76例育龄女性胸腔积液病因结构及临床特点分析

目的了解育龄女性胸腔积液的病因结构及临床特点。方法回顾我院76例育龄女性胸腔积液的临床资料,分析其病因结构并分组（结核组、狼疮组、肿瘤组及混合组）,对比各组胸腔积液的临床特征,包括症状、血液及胸水生化。结果育龄女性胸腔积液以结核性为主（40.7%）,其次为狼疮性（19.7%）;不同病因的主要伴随症状有所不同;各组的血浆球蛋白浓度及C反应蛋白水平均无明显差异（P〉0.05）;结核组胸水ADA值明显高于其他病因组（P〈0.01）,狼疮组胸水ANA水平显著高于其他病因组（P〈0.05）。结论育龄女性的胸腔积液以结核性为主,其次为狼疮性,伴随症状、胸液ADA及ANA水平对病因鉴别诊断有一定帮助。     

外源性棕榈酸减轻儿茶酚胺和血管紧张素II共同介导的大鼠乳鼠心肌细胞损伤机制的初步探讨

目的:初步探讨棕榈酸减轻儿茶酚胺和血管紧张素II共同介导的心肌细胞损伤的可能机制,以及外源性棕榈酸的心脏保护作用。方法:培养原代大鼠乳鼠心肌细胞,随机分为:正常对照组(Control),药物损伤组[进一步分为低(LDC),中(MDC),高(HDC)三种药物浓度]组和棕榈酸保护组(对照组及三种药物浓度组分别加入0.3 mmol/L棕榈酸Palmic acid,PA),通过倒置显微镜和苏木精-伊红(hematoxylin-eosin,HE)染色观察细胞形态学变化,测量心肌细胞表面积。噻唑兰(MTT)法检测心肌细胞活力,采用高效液相色谱法测定心肌细胞总ATP含量,全自动生化分析仪测定心肌细胞培养液中乳酸脱氢酶释放量。结果:与药物组相比,棕榈酸保护组细胞损伤减轻,乳酸脱氢酶(LDH)释放减少,达到形态学改善,心肌细胞存活率及细胞内三磷酸腺苷(ATP)含量升高。结论:儿茶酚胺和血管紧张素II可共同介导心肌细胞损伤,机制可能与药物作用使细胞耗氧量增加,能量代谢障碍,细胞内ATP含量下降有关。一定浓度的棕榈酸可增加代谢底物,提高心肌细胞内ATP含量,保护心肌细胞。     

Association of G22A and A4223C ADA1 gene polymorphisms and ADA activity with PCOS

Adenosine deaminase-1 (ADA1) regulates the concentration of adenosine as the main modulator of oocyte maturation. There is compelling evidence for the association of ADA1 gene polymorphisms with many diseases but the importance of ADA1 polymorphisms in polycystic ovary syndrome (PCOS) has not been studied before. This study investigates serum total ADA activity (tADA), ADA1 and ADA2 isoenzyme activities, and genotype and allele frequencies of G22A and A4223C polymorphisms in healthy and PCOS women. In this case-control study 200 PCOS patients and 200 healthy women were enrolled. Genomic DNA was extracted from whole blood and the PCR-RFLP technique was used to determine the G22A and A4223C variants. The genotype frequencies were calculated and the association between polymorphic genotypes and enzyme activities were determined. tADA activity was significantly lower in the PCOS group compared with the control group (27.76±6.0 vs. 39.63±7.48, respectively). PCOS patients also showed reduced activity of ADA1 and ADA2. PCOS was not associated with G22A polymorphism whereas AA, AC, and CC genotypes of A4223C polymorphism were found distributed differently between the control and the PCOS women where the C allele showed a strong protective role for PCOS (odds ratio=1.876, p=0.033). The present study for the first time showed that lower ADA activity may be involved in pathogenesis of PCOS by maintaining a higher concentration of adenosine affecting follicular growth. As a novel finding, we also showed great differences in genotype distribution and allele frequencies of A4223C polymorphism between groups indicating a protective role for C allele against PCOS.

