乙型肝炎病人重叠感染丙型肝炎的评价

应用ＥＬＩＳＡ和ＰＣＲ法检测５０２例乙肝病人血清,４０１例ＨＢｓＡｇ阳性血清中,有１１４例（２８．４％）抗－ＨＣＶ和ＨＣＶＲＮＡ双项阳性,２５例（６．２％）ＨＣＶＲＮＡ单项阳性;２１例（５．２％）抗－ＨＣＶ单项阳性。将ＨＢｓＡｇ乙肝病人分成ＨＢＶＤＮＡ,ＨＢｅＡｇ阳性组和ＨＢＶＤＮＡ,ＨＢｅＡｇ阴性组。前者抗－ＨＣＶ阳性率为１１．６％～２０．５％,ＨＣＶＲＮＡ阳性率为１６．２％～２０．５％。后者抗－ＨＣＶ阳性率为２０．２％～５５．６％,ＨＣＶＲＮＡ阳性率为２３％～６０．３％。结果说明长期携带ＨＢＶ者和慢性乙肝病人均可重叠ＨＣＶ感染。ＨＢＶＤＮＡ阳性组抗－ＨＣＶ和ＨＣＶＲＮＡ阳性率明显高于ＨＢＶＤＮＡ阳性组     

HBsAg携带者重叠感染HCV、HDV的血清学调查

对３６２名无症状高滴度ＨＢｓＡｇ携带者用ＲＩＡ法检测ＨＢｅＡｇ、Ａｎｔｉ－ＨＢｅ、Ａｎｔｉ－ＨＣＶ、Ａｎｔｉ－ＨＤＶ。结果表明,ＨＢｅＡｇ阳性率随ＨＢｓＡｇ滴度的增高而增加,且有显著性差异（Ｐ＜０．０５）。重叠感染以ＨＢＶ＋ＨＣＶ最高,占２７．６％;其次是ＨＢＶ＋ＨＤＶ,占９．１％;ＨＢＶ＋ＨＣＶ＋ＨＤＶ最少,占６．４％。但是,以上重叠感染率均与ＨＢｓＡｇ滴度及／或ＨＢｅＡｇ阳性率高低无关（Ｐ＞０．０５）。调查显示,无症状ＨＢｓＡｇ携带者中ＨＢＶ＋ＨＣＶ,或ＨＢＶ＋ＨＤＶ,或ＨＢＶ＋ＨＣＶ＋ＨＤＶ的重叠感染均可发生。     

用套多聚酶链反应技术监测乙型肝炎病毒的母婴垂直传播

用套式多聚酶链反应（Ｎｅｓｔｅｄ－ＰＣＲ）技术对１６９对ＨＢｓＡｇ及ＨＢｓＡｇ／ＨＢｅＡｇ阳性孕妇及其新生儿外周血清进行了ＨＢＶ－ＤＮＡ检测,１０３对ＨＢｓＡｇ阳性孕妇及其新生儿外周务中ＨＢＶ－ＤＮＡ阳性率分别为７２．８％和３３．０％;６６对ＨＢｓＡｇ和ＨＢｅＡｇ双阳性的孕妇及其新生儿外周血清中ＨＢＶ－ＤＮＡ阳性率分别为８６．４％和４３．９％,对５５例ＨＢｓＡｇ及ＨＢｓＡｇ／ＨＢｅＡｇ阳性产妇产后     

