老年及青年Wistar大鼠心电图QRS波时域及频域分析的比较研究

本文报道了老年及青年Ｗｉｓｔａｒ大鼠Ⅱ导联心电图ＱＲＳ波的时程、波幅及频谱特性，并分析了老龄对其时域值及频谱的影响，结果如下：（１）ｍ青年及老年鼠ＱＲＳ波时程及波幅；老年鼠与青年鼠相比，ＱＲＳ波时程延长（Ｐ〈０．０１）崦波幅减少（Ｐ〈０．０５）；（２）青年及老年鼠ＱＲＳ波频谱特征；青年鼠ＱＲＳ波频产呈双峰型，可分为两型：大部分鼠（１３／２１只）第一峰大，少部分鼠（８／２１只）第二峰大，老年鼠频谱图     

大鼠心电信号时频域及混沌分析

本文利用采样频率１５００Ｈｚ，精度１２位的“计算机化大鼠心电信号获取和分析系统”获得了Ｗｉｓｔａｒ大鼠的高分辨心电图表象，并将心室去极化波命名为ＱＲＸＹＳ复合波。对ＱＲＸＹＳ作了５１２点的功率谱分析，获得了不同于人的ＱＲＳ复合波的（单峰或指数下降特征）具有双峰特征的功率谱。     

基于微机的心电信号实时自动分析系统

作者介绍了在３８６微机上研制开发的心电信号实时自动分析系统，着重介绍了ＱＲＳ复合波的帝时检测算法和心律失常自动分析软件。该系统能实时显示任一导联心电波形，同时显示心率（ＨＲ）和早搏（ＰＶＣ）累积数；能自动识别十余种心律失常并报警；具有ＳＴ段分析功能，能实时检测ＳＴ段电平和斜率，经用美国ＭＩＴ心电数据库的部分数据对该系统进行测试，准确率达９５％以上。     

兔心电QRS波的三维频谱分析

应用小波转换的三维频谱分析技术,对４０只兔心电ＱＲＳ波进行分析,观察其三维心电频谱的特征。结果显示：正常兔心电ＱＲＳ波的三维频谱形态呈双侧对称的山坡状,频谱宽度约为２４０Ｈｚ,高频成分主要分布在ＱＲＳ波的中部,能幅随频率增加呈下降趋势,其中１００—１０００Ｈｚ与６０—１００Ｈｚ的能量比约为１０,１５０—２５０Ｈｚ与６０—１００Ｈｚ的能量比约为０３５,并证明性别和体重对心电ＱＲＳ波三维频谱各参数不产生严重影响。     

多导同步心电图的QRS波检测及起止点的确定

本文采用从单导到多导的检测方法,首先利用小波变换实现单导ＱＲＳ波的检测,在此基础上,利用位置相关法进行多导ＱＲＳ波的检测,并利用心电信号的２＾１迟度小波变换的平方值来确定ＱＲＳ波的起止点,经过大量数据的检测证明取得了很好的效果。     

一种高效的QRS波实时检测方法

本文介绍一种高效的ＱＲＳ波实时检测方法。该检测方法由检测电路和判断子程序组成。结合Ｒ波斜率、ＱＲＳ波幅度、持续期，频带等特征进行ＱＲＳ波的综合检测。判断子程序可在单片机系统内实时实现。对检测方法噪声敏感性和检测准确性的测试和临床应用表明该方法具有抗干扰性强，准确率高等特点。     

A Method for Detecting QRS Waves

作者提出了一种心电图ＱＲＳ波检测方法。该方法采用硬件和软件结合检测ＱＲＳ波，集中了硬件检测的快速性和软件检测的灵活性的优点，经过在多参数病人监护系统中应用，表明该方法准确可靠、快速实用。     

一种心电图QRS波检测方法

作者提出了一种心电图ＱＲＳ波检测方法，该方法采用硬件和软件结合检测ＱＲＳ波，集中了硬件检测的快速性和软件检测的灵活性的优点，经过在多参数病人监护系统中应用，表明该方法准确可靠，快速实用。     

