心肌肌钙蛋白I-C复合物酶联免疫检测方法的建立

为了制备抗人心肌肌钙蛋白I(cTnI)单克隆抗体、建立检测人cTnI链酶亲和素-生物素双抗体夹心酶联免疫吸附测定(ELISA)方法,用基因工程表达的人cTnI免疫雌性BALB/c小鼠,以杂交瘤技术制备得到三株特异性抗人cTnI的单克隆抗体记为6G3,6A6,3G9.三株杂交瘤细胞中6G3和6A6为IgG1,3G9为IgG2b,腹水效价分别为4×10-5,4×10-5和10-5.亲和常数为5.0×109,6.4×109和3.8×109mol-1.Westernblotting结果表明6G3和6A6能够识别cTnI-C复合物.把6G3抗体生物素化并制备抗cTnI、cTnC和cTnI-C的大鼠多克隆抗体.以多抗作为固相捕捉抗体,生物素化6G3抗体作为检测抗体,建立检测cTnI的双抗体夹心ELISA方法并初步应用于临床病人标本检测.以cTnI-C复合物多抗捕捉检测方法具有良好的灵敏度、特异性和准确性,灵敏度为0.9ng/mL,较包被其他抗体捕捉方法提高1~2倍.批内变异系数为5.03%,回收率为94.56%.测定17例AMI病人和18例血清样本临床诊断结果符合率为100%.     

Overexpressing dominant negative MyD88 induces cardiac dysfunction in transgenic mice

Myeloid differentiation protein-88 (MyD88) is a crucial adaptor protein in the innate immune response. A protective role for MyD88 in normal cardiac function has been proposed in a surgical hypertrophic model. To assess the in vivo role of MyD88 in cardiac remodeling, we generated transgenic mice with cardiac-restricted expression of a dominant negative mutant of MyD88 (dnMyD88). Surprisingly, dnMyD88 transgenic mice displayed characteristic features of heart failure; including heart weight increase, cardiomyocytes enlargement, interstitial fibrosis, and re-expression of “fetal” genes. Echocardiographic examination of dnMyD88 hearts revealed dilated chamber volume and reduced cardiac contractility. DnMyD88 mice died from heart failure before they were 7 months old, as shown by Kaplan-Meier analysis. Additionally, the heart failure phenotype of dnMyD88 mice was associated with abnormal activation of the Akt/GSK-3β signaling pathway. These data provide the first evidence that normal MyD88 signaling is crucial for maintaining the physiological function of the adult heart.     

生命科学及其相关学科的研究（八）

阐述了含有人凝血因子转基因羊、应用细胞工程及有性杂交法培育异源四倍体鲫鲤鱼、基因对人类思维的作用、转基因植物生产人胰岛素、细胞衰老的决定因素、心肌细胞再生方法及基因工程灭蚊等方面的研究进展。     

Quantitative differences in the pharmacological effects of (+)- and (−)-cathinone

Summary The optically pure isomers of cathinone were prepared by separating synthetic cathinone racemate and used to study central and peripheral effects of these indirect sympathomimetics in rats and guinea pigs. The (–)-isomer was significantly more potent than the (+)-isomer in stimulating locomotor activity whereas no difference was observed with respect to their cardiac effects. In analogy to observations with (+)- and (–)-amphetamine such variable isomer discrimination may be due to different stereoselectivities of amine uptake mechanisms in the target tissues.     

破伤风抗毒素过敏反应二例

破伤风抗毒素（ＴＡＴ）在临床上的使用比较多见，ＴＡＴ皮试引起过敏性休克是过敏反应中最危险的一种，应引起基层医务人员的高度重视。本文报告此类过敏反应二例，并简述在使用ＴＡＴ时，应注意的几个问题     

Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells is mediated through arrest of the cell cycle at the G2-M phase

Elemene is a natural antitumor plant drug. However, the effect of elemene on cell growth in ovarian cancer is unknown. In this study, we show that -elemene inhibited the proliferation of cisplatin-resistant human ovarian cancer cells and their parental cells, but had only a marginal effect in human ovary cells, indicating differential inhibitory effects on cell growth between ovarian cancer cells and normal ovary cells. We also demonstrated for the first time that -elemene markedly enhanced cisplatin-induced growth inhibition in resistant cells compared to sensitive cells. In addition, cell cycle analysis revealed a synergistic effect of -elemene and cisplatin on the induction of cell cycle G2-M arrest in our resistant ovarian carcinoma cells. Furthermore, we showed that treatment of these cells with both drugs downregulated cyclin B1 and Cdc2 expression, but elevated the levels of p53, p21waf1/cip1, p27kip1 and Gadd45. Finally, the combination of -elemene and cisplatin was found to increase the phosphorylation of Cdc2 and Cdc25C, which leads to a reduction in Cdc2-cyclin B1 activity. These novel findings suggest that -elemene sensitizes chemoresistant ovarian carcinoma cells to cisplatin-induced growth suppression partly through modulating the cell cycle G2 checkpoint and inducing cell cycle G2-M arrest, which lead to blockade of cell cycle progression.Received 19 January 2005; accepted 5 February 2005     

中华鳖心肌有限细胞系的建立及其生物学特性

首次对中华鳖的心肌细胞进行了体外原代和传代培养获得成功。并对其细胞形态,生长速率等细胞生物学特性以及温度和ＰＨ值对细胞生长的影响进行了观察研究。     

一种带心肌瘢痕的心脏磁共振图像左室壁分割方法

从心脏磁共振图像中分割出左心室内外膜轮廓线,是心脏三维重建及心脏功能评定的先决条件.针对带心肌瘢痕的心脏磁共振图像,提出了一种基于显著性检测定位的左心室内外膜分割方法.方法采用视觉显著性检测和分水岭变换,提取左心室血池区域,准确确定了左心室位置;然后提取血池区域轮廓线作为内膜初始轮廓,在带形状约束的活动轮廓模型作用下演化得到左心室内外膜.实验结果证明,该方法定位较为准确,能使初始轮廓迅速收敛到内膜边界,分割得到的内外膜以及心肌区域均较为准确.     

Effect of wortmannin and 3-AB on G2 phase arrest and transient failure to activate MPF induced by ionizing irradiation

Active mitosis promoting factor (MPF) composed of p34 cdc2 with cyclin B1 is required for the cell cycle transition from G 2 to M phase. Recent studies have demonstrated that ionizing radiation (IR) exposures associated with inhibition of p34 cdc2 activity was the mechanism of G 2 arrest. At low dose, IR causes transient failure to dephosphorylate p34 cdc2 instead of suppression of cyclin B or MPF formation of cyclin B with p34 cdc2 