用套式多聚酶链反应技术监测乙型肝炎病毒的母婴垂直传播

用套式多聚酶链反应（Ｎｅｓｔｅｄ－ＰＣＲ）技术对１６９对ＨＢｓＡｇ及ＨＢｓＡｇ／ＨＢｅＡｇ阳性孕妇及其新生儿外周血清进行了ＨＢＶ－ＤＮＡ检测。１０３对ＨＢｓＡｇ阳性孕妇及其新生儿外周血清中ＨＢＶ－ＤＮＡ阳性率分别为７２．８％和３３．０％;６６对ＨＢｓＡｇ和ＨＢｅＡｇ双阳性的孕妇及其新生儿外周血清中ＨＢＶ－ＤＮＡ阳性率分别为８６．４％和４３．９％。对５５例ＨＢｓＡｇ及ＨＢｓＡｇ／ＨＢｅＡｇ阳性产妇产后的初乳进行了ＨＢＶ－ＤＮＡ检测,结果ＨＢＶ－ＤＮＡ阳性率为３６．４％。结果表明ＨＢｓＡｇ和ＨＢｅＡｇ双阳性的孕妇及其新生儿外周血清ＨＢＶ－ＤＮＡ检出率较ＨＢｓＡｇ单阳性的孕妇及其新生儿要高,其初乳中ＨＢＶ－ＤＮＡ的检出率也高。还对１０５例注射了乙肝疫苗及高价乙肝特异性免疫球蛋白的６月龄婴儿的外周血清进行了ＨＢＶ－ＤＮＡ检测,结果有２３例阳性。     

家兔离体心脏组织的不应期及房室结的滤波特性

一般认为房室结具有滤波特性,即它能阻止过快或过于提前的心房冲动传到心室。本实验旨在研究家兔离体心脏组织的不应期及房室结的滤波牧场生（ｎ＝１８）。实验中发现：（１）在短基础周期（２００－３００ｍｓ）房室结的相对不应期最长,而在长基础周期（６００,７００ｍｓ）希浦系（ＨｉｓＰｕｒｋｉｎｊｅ ｓｙｔｅｍ）的相对不应期最长;（２）在多种基础周期下,大多数心脏（１６／１８）房室结有效不应期小于心房功能不应期     

乙型肝炎病人尿细胞中HBV的实验研究

本文采用间接免疫荧光法（ＩＦ）,ＲＰＨＡ法,ＥＬＩＳＡ法及斑点杂交技术检测１０例无症状ＨＢ－ｓＡｇ携带者及８９例乙肝病人尿细胞中的ＨＢｓＡｇ、ＨＢｅＡｇ及ＨＢＶＤＮＡ,发现尿细胞中有ＨＢｓＡｇ、ＨＢｅＡｇ、ＨＢＶＤＮＡ存在。结果提示：乙肝无症状携带者及乙肝病人尿细胞中具有ＨＢｓＡｇ、ＨＢｅＡｇ、ＨＢＶＤＮＡ,因此更进一步证实尿液具有传染性。     

HRP-HBVDNA探针在临检应用中的研究

本文介绍了一种简便的检测血清ＨＢＶＤＮＡ的方法。参照Ｒｅｎｚ等人的标记方法,构建了直接酶标ＨＲＰ ＨＢＶＤＮＡ探针。此探针经与固定在硝酸纤维素滤膜上的血清靶ＤＮＡ杂交后,可通过化学发光自显影检测技术观察结果。敏感度可检测０－１ｐｇ靶ＤＮＡ,相当于同位素探针的灵敏度。对６３份ＨＢｓＡｇＨＢｅＡｇ和Ａｎｔｉ ＨＢｃＥＬＩＳＡ阳性血清以及２４份ＨＢｓＡｇＡｎｔｉ ＨＢｃ阳性,ＨｂｅＡｇ阴性血清用ＨＲＰ ＨＢＶＤＮＡ探针进行检测,结果探针ＨＢＶＤＮＡ阳性率分别为１００％（６３）和５８％（１４）;对５０份ＨＢｓＡｇ,ＥＬＩＳＡ阴性和ＡＬＴ正常的血清,探针ＨＢＶＤＮＡ全部阴性。实验结果表明本方法具有很大的推广应用价值。     

乙型肝炎病毒重组腺病毒载体疫苗的免疫研究进展

以人类腺病毒（Ａｄ）为表达载体发展多价展组口服活疫苗,尤其在乙型肝炎病毒（ＨＢＶ）疫苗研制上成效显著,表达ＨＢｃＡｇ,ＨＢｅＡｇ和ＨＢｓＡｇ的重组人类Ａｄ７型（ｄ７）活载体疫苗在实验动物免疫上取得良好效果。在重组Ａｄ活载体疫苗研制方面是一项重大进展,表达ＨＢｓＡｇ的重组Ａｄ７活载体口服疫苗已有人体初次免疫试验的报道。     

