：ＢｏｄｙＳｕｒｆａｃｅＰｏｔｅｎｔｉａｌＭａｐｐｉｎｇｓ）特征参数的关系,用ＢＳＰＭ的预激旁道位置敏感参数构造了优化系统的数学模型,给出了相应的优化算法及预激综合征旁道定位结果。研究结果表明：这种新的心电逆问题研究方法是可行、有效的,对心室内预激点的定位精度在三个心肌单元以内（即４．５ｍｍ）。     

从体表电位分布图中提取陈旧性心肌梗塞诊断信息的研究

如何从体表电位分布图（ＢｏｄｙＳｕｒｆａｃｅＰｏｔｅｎｔｉａｌＭａｐｐｉｎｇｓ：ＢＳＰＭ）中得到有价值的诊断特征或信息是将ＢＳＰＭ技术应用于临床的重要研究课题之一。基于计算机心脏仿真模型,详细研究了ＢＳＰＭ中能够对陈旧性心肌梗塞的发生部位与范围进行准确诊断的特征与信息。研究结果表明：ＱＲＳ期间正常ＢＳＰＭ中为正电位、陈旧性心肌梗塞ＢＳＰＭ中为负电位的导联分布区域与出现Ｑ波的导联分布区域是陈旧性心肌梗塞发生部位较准确、可靠的定位信息;可以用正常ＢＳＰＭ为正电位、而梗塞ＢＳＰＭ为负电位的导联区域的面积或导联数来识别陈旧性心肌梗塞的发生范围或大小。     

小波变换与生物医学信号处理

作为数字信号处理领域的一个重要分支,生物医学信号处理理论与技术的研究一直受到国内外科技工作者的高度重视。小波变换是近年来发展起来的一种新的信号分析工具。本文结合生物医学信号与小波变换的特点,探讨了小波变换在生物医学信号处理领域的应用前景。     

基于小波变换的混合二维ECG数据压缩方法

提出了一种新的基于小波变换的混合二维心电(electrocardiogram,ECG)数据压缩方法。基于ECG数据的两种相关性,该方法首先将一维ECG信号转化为二维信号序列。然后对二维序列进行了小波变换,并利用改进的编码方法对变换后的系数进行了压缩编码:即先根据不同系数子带的各自特点和系数子带之间的相似性,改进了等级树集合分裂(setpartitioninghierarchicaltrees,SPIHT)算法和矢量量化(vectorquantization,VQ)算法;再利用改进后的SPIHT与VQ相混合的算法对小波变换后的系数进行了编码。利用所提算法与已有具有代表性的基于小波变换的压缩算法和其他二维ECG信号的压缩算法,对MIT/BIH数据库中的心律不齐数据进行了对比压缩实验。结果表明:所提算法适用于各种波形特征的ECG信号,并且在保证压缩质量的前提下,可以获得较大的压缩比。     

小波分析在生态环境研究中的应用初探

小波分析(Wavelet Analysis)是时间-频率分析领域近年来迅速发展的一种新技术,具有多时间尺度,多层次和多分辨的特性,已被广泛地应用在信号分析、信息分析和地球科学研究上.本文以大亚湾大鹏澳水域2002年春秋两季浮游植物30d连续观测资料为例,首次运用小波技术分析浮游植物对生境变化的响应特征.结果表明,通过小波变换的浮游植物数量(细胞密度)的时间序列,存在各自的优势周期和多时间尺度结构特征,而春秋两季浮游植物细胞密度的优势周期和多时间尺度结构,在大尺度上大致相同,但在小尺度结构上稍有差别;使用不同小波变换(如Mexh小波变换和Morlet小波变换)可以取得各自不同特点的结果.本文对小波分析技术在生态环境研究的初步应用说明,小波分析技术可以对生态系统中浮游植物的动态变化进行多时间尺度,多层次和多分辨的分析,为深入研究和预测浮游植物的动态变化提供一种新的分析手段.     

环境因素引起植物表面电位变化的小波分析

许多外界环境因子都能引发植物局部表面电位发生变化。在植物电生理研究中如何解读表面电位变化所包含的对环境的反应是一个长期没有解决的问题。小波分析能有效地提取某种信号的时、频域特征。本文首次将小波分析方法用于植物电信号的解析,结果表明,在环境因子引发的表面电位变化中,具有明显的时域和频域的特征。在不同频域中,主要在低频尺度上反映植物对光、温及光和温度共同作用的特定响应。     

体表电位标测系统及心电逆问题

一、前言 心电学的研究分正问题研究和逆问题研究,前者研究体表心电是如何产生和形成的;后者研究的是如何从体表电位推断心脏状态。广义地讲,目前临床医生根据无损地从体表测得的12导联心电图或心向量图来作诊断也是心电逆问题求解。只是这种对心脏状态的推断依据的是书本知识和医生的临床经验,而且一般只能作定性的推断。     

