超声心动图与心电图判定左室心肌梗塞部位和范围对比研究

目的:比较二维超声心动图(2DE)和心电图(ECG)对心肌梗塞(MI)定位诊断的异同、优劣。方法:对59例 MI 患者进行了2DE 和 ECG 检查。在2DE 上将左室分为16个节段而分别确定与 ECG 各导联的对应关系,分别计数2DE 上室壁运动异常(WMA)节段数和 ECG 上有异常 Q 波导联所对应节段数,对比分析两种方法检查结果的一致性。结果:2DE 和 ECG 分别检出338和311个节段阳性,两种方法阳性一致率57.9%,两种方法阳性一致率在各壁的高低依次为下壁、前壁、后壁、前间隔、侧壁;两种方法检测结果的差别有显著性(P<0.05);两种方法检测结果的相关系数 r=0.595(P=0.0000)。结论:两种方法的检查结果有较好的一致性,2DE 优于 ECG。     

黄芪、小柴胡冲剂联合辅酶Q10治疗病毒性心肌炎

目的观察黄芪、小柴胡冲剂联合辅酶Q10治疗病毒性心肌炎(VMC)的临床疗效.方法治疗组(30例)应用黄芪注射液、小柴胡冲剂和辅酶Q10;对照组(30例)用GIK极化液、辅酶Q10和维生素C,两组患者无禁忌证者均给予β-受体阻滞剂,钙拮抗剂和对症治疗.两组疗程均为3个月.结果治疗组临床症状和心律失常总有效率分别为73.3%和86.6%,高于对照组的43.3%和63.3%(p＜0.05).结论黄芪、小柴胡冲剂联合辅酶Q10对VMC有较好疗效,且无明显不良反应.     

体表电位标测微机系统(Ⅰ型)

本系统的107个电极中,103个分布于胸、背部,1个为参考电极,1个为V_3,其余用于肢导。本系统除能绘出2、4、8ms任意间隔的103通道同步的体表等电位图,常规12导联和V_(7 9)心电图,胸、背部位的心电图外,还可记录R峰值等电位图,∑R,Q波等电位图,nQ30、40,极大、极小轨迹图等。     

辅酶Q10对大鼠阿霉素心脏毒性的保护作用

目的：研究辅酶Q10（CoQ10）对大鼠阿霉素心脏毒性的保护作用，并探讨可能的机理。方法：采用离体心脏灌流方法，实验分3组：对照组、阿霉素组、CoQ10组，监测大鼠心肌收缩幅度、冠脉流量、心电图的变化，并测定冠脉流出液肌酸磷酸激酶（CPK）活力和大鼠心肌丙二醛含量、超氧化物歧化酶、谷胱甘肽过氧化物酶（GSH-Px）活力以及电镜下超微结构的改变。结果：CoQ10可改善阿霉素引起的大鼠心肌收缩幅度、冠脉流量下降，减少心律失常的发生，降低冠脉流出液CPK活力；CoQ10组心肌丙二醛含量明显低于阿霉素组、SOD和GSH-Px活力高于阿霉素组，电镜下超微结构变化亦优于阿霉素组。结论：CoQ10对阿霉素引起的心脏毒性具有保护作用，其机理可能与CoQ10拮抗阿霉素的氧自由基损伤有关。     

儿童虐待史问卷的信度效度分析

目的引入儿童虐待史问卷(CECA.Q),并对它进行初步的信度、效度分析.方法对308例某一社区人群和60例抑郁症患者人群进行了CECA.Q测试,分析CECA.Q的内部一致性,重测信度,内容及校标效度.结果 CECA.Q的精神虐待部分的Cronbach's α系数为0.97(其中母亲为0.96,父亲为 0.94),其中憎恶因子为0.93(其中母亲为0.90,父亲为0.88),忽视因子为0.97(其中母亲0.96,父亲 0.95).精神虐待的重测信度0.82(其中母亲0.80,父亲0.83),其中憎恶因子为0.80(其中母亲为0.80,父亲为 0.67),忽视因子为0.78(其中母亲0.75,父亲0.77);躯体及性虐待的两次测评的一致性好(Kappa值为 0.78).精神虐待分值与抑郁自评量表 (SDS)分值正相关(r=0.61,P ＜0.01),CECA.Q与儿童虐待史晤谈评定提纲(CECA)评定躯体及性虐待史的一致性好(Kappa值为0.87),抑郁症患者的精神虐待分值高于社区人群的精神虐待分值(P ＜0.05).结论儿童虐待史问卷具有较好的信、效度,在我国也可作为回顾性儿童虐待史筛选调查的自评工具.     

我国河南汉族正常人群凝血因子VII基因MspⅠ多态性观察

目的 研究我国汉族正常人群凝血因子Vll基因MspI多态性的分布特点.方法 利用聚合酶链反应-限制性内切酶片段长度多态性(PCR-RFLP)技术,分析560名河南汉族正常人群凝血因子VII(FVII)基因R353Q突变的分布情况.结果 我国河南汉族正常人群FVII基因R353Q的RR,RQ,QQ,基因型频率分别是0.864,0.132,0.004;R,Q等位基因频率分别是0.930,0.070;与国外其他种族相比,基因型及等位基因频率与日本人差异无统计学意义(χ2=2.475,P＞0.05χ2=0.000,P＞0.05);RQ及QQ基因型明显低于意大利人,差异具有统计学意义(χ2=38.536,P＜0.01;χ2=16.311,P＜0.01);Q等位基因明显低于意大利人,差异具有统计学意义(χ2=50.228,P＜0.01).结论 我国河南汉族正常人群FVII基因R353Q突变的基因型分布不同于国外其它种族,具有种族或地域的差异.     

AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)‐activated protein kinase (AMPK)‐activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol‐3‐phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5‐aminoimidazole 4‐carboxamide‐riboside (AICAR), further indicating that the exercise‐induced alterations in these enzymes were AMPK‐mediated. Conclusions: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post‐exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

Atypical respiratory pathogens

The main atypical pathogens in respiratory tract infections are classified on the basis of their ability to cause atypical pneumonia. This is not a well-defined clinical entity, and it is evident that atypical pathogens can sometimes cause 'typical' pneumonias and vice versa. This emphasizes the need for microbiological diagnosis, since it affects the selection of proper treatment, in which β-lactam antibiotics and aminoglycosides are not effective. Moreover, mixed infections caused by atypical and typical pathogens together are common. At this moment rapid and sensitive diagnostic methods are lacking. Besides numerous viruses, the main bacterial pathogens causing atypical pneumonias are Mycoplasma pneumoniae , two chlamydia species. Chlamydia pneumoniae and C. psittaci , one rickettsia, Coxiella burnetti , and several Legionella species. The majority of these pathogens cause upper respiratory tract infections more often than overt pneumonias. An atypical agent, Chlamydia pneumoniae , has also been associated with chronic inflammatory conditions in the cardiovascular system. The most recently discovered pathogen in atypical pneumonias is a hantavirus causing hantavirus pulmonary syndrome.