乙型肝炎病毒表面抗原aa126 Ile→Ser变异株HBsAg的暂时表达和抗原性鉴定

曾在一个儿童患者体内,发现一个新的乙型肝炎病毒（ＨＢＶ）变异株,其ＨＢｓＡｇ主蛋白ａａ１２６发生Ｉｌｅ（ＡＴＴ）到Ｓｅｒ（ＡＧＴ）的取代。已知ａｄｒ／ａｙｒ亚型ＨＢｓＡｇ１２６位为Ｉｌｅ,而ａｄｗ／ａｙｗ亚型ＨＢｓＡｇ１２６位为Ｔｈｒ,表明ＨＢｓＡｇ１２６Ｓｅｒ是一个新的变异株。用计算机做结构分析的结果表明,突变体ＨＢｓＡｇ１２６Ｓｅｒ主蛋白ａａ１２０－ａａ１３０区段的二级结构与野生型ａｄｒＨＢＶＨＢｓＡｇ１２６Ｉｌｅ相比发生明显的改变。这种构象的变化可能会影响ａ抗原决定簇（ａ１２４－ａａ１４７）的抗原性。为了证实这一点,构建了突变Ｓ基因表达质粒,在ＳＶ４０早期启动子的控制下进行抗原表达。利用ＨＢｓＡｇ９肽（Ｔｈｒ－Ｉｌｅ１２６－Ｐｒｏ－Ａｌａ－Ｇｌｎ－Ｇｌｙ－Ｔｈｒ－Ｓｅｒ－Ｍｅｔ）抗ｉ单克隆抗体和９肽（Ｔｈｒ－Ｔｈｒ１２６－Ｐｒｏ－Ａｌａ－Ｇｌｎ－Ｇｌｙ－Ｔｈｒ－Ｓｅｒ－Ｍｅｔ）抗ｔ单克隆抗体进行放射免疫测定,结果表明,这种Ｓｅｒ１２６突变蛋白对抗ｉ单克隆抗体的反应性比野生蛋白减弱,对抗ｔ单克隆抗体的反应性则与ＨＢｓＡｇ１２６Ｔｈｒ接近。但用三种抗－ａ单克隆抗体的检测结果揭示,突变蛋白ＨＢｓＡｇ１２６     

反义寡聚硫代磷酸脱氧核苷抑制体外细胞培养系统中乙肝抗原表达的研究

设计合成了两个分别互补于乙肝病毒２．１ｋｂ ｍＲＮＡ起始区（片段Ａ）和增强子区（片段Ｂ）的硫代磷酸的ＤＮＡ片段,在经克隆ＨＢＶ ＤＮＡ转染ＨｅｐＧ２细胞建立的ＨＢＶ短暂表达系统及稳定产生ＨＢＶ的２２１５细胞中研究二者对ＨＢｓＡｇ及ＨＢｅＡｇ表达的抑制作用。结果表明反义寡聚物能不同程序抑制乙肝抗原表达,并与剂量呈一定正相关。在ＨｅｐＧ２细胞ＨＢＶ短暂表达系统中,６μｍｏｌ／Ｌ浓度时,片段Ａ、Ｂ对ＨＢ     

A quantitative description of normal AV nodal conduction curve in man.

The AV nodal conduction curve generated by the atrial extrastimulus technique has been described only qualitatively in man, making clinical comparison of known normal curves with those of suspected AV nodal dysfunction difficult. Also, the effects of physiological and pharmacological interventions have not been quantifiable. In 50 patients with normal AV conduction as defined by normal AH (less than 130 ms), normal AV nodal effective and functional refractory periods (less than 380 and less than 500 ms), and absence of demonstrable dual AV nodal pathways, we found that conduction curves (at sinus rhythm or longest paced cycle length) can be described by an exponential equation of the form delta = Ae-Bx. In this equation, delta is the increase in AV nodal conduction time of an extrastimulus compared to that of a regular beat and x is extrastimulus interval. The natural logarithm of this equation is linear in the semilogarithmic plane, thus permitting the constants A and B to be easily determined by a least-squares regression analysis with a hand calculator.     