用移动平均幅值微分算法检测胎儿R波

用移动平均幅值微分算法检测胎儿Ｒ波［英］／Ｐａｒｋ　ＹＣ…／／ＩＥＥＥＴｒａｎｓＢＭＥ．－１９９２，３９（８）．－８６８胎儿ＥＣＧ信号处理问题包括从腹导ＥＣＧ信号中去除母体ＱＲＳ复合波增强胎儿ＱＲＳ复合波，检测胎儿Ｒ波计算胎儿心率。ＡＭＤＦ（ａｖｅｒ...     

心电记录仪频响范围不同时人和小鼠QRS波群峰峰值及波宽的比较研究

本文分析了当心电记录仪频响范围分别在０～５０Ｈｚ,０～１００Ｈｚ,０～２００Ｈｚ,０～５００Ｈｚ,０～１０００Ｈｚ５个频响范围时正常人和小鼠ＱＲＳ波群的峰峰值（Ｖｐ－ｐ）及波宽的变化。结果：正常人（ｎ＝２０）和正常小鼠（ｎ＝２０）,Ⅱ导联、ａＶＦ导联及Ｖ３导联的ＱＲＳ波群的Ｖｐ－ｐ,在０～１０００Ｈｚ频响范围内,均随着记录仪频响范围的增宽而增大。但正常人增幅极小,Ⅱ导联０～１０００Ｈｚ频响范围的ＱＲＳ波群的Ｖｐ－ｐ比０～１００Ｈｚ的仅增加了００３５ｍｖ,增幅仅为５９％;而小鼠的ＱＲＳ的Ｖｐ－ｐ增幅比人的大得多,Ⅱ导联０～１０００Ｈｚ频响范围的ＱＲＳ波群的Ｖｐ－ｐ比０～１００Ｈｚ的增加了０２５２ｍｖ,增幅为５２６％,是人的８９倍。小鼠及人的心电信号是在同一条件下记录的,通过对二者的比较,可认为小鼠的心电活动中,确实存在着高频信号,即小鼠高频心电图中的高频信号并非来自外界环境。人与小鼠Ⅱ、ａＶＦ、Ｖ３三个导联各频响范围的ＱＲＳ波宽均无明显差异。     

心电信号时频特性的对比研究

对心电信号的分析存在着时域频域两种方法,我对此作了对照研究。用频域滤波的方法,分别滤去一定低频成分,再IFFT恢复时域波形,时域信号出现了双相T波。滤去一定高频成分,再IFFT恢复时域波形,经适当放大,可明显看出高频心电的时域表象：P波、T波的高频时域表象没有明显结构,而QRS波有明显的结构。QRS波时限与高频成分有关,滤去一定的高频成分QRS时限延长。QRS波顿挫是高频成分增多所致。心室去极化QRS复合波有三角脉冲样波形,也有非三角脉冲样波形,其功率谱具有单峰和指数下降（倒幂）特征两种类型。整个心动周期信号、P、波、T波的高频谱无明显的规律性,而QRS波有一定的结构。     

Impairment of different protein domains causes variable clinical presentation within Pitt-Hopkins syndrome and suggests intragenic molecular syndromology of TCF4