AbbreviationsADA: adenosine deaminase PCOS: polycystic ovary syndrome PCR-RFLP: polymerase chain reaction–restriction fragment length polymorphism tADA: total adenosine deaminase     

药物负荷核素心肌灌注显影对冠心病的诊断价值

目的探讨药物负荷核素心肌灌注显像（MPI）对冠心病的诊断价值。方法回顾性分析88例疑有冠心病且同时行冠状动脉造影（CAG）和双嘧达莫或腺苷药物负荷核素MPI患者,CAG与MPI检查日期相差不超过14 d,以CAG检查结果作为诊断冠心病的金标准,对比分析药物负荷核素MPI敏感度、特异性等指标。结果药物负荷核素MPI诊断冠心病的敏感度、特异性、准确率分别为91.4%、73.3%、85.2%;在5例假阴性患者中,4例为单支病变,1例为双支病变,侧支循环均良好;8例假阳性患者中,3例为X综合征,4例为冠状动脉血流缓慢。结论药物负荷核素心肌灌注显像是无创诊断冠心病及心肌缺血的有效途径,其假阳性和假阴性患者多有相应的冠状动脉或心肌的病理生理基础。     

Tuberculous Pleural Effusion

Tuberculous pleural effusion (TBPE) is the most common form of extrapulmonary tuberculosis (TB) in Spain, and is one of the most frequent causes of pleural effusion. Although the incidence has steadily declined (4.8 cases/100 000 population in 2009), the percentage of TBPE remains steady with respect to the total number of TB cases (14.3%–19.3%). Almost two thirds are men, more than 60% are aged between 15 and 44 years, and it is more common in patients with human immunodeficiency virus. The pathogenesis is usually a delayed hypersensitivity reaction. Symptoms vary depending on the population (more acute in young people and more prolonged in the elderly). The effusion is almost invariably a unilateral exudate (according to Light's criteria), more often on the right side, and the tuberculin test is negative in one third of cases.There are limitations in making a definitive diagnosis, so various pleural fluid biomarkers have been used for this. The combination of adenosine deaminase and lymphocyte percentage may be useful in this respect. Treatment is the same as for any TB. The addition of corticosteroids is not advisable, and chest drainage could help to improve symptoms more rapidly in large effusions.     

三磷酸腺苷促进肌源性干细胞增殖的作用及机制研究

目的 研究三磷酸腺苷(ATP)促进肌源性干细胞(MDSCs)增殖的作用机制.方法 采用差速贴壁法分离出小鼠MDSCs,将细胞分为两组:实验组(100 μmol/L ATP)和对照组,观察MDSCs的生长情况,用流式细胞仪检测细胞周期,RT-PCR检测MDSCs中ATP受体的表达.结果 ATP作用3d后,实验组的细胞数显著多于对照组.与对照组相比,实验组的G1％(处于G1期的细胞百分率)降低,S％(处于S期的细胞百分率)和PrI值(增殖指数)升高.实验组MDSCs各亚周期(G1期、S期和G2M期)时间分别为21.5 h、4.4h和10.8 h,对照组MDSCs各亚周期时间分别为27.1h、9.6h和13.5 h.与对照组相比,实验组细胞G1期和S期明显缩短.ATP作用后,小鼠MDSCs中P2Y1受体表达显著升高,在3d时达到最高水平,之后开始下降,但仍然维持高水平.结论 ATP上调MSCs中P2Y1受体的表达,缩短G1期和S期,促使细胞从G1期进入S期,从而刺激MDSCs增殖.     

Adenosine-sensitive atrial tachycardia originating from the proximal coronary sinus

BACKGROUND: Atrial tachycardia (AT) can originate from the proximal coronary sinus (CS). However, detailed electrophysiologic characteristics of the tachycardia are not available. OBJECTIVES: We describe the electrophysiologic characteristics, response to adenosine 5'-triphosphate, and results of radiofrequency ablation of AT with the earliest activation in the proximal CS. METHODS: In 7 of 54 patients (age 57 +/- 18 years) with nonmacroreentrant "focal" AT undergoing electrophysiologic study and radiofrequency ablation, the earliest atrial activation site was located in the proximal CS. RESULTS: The earliest activation site was inside the CS 13 +/- 3 mm from the ostium. The AT could be induced and terminated by atrial extrastimuli or burst pacing. In all patients, the AT was also terminated by a very small dose of adenosine 5'-triphosphate (4.2 +/- 1.1 mg). Rapid ventricular pacing during the tachycardia produced ventriculoatrial dissociation. Radiofrequency ablation directed at the earliest atrial activation site was effective in only three patients (group A). In the remaining four patients (group B), after the radiofrequency energy deliveries, the earliest activation site shifted to an adjacent site with a small increase in the cycle length. Three group B patients underwent successful ablation in the slow pathway region. No recurrence was observed over a follow-up period of 22 +/- 5 months. CONCLUSION: AT with earliest activation in the proximal CS is sensitive to a small dose of adenosine 5'-triphosphate. In some patients, radiofrequency applications in the slow pathway region are effective even if the local activation is not early.     