Dynamic sympathetic control of atrioventricular conduction time and heart period

Although power spectra of R-R and P-R intervals in response to random respiration show similar frequency distributions, the way in which dynamic sympathetic regulation contributes to such similarity remains unknown. We estimated the transfer function from sympathetic stimulation to the atrioventricular interval (AV conduction time; T(AV)) with and without constant atrial pacing in seven anesthetized cats. The transfer function from sympathetic stimulation to T(AV), except for absolute gain values, approximated a low-pass filter similar to that from sympathetic stimulation to the A-A interval (heart period; T(AA)). The 90%-rise times did not differ between the T(AA) and T(AV) step responses (32.3 +/- 1.8 vs. 29.6 +/- 3.2 s). Constant pacing augmented the T(AV) step response (-0.58 +/- 0.10 vs. -0.86 +/- 0.12 ms/Hz, P < 0.05) without affecting the 90%-rise time. These findings suggest that the dynamic characteristics of sympathetic control are similar between T(AA) and T(AV) despite the different electrophysiological mechanisms determining T(AA) and T(AV). A numerical simulation indicated that if the dynamic characteristics of the sympathetic control do not match between T(AA) and T(AV), a critical condition for initiation of reentrant tachycardia would be encountered.     

Arrhythmia and sudden death associated with elevated cardiac chloride channel activity

The identification and analysis of several cationic ion channels and their associated genes have greatly improved our understanding of the molecular and cellular mechanisms of cardiac arrhythmia. Our objective in this study was to examine the involvement of anionic ion channels in cardiac arrhythmia. We used a transgenic mouse model to overexpress the human cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-regulated chloride channel. We used RNase protection and in situ hybridization assays to determine the level of CFTR expression, and radiotelemetry and in vivo electrophysiological study in combination with pharmacological intervention to analyse the cardiac function. Cardiac CFTR overexpression leads to stress-related sudden death in this model. In vivo intracardiac electrophysiological studies performed in anaesthetized mice showed no significant differences in baseline conduction parameters including atrial-His bundle (AH) or His bundle-ventricular (HV) conduction intervals, atrioventricular (AV) Wenckebach or 2:1 AV block cycle length and AV nodal functional refractory period. However, following isoproterenol administration, there was marked slowing of conduction parameters, including high-grade AV block in transgenic mice, with non-sustained ventricular tachycardia easily inducible using programmed stimulation or burst pacing. Our sudden death mouse model can be a valuable tool for investigation of the role of chloride channels in arrhythmogenesis and, potentially, for future evaluation of novel anti-arrhythmic therapeutic strategies and pharmacological agents.     

Correlation between the sudden jump-like increases of the atrio-Hisian interval induced during burst atrial pacing and during programmed atrial stimulation in patients with atrioventricular nodal reentrant tachycardia

Purpose

To study the correlation between the sudden prolongations of the atrio-Hisian (AH) interval with ≥50 ms during burst and programmed atrial stimulation, and to define whether the AH jump during burst atrial pacing is a reliable diagnostic criterion for dual AV nodal physiology.

Ventricular Pacing on the Prognosis of Patients with Pacemaker Implantation

Excessive right ventricular apex pacing has significant adverse effects on the cardiac function and hence, it is necessary to clinically optimize pacing parameters and advocate suitable physiological pacing to safeguard the cardiac function after pacemaker implant. Minimizing ventricular pacing is an atrioventricular node priority function, to encourage ventricular self conduction and to reduce unnecessary right ventricular pacing. Minimized ventricular pacing reduces ventricular pacing by encouraging self atrioventricular conduction function and extending the AV interval. This study is a prospective cohort study to evaluate the changes of cardiac function in patients and serum amino-terminal natriuretic peptide (NT-proBNP) before and after pacing, and the risk of atrial fibrillation with different CUM% VP. The study has shown that the cardiac function will deteriorate with an increase in pacing rate.     

Quantification of concealed conduction in the atrioventricular node

Twenty-eight anaesthetized open-chest mongrel dogs were used. Programmed atrial pacing was used and Hisian electrograms recorded through endocavitary electro-catheters to study and quantify the concealed conduction of non-transmitted atrial impulses in the A-V node. An exponential model was used in three situations to quantify the nodal conduction during incremental atrial pacing: a) during 1:1 conduction, b) during 2:1 nodal block, and c) during pacing, coupling an atrial impulse delivered at fixed intervals and blocked in the A-V node to each transmitted impulse. The relation between intranodal conduction times was analyzed both with and without the presence of blocked impulses, and the quotient between the obtained functions in situations b, c and situation a was determined. In a subgroup of 13 dogs the study was repeated following pharmacological block of the autonomic nervous system. In dogs with autonomic block, this relation always tended to decrease when the atrial pacing rate increased. The variations in the group of dogs with intact autonomic nervous systems were not homogeneous. During pacing with coupled block impulses, the progressive removal of conduction curves obtained for each coupling interval with respect to those obtained during 1:1 transmission, expresses the interval with respect ot those obtained during 1:1 transmission, expresses the lesser influence of the blocked impulses on decreasing their coupling interval.     

Functional mathematical model of dual pathway AV nodal conduction

Dual atrioventricular (AV) nodal pathway physiology is described as two different wave fronts that propagate from the atria to the His bundle: one with a longer effective refractory period [fast pathway (FP)] and a second with a shorter effective refractory period [slow pathway (SP)]. By using His electrogram alternance, we have developed a mathematical model of AV conduction that incorporates dual AV nodal pathway physiology. Experiments were performed on five rabbit atrial-AV nodal preparations to develop and test the presented model. His electrogram alternances from the inferior margin of the His bundle were used to identify fast and slow wave front propagations. The ability to predict AV conduction time and the interaction between FP and SP wave fronts have been analyzed during regular and irregular atrial rhythms (e.g., atrial fibrillation). In addition, the role of dual AV nodal pathway wave fronts in the generation of Wenckebach periodicities has been illustrated. Finally, AV node ablative modifications have been evaluated. The model accurately reproduced interactions between FP and SP during regular and irregular atrial pacing protocols. In all experiments, specificity and sensitivity higher than 85% were obtained in the prediction of the pathway responsible for conduction. It has been shown that, during atrial fibrillation, the SP ablation significantly increased the mean HH interval (204 ± 39 vs. 274 ± 50 ms, P < 0.05), whereas FP ablation did not produce significant slowing of ventricular rate. The presented mathematical model can help in understanding some of the intriguing AV node mechanisms and should be considered as a step forward in the studies of AV nodal conduction.     

Normalisation of the ECG in a patient with right bundle branch block by cardiac pacing

Right ventricular apical pacing (RVA) appears to have potential deleterious effects on myocardial systolic and diastolic left ventricular function, especially in patients with intact AV conduction. Therefore, new pacing sites in the right ventricle are being explored to overcome these detrimental effects. Alternative pacing sites in the right ventricle are the right ventricular outflow tract (RVOT) and the right ventricular septum (RVS). In this case report, we demonstrate an exceptional form of ventricular fusion, namely normalisation of the QRS complex in a patient with pre-existing right bundle branch block by RVS pacing. To our knowledge, this is the first report in the literature where right ventricular pacing could restore a complete RBBB to a normal QRS complex by stimulating distally from the anatomical position of the RBBB, due to fusion between artificial right ventricular stimulation and intrinsic conduction over the left bundle of the specific His-Purkinje system.     

降钙素基因相关肽在豚鼠冠脉血流量和心脏传导系统作用的比较

本文目的在于深入研究降钙素基因相关肽（ＣＧＲＰ）对豚鼠冠状血流量以及心脏传导系统各部分的作用。采用Ｌａｎｇｅｎｄｏｒｆｆ法灌流心脏,同步记录心脏表面电图和希氏束电活动。观察应用ＣＧＲＰ前后的冠脉流量、自主心率、在相同心房周期下的房室结（ＡＨ）及希浦系传导时间（ＨＶ）、心脏出现３：２文氏传导及２：１房室传导阻滞所需的最长起搏周期（ＰＣＬ３：２,ＰＣＬ２：１）。ＣＧＲＰ（３－３０ｎｍｏｌ／Ｌ）可显著增     

Phasic influences of vagal stimulation on atrioventricular conduction

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.