Pitt-Hopkins syndrome is a neurodevelopmental disorder characterized by severe intellectual disability and a distinctive facial gestalt. It is caused by haploinsufficiency of the TCF4 gene. The TCF4 protein has different functional domains, with the NLS (nuclear localization signal) domain coded by exons 7–8 and the bHLH (basic Helix-Loop-Helix) domain coded by exon 18. Several alternatively spliced TCF4 variants have been described, allowing for translation of variable protein isoforms. Typical PTHS patients have impairment of at least the bHLH domain. To which extent impairment of the remaining domains contributes to the final phenotype is not clear. There is recent evidence that certain loss-of-function variants disrupting TCF4 are associated with mild ID, but not with typical PTHS. We describe a frameshift-causing partial gene deletion encompassing exons 4–6 of TCF4 in an adult patient with mild ID and nonspecific facial dysmorphisms but without the typical features of PTHS, and a c.520C > T nonsense variant within exon 8 in a child presenting with a severe phenotype largely mimicking PTHS, but lacking the typical facial dysmorphism. Investigation on mRNA, along with literature review, led us to suggest a preliminary phenotypic map of loss-of-function variants affecting TCF4.An intragenic phenotypic map of loss-of-function variants in TCF4 is suggested here for the first time: variants within exons 1–4 and exons 4–6 give rise to a recurrent phenotype with mild ID not in the spectrum of Pitt-Hopkins syndrome (biallelic preservation of both the NLS and bHLH domains); variants within exons 7–8 cause a severe phenotype resembling PTHS but in absence of the typical facial dysmorphism (impairment limited to the NLS domain); variants within exons 9–19 cause typical Pitt-Hopkins syndrome (impairment of at least the bHLH domain). Understanding the TCF4 molecular syndromology can allow for proper nosology in the current era of whole genomic investigations.     

Pyruvate carboxylase deficiency type A and type C: Characterization of five novel pathogenic variants in PC and analysis of the genotype–phenotype correlation

Pyruvate carboxylase deficiency (PCD) is caused by biallelic mutations of the PC gene. The reported clinical spectrum includes a neonatal form with early death (type B), an infantile fatal form (type A), and a late‐onset form with isolated mild intellectual delay (type C). Apart from homozygous stop‐codon mutations leading to type B PCD, a genotype–phenotype correlation has not otherwise been discernible. Indeed, patients harboring biallelic heterozygous variants leading to PC activity near zero can present either with a fatal infantile type A or with a benign late onset type C form. In this study, we analyzed six novel patients with type A (three) and type C (three) PCD, and compared them with previously reported cases. First, we observed that type C PCD is not associated to homozygous variants in PC. In silico modeling was used to map former and novel variants associated to type A and C PCD, and to predict their potential effects on the enzyme structure and function. We found that variants lead to type A or type C phenotype based on the destabilization between the two major enzyme conformers. In general, our study on novel and previously reported patients improves the overall understanding on type A and C PCD.     

Nonlinear and Frequency-Dependent Mechanical Behavior of the Mouse Respiratory System

The assessment of the mechanical properties of the respiratory system is typically done by oscillating flow into the lungs via the trachea, measuring the resulting pressure generated at the trachea, and relating the two signals to each other in terms of some suitable mathematical model. If the perturbing flow signal is broadband and not too large in amplitude, linear behavior is usually assumed and the input impedance calculated. Alternatively, some researchers have used flow signals that are narrow band but large in amplitude, and invoked nonlinear lumped-parameter models to account for the relationship between flow and pressure. There has been little attempt, however, to deal with respiratory data that are both broadband and reflective of system nonlinearities. In the present study, we collected such data from mice. To interpret these data, we first developed a time-domain approximation to a widely used model of respiratory input impedance. We then extended this model to include nonlinear resistive and elastic terms. We found that the nonlinear elastic term fit the data better than the linear model or the nonlinear resistance model when amplitudes were large. This model may be useful for detecting overinflation of the lung during mechanical ventilation. © 2003 Biomedical Engineering Society. PAC2003: 8719Rr, 8719Uv     

脉搏波分析方法及其应用

脉搏波包含大量的人体生理病理信息。如何有效提取其中包含的信息,一直为国内外研究者所关注。目前脉搏波分析的主要方法有时域分析、频域分析、时频分析、数学建模分析和脉搏波速度分析等。研究者们应用上述脉搏波分析方法提取相应的脉搏波特征参数,用于评估心血管功能状态,分析人体的生理病理状况,进行中医脉象方面的研究。本文全面、系统地介绍了脉搏波分析方法及其应用研究,对脉搏波分析研究的成果和局限性进行了总结,并对下一步研究方向进行了展望。     