腺苷对猪急性心肌梗死再灌注后无再流的影响

目的评价腺苷防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪24只随机分成对照组、腺苷组(100μg·kg-1·min-1持续静点)和假手术组,每组8只。前2组行冠状动脉结扎3h,松解1h建立AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定和心肌声学造影检查,最终行病理学分析。结果(1)与AMI前相比,对照组AMI后3h主动脉收缩和舒张压、左室收缩压、心排量和左室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05～0.01),肺毛细血管楔压和左室舒张末压均显著升高(P<0.01);再灌注后1h仅左室舒张末压显著恢复(P<0.05)然而±dp/dtmax继续显著下降(P<0.05);而腺苷组AMI后3h各项指标变化与对照组相同;但再灌注后1h左室收缩压、左室舒张末压、±dp/dtmax和心排量均显著恢复(P均<0.05),且比对照组更显著(P均<0.05)。(2)对照组心肌声学造影和病理染色所测的冠状动脉结扎区心肌范围高度一致,再灌注后无再流面积分别为67.5%和69.3%,心肌坏死面积(NA)占结扎区心肌面积(LA)的98.5%;而腺苷组LA均与对照组相当,但两方法所测无再流面积仅分别为21.5%和20.8%,NA仅为75.2%,均显著小于对照组(P<0.05～0.01)。(3)对照组再灌注即刻和再灌注后1h冠状动脉血流量仅占AMI前的45.8%和50.6%(P均<0.01),而腺苷组冠     

冠状动脉慢血流与心肌缺血的关系

目的:通过腺苷负荷心肌灌注显像(SPECT),评价冠状动脉慢血流现象(CSF)与心肌缺血的关系。方法:选择经冠状动脉造影(CAG)诊断为CSF者20例,CAG显示无管腔狭窄及无慢血流者20例为对照组。使用校正的TIMI血流分级(CTFC)方法评价冠状动脉血流速度,2组均行心电图及腺苷负荷SPECT检查。结果:CSF者发生心电图及腺苷负荷SPECT异常的例数比对照组明显增多,同时心肌缺血的范围与缺血程度也均大于血流正常者(P<0.01)。结论:腺苷负荷SPECT发现CSF存在可逆性心肌缺血,可能CSF与心肌缺血关系密切。     

DeltaPKC-mediated activation of epsilonPKC in ethanol-induced cardiac protection from ischemia

Previous studies have demonstrated that acute ethanol exposure induces activation of delta protein kinase C (deltaPKC) and epsilonPKC, and mimics ischemic preconditioning via epsilonPKC activation. However, the role of deltaPKC isozyme in ischemia and reperfusion is still controversial. Here, we investigated the role of deltaPKC in ethanol-induced cardioprotection using a selective deltaPKC activator (psideltaRACK), or inhibitor (deltaV1-1), and a selective epsilonPKC inhibitor (epsilonV1-2) in isolated mouse hearts. Mice were injected intraperitoneally or by gavage with ethanol, regulators of delta and epsilonPKC or an adenosine A1 receptor blocker (DPCPX). Isolated perfused mouse hearts were subjected to a 30-min global ischemia and a 120-min reperfusion, ex vivo. Injection of 0.5 g/kg ethanol 1 h, but not 10 min, before ischemia reduced infarct size and CPK release. Pretreatment with epsilonV1-2 abolished this ethanol-induced cardioprotection. Pretreatment with deltaV1-1 induced cardioprotection when injected with ethanol (0.5 g/kg) 10 min before ischemia, but deltaV1-1 partly inhibited ethanol-induced cardioprotection when injected with ethanol 1-h before the onset of ischemia. psideltaRACK injection 1 h, but not 10 min, before ischemia induced cardioprotection and translocation of epsilonPKC from the cytosol to the particulate fraction. Pretreatment with DPCPX or epsilonV1-2 inhibited psideltaRACK-induced cardioprotection and translocation of epsilonPKC. Therefore, activation of deltaPKC-induced by ethanol or by the deltaPKC activator is cardioprotective, provided that sufficient time passes to allow deltaPKC-induced activation of epsilonPKC, an A1 adenosine receptor-dependent process.