一个新的脑电信号分析系统：小波分析理论的运用

小波变换是一种把时间、频率（或尺度）两域结合起来的分析方法。它被誉为“分析信号的数学显微镜”。本系统将小波变换用于脑电信号分析,是一个在Ｗｉｎｄｏｗｓ３．１下开发的脑电分析系统。     

心音信号奇异点的小波分析方法

本文利用小波变换方法,提出以确定奇异点的位置以及幅值的变化对心音信号进行参数估计.通过PhysioBank数据库中的相关数据,运用Madab对正常心音和病理性心音信号进行小波变换分析,对奇异点做了检测.并与傅里叶变换结果作对比分析.通过对变换后的心音信号进行分析,研究结果表明:利用小波变换技术分析与处理心音信号是一种新的有效和实用的方法.可以为心音信号的分析或医学诊断提供有价值的信息.     

基于心脏模型推断心肌病理状态的仿真研究

采用有限元方法建立了人体心脏力学模型, 并基于该仿真模型提出了一种无创推断心肌病理状态的新方案,并通过心肌梗塞定位试验加以验证。仿真研究表明这种基于模型参数优化解的方法能将心肌梗塞定位到模型基本单元的空间范围,可用于提取心肌疾病信息。     

Diagnosis of Coronary Heart Diseases Using Gene Expression Profiling; Stable Coronary Artery Disease,Cardiac Ischemia with and without Myocardial Necrosis

Cardiovascular disease (including coronary artery disease and myocardial infarction) is one of the leading causes of death in Europe, and is influenced by both environmental and genetic factors. With the recent advances in genomic tools and technologies there is potential to predict and diagnose heart disease using molecular data from analysis of blood cells. We analyzed gene expression data from blood samples taken from normal people (n = 21), non-significant coronary artery disease (n = 93), patients with unstable angina (n = 16), stable coronary artery disease (n = 14) and myocardial infarction (MI; n = 207). We used a feature selection approach to identify a set of gene expression variables which successfully differentiate different cardiovascular diseases. The initial features were discovered by fitting a linear model for each probe set across all arrays of normal individuals and patients with myocardial infarction. Three different feature optimisation algorithms were devised which identified two discriminating sets of genes, one using MI and normal controls (total genes = 6) and another one using MI and unstable angina patients (total genes = 7). In all our classification approaches we used a non-parametric k-nearest neighbour (KNN) classification method (k = 3). The results proved the diagnostic robustness of the final feature sets in discriminating patients with myocardial infarction from healthy controls. Interestingly it also showed efficacy in discriminating myocardial infarction patients from patients with clinical symptoms of cardiac ischemia but no myocardial necrosis or stable coronary artery disease, despite the influence of batch effects and different microarray gene chips and platforms.     

Overexpression of Na+/Ca2+ exchanger gene attenuates postinfarction myocardial dysfunction

We monitored myocardial function in postinfarcted wild-type (WT) and transgenic (TG) mouse hearts with overexpression of the cardiac Na(+)/Ca(2+) exchanger. Five weeks after infarction, cardiac function was better maintained in TG than WT mice [left ventricular (LV) systolic pressure: WT, 41 +/- 2; TG, 58 +/- 3 mmHg; P < 0.05; maximum rising rate of LV pressure (+dP/dt(max)): WT, 3,750 +/- 346; TG, 5,075 +/- 334 mmHg/s; P < 0.05]. The isometric contractile response to beta-adrenergic stimulation was greater in papillary muscles from TG than WT mice (WT, 13.2 +/- 0.9; TG, 16.3 +/- 1.0 mN/mm(2) at 10(-4) M isoproterenol). The sarcoplasmic reticulum (SR) Ca(2+) content investigated by rapid cooling contractures in papillary muscles was greater in TG than WT mouse hearts. We conclude that myocardial function is better preserved in TG mice 5 wk after infarction, which results from enhanced SR Ca(2+) content via overexpression of the Na(+)/Ca(2+) exchanger.     

The proteoglycan biglycan enhances antigen-specific T cell activation potentially via MyD88 and TRIF pathways and triggers autoimmune perimyocarditis

Biglycan is a proteoglycan ubiquitously present in extracellular matrix of a variety of organs, including heart, and it was reported to be overexpressed in myocardial infarction. Myocardial infarction may be complicated by perimyocarditis through unknown mechanisms. Our aim was to investigate the capacity of TLR2/TLR4 ligand biglycan to enhance the presentation of specific Ags released upon cardiomyocyte necrosis. In vitro, OVA-pulsed bone marrow-derived dendritic cells from wild-type (WT; C57BL/6) and TLR2-, TLR4-, MyD88-, or TRIF-deficient mice were cotreated with LPS, biglycan, or vehicle and incubated with OVA-recognizing MHC I- or MHC II-restricted T cells. Biglycan enhanced OVA-specific cross-priming by >80% to MHC I-restricted T cells in both TLR2- and TLR4-pathway-dependent manners. Accordingly, biglycan-induced cross-priming by both MyD88- and TRIF-deficient dendritic cells (DCs) was strongly diminished. OVA-specific activation of MHC II-restricted T cells was predominantly TLR4 dependent. Our first in vivo correlate was a model of experimental autoimmune perimyocarditis triggered by injection of cardiac Ag-pulsed DCs (BALB/c). Biglycan-treated DCs triggered perimyocarditis to a comparable extent and intensity as LPS-treated DCs (mean scores 1.3 ± 0.3 and 1.5 ± 0.4, respectively). Substitution with TLR4-deficient DCs abolished this effect. In a second in vivo approach, WT and biglycan-deficient mice were followed 2 wk after induction of myocardial infarction. WT mice demonstrated significantly greater myocardial T lymphocyte infiltration in comparison with biglycan-deficient animals. We concluded that the TLR2/4 ligand biglycan, a component of the myocardial matrix, may enhance Ag-specific T cell priming, potentially via MyD88 and TRIF, and stimulate autoimmune perimyocarditis.     

A new theory of infarction-genesis in cats

It can be shown that a number of substances that are derived from incubation have a good blocking capacity in myocardial infarction. There exists also a natural substance (intrinsic factor, i.f.) which can also block infarction. The same substances also inhibit arrhythmias of ischaemic origin. Thus a common root for myocardial infarction and arrhythmias could be inferred. A new dynamic method (T/2 velocity) was elaborated for evaluating anti-infarction drugs instead of using static T/2 values. Oxidation of i.f. in vitro and in vivo enhances the blocking capacity of artificial drugs reagented previously each other. The natural substance (i.f.) lost its blocking capacity after oxygenation, thus may be unable to compete with the above mentioned artificial substances. Ligation of the coronaries i.e. its myocardial infarction producing effect can also be inhibited by the same substances. No matter how infarction is produced, the same substances can block it. Since after cutting the vagi KCl elicits the same phenomena their reflex origin can be excluded.     

Musculoskeletal model of the upper limb based on the visible human male dataset

A mathematical model of the human upper limb was developed based on high-resolution medical images of the muscles and bones obtained from the Visible Human Male (VHM) project. Three-dimensional surfaces of the muscles and bones were reconstructed from Computed Tomography (CT) images and Color Cryosection images obtained from the VHM cadaver. Thirteen degrees of freedom were used to describe the orientations of seven bones in the model: clavicle, scapula, humerus, radius, ulna, carpal bones, and hand. All of the major articulations from the shoulder girdle down to the wrist were included in the model. The model was actuated by 42 muscle bundles, which represented the actions of 26 muscle groups in the upper limb. The paths of the muscles were modeled using a new approach called the Obstacle-set Method [33]. The calculated paths of the muscles were verified by comparing the muscle moment arms computed in the model with the results of anatomical studies reported in the literature. In-vivo measurements of maximum isometric muscle torques developed at the shoulder, elbow, and wrist were also used to estimate the architectural properties of each musculotendon actuator in the model. The entire musculoskeletal model can be reconstructed using the data given in this paper, along with information presented in a companion paper which defines the kinematic structure of the model [26].     

瞬时受体电位香草酸亚型1激活释放的P物质在小鼠急性心肌梗死后凋亡中的保护作用

瞬时受体电位香草酸亚型1 (transient receptor potential vanilloid 1, TRPV1)在心肌缺血激活后可传导心绞痛信号和释放P物质(substance P, SP).SP是速激肽家族成员之一,主要通过结合并激活神经激肽1 (neurokinin 1,NK1)受体发挥作用. TRPV1和SP在缺血性心脏病中对心功能的恢复和重塑有一定保护作用,但对心肌梗死后凋亡的作用及具体机制尚不明确.本研究用TRPV1基因敲除(TRPV1-/- )小鼠和野生型(wide type, WT)小鼠建立心肌梗死模型,并外源性给予SP和NK1受体拮抗剂RP67580,用TTC染色法观察梗死的面积,TUNEL法检测心肌细胞凋亡指数,Western印迹方法检测caspase-3、Bcl-2、Bax、p53的蛋白表达.结果发现,心肌梗死24 h后,TRPV1-/-小鼠比WT小鼠梗死面积更大,凋亡指数和caspase-3活性更高,Bcl-2/Bax和p53蛋白表达更低. SP预处理可以明显缩小TRPV1-/-小鼠梗死面积,降低凋亡指数、caspase-3活性和升高Bcl-2/Bax比值,而在WT小鼠中改善不明显.外源性给予RP67580,阻断SP与NK1受体结合后,与相应对照组相比,WT小鼠梗死面积和凋亡指数更大,caspase-3蛋白表达更高,Bcl-2/Bax比值更低;TRPV1-/-小鼠与相应对照组比较,凋亡指数和caspase-3表达升高,Bcl-2/Bax比值降低.研究结果表明,SP可能介导了TRPV1在急性心肌梗死后凋亡中的保护作用.     

心肌酶和红细胞形态学参数与心肌梗死的相关性研究

目的:研究红细胞形态学参数对心肌梗死患者诊断作用及其与心肌酶谱的相关性。方法:选取40例心肌梗死患者,40例稳定型心绞痛组患者,40例健康对照组人群。对比分析稳定性心绞痛、急性心肌梗死(入院1h内)和对照组红细胞形态学参数(MCV、MCH、MCHC、RDW)、及心肌酶谱(CK-MB、c Tn I)。分析心肌梗死不同时间MCV、MCH、MCHC、RDW变化趋势。结果:稳定性心绞痛、心肌梗死组1 h内MCV、RDW明显高于正常对照组,差异有统计学意义(P0.05);稳定性心绞痛、心肌梗死组1 h内MCHC、MCH低于对照组,差异有统计学意义(P0.05)。心肌梗死组MCV、RDW在发病后1 h、24 h、48 h、7 d水平逐渐升高,各时间点间差异有统计学意义(P0.05)。心肌梗死组发病后1 h、24 h、48 h、7 d、14 d MCHC、MCH水平逐渐降低,各时间点间差异有统计学意义(P0.05)。RDW和CK-MB、c Tn I呈正相关性(P0.05)。RDW对心肌梗死诊断的灵敏度最高达到93.4%,特异度为69.7%,RDW对急性心肌梗塞的诊断临界值为14.04%。结论:RDW对心肌梗死的诊断具有较高的敏感性,可用于临床早期诊断心肌梗死,为临床诊断提供一新的诊断标准。     

Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice

MyD88 is an adaptor protein critical for innate immune response against microbial infection and in certain noninfectious tissue injury. The present study examined the role of MyD88 in myocardial inflammation and injury after ischemia-reperfusion (I/R). I/R was produced by coronary artery ligation for 30 min followed by reperfusion. The ratios of area at risk to left ventricle (LV) were similar between wild-type (WT) and MyD88-deficient (MyD88-/-) mice. However, 24 h after I/R, the ratios of myocardial infarction to area at risk were 58% less in MyD88(-/-) than in WT mice (14 +/- 2% vs. 33 +/- 6%, P = 0.01). Serial echocardiographic studies demonstrated that there was no difference in baseline LV contractile function between the two groups. Twenty-four hours after I/R, LV ejection fraction (EF) and fractional shortening (FS) in WT mice were reduced by 44% and 62% (EF, 51 +/- 2%, and FS, 22 +/- 1%, P < 0.001), respectively, and remained depressed on the seventh day after I/R. In comparison, EF and FS in MyD88(-/-) mice were 67 +/- 3% and 33 +/- 2%, respectively, after I/R (P < 0.001 vs. WT). Similarly, LV function, as demonstrated by invasive hemodynamic measurements, was better preserved in MyD88(-/-) compared with WT mice after I/R. Furthermore, when compared with WT mice, MyD88(-/-) mice subjected to I/R had a marked decrease in myocardial inflammation as demonstrated by attenuated neutrophil recruitment and decreased expression of the proinflammatory mediators keratinocyte chemoattractant, monocyte chemoattractant protein-1, and ICAM-1. Taken together, these data suggest that MyD88 modulates myocardial inflammatory injury and contributes to myocardial infarction and LV dysfunction during I/R.     

Detailed Anatomical and Electrophysiological Models of Human Atria and Torso for the Simulation of Atrial Activation

Atrial arrhythmias, and specifically atrial fibrillation (AF), induce rapid and irregular activation patterns that appear on the torso surface as abnormal P-waves in electrocardiograms and body surface potential maps (BSPM). In recent years both P-waves and the BSPM have been used to identify the mechanisms underlying AF, such as localizing ectopic foci or high-frequency rotors. However, the relationship between the activation of the different areas of the atria and the characteristics of the BSPM and P-wave signals are still far from being completely understood. In this work we developed a multi-scale framework, which combines a highly-detailed 3D atrial model and a torso model to study the relationship between atrial activation and surface signals in sinus rhythm. Using this multi scale model, it was revealed that the best places for recording P-waves are the frontal upper right and the frontal and rear left quadrants of the torso. Our results also suggest that only nine regions (of the twenty-one structures in which the atrial surface was divided) make a significant contribution to the BSPM and determine the main P-wave characteristics.