Mutations in the motor and stalk domains of KIF5A in spastic paraplegia type 10 and in axonal Charcot-Marie-Tooth type 2

Spastic paraplegia type 10 (SPG10) is an autosomal dominant form of hereditary spastic paraplegia (HSP) due to mutations in KIF5A, a gene encoding the neuronal kinesin heavy chain implicated in anterograde axonal transport. KIF5A mutations were found in both pure and complicated forms of the disease; a single KIF5A mutation was also detected in a CMT2 patient belonging to an SPG10 mutant family. To confirm the involvement of the KIF5A gene in both CMT2 and SPG10 phenotypes and to define the frequency of KIF5A mutations in an Italian HSP patient population, we performed a genetic screening of this gene in a series of 139 HSP and 36 CMT2 affected subjects. We identified five missense changes, four in five HSP patients and one in a CMT2 subject. All mutations, including the one segregating in the CMT2 patient, are localized in the kinesin motor domain except for one, falling within the stalk domain and predicted to generate protein structure destabilization. The results obtained indicate a KIF5A mutation frequency of 8.8% in the Italian HSP population and identify a region of the kinesin protein, the stalk domain, as a novel target for mutation. In addition, the mutation found in the CMT2 patient strengthens the hypothesis that CMT2 and SPG10 are the extreme phenotypes resulting from mutations in the same gene.     

T细胞免疫球蛋白及黏蛋白域蛋白4的生物学功能及其与过敏性疾病的关系

T细胞免疫球蛋白及黏蛋白域家族是一个影响Th1／Th2细胞分化的基因家族。T细胞免疫球蛋白及粘蛋白域蛋白4（TIM4）是TIM家族的一个成员,主要表达于树突状细胞和巨噬细胞。TIM4与TIM1结合后参与对Th2细胞的激活,影响机体的免疫功能：TIM4同时是一个黏附分子,其与磷脂酰丝氨酸结合后可介导巨噬细胞对凋亡细胞的吞噬。另外,TIM4与儿童过敏性鼻炎,过敏性哮喘之间存在着遗传相关性,     

Seven single nucleotide substitutions in human Fc(gamma) receptor IIB gene

Variation screening for the immunoglobulin G Fc receptor IIB (Fc(gamma)RIIB) gene was performed with the genomic DNA from 100 healthy Japanese subjects. We identified 3 non-synonymous and 2 synonymous substitutions and 2 single-nucleotide polymorphisms in an intron region. These substitutions were found to be located in the ligand-binding domain and the intron, which might alter the function of Fc(gamma)RIIb.     

Tim-3启动子区-574基因多态性与变应性哮喘的关系

目的:探讨引物特异PCR-核酸序列测定技术检测T细胞免疫球蛋白域粘蛋白域蛋白-3(Ti m-3)启动子区-574G>T单核苷酸变异及其与湖北地区汉族人群支气管哮喘易感性之间的关系。方法:分别采用引物特异聚合酶链反应(PCR)-核酸序列测定技术检测湖北地区296例哮喘患者和202例健康对照人群Ti m-3启动子区-574G>T单核苷酸变异,计算基因型和等位基因频率。结果:湖北健康人群中Ti m-3启动子区-574位G/G、G/T和T/T基因型频率分别是0.990、0.010和0,而哮喘患者频率分别为0.929、0.071、0,其基因型频率与对照组差异有显著性(χ2=10.14,P<0.01)。结论:引物特异PCR-核酸序列测定技术可用于检测Ti m-3启动子区-574G>T单核苷酸变异的检测;湖北汉族人群中Ti m-3启动子区存在多态性变异,其中-574G>T多态性可能与湖北汉族人群变应性哮喘易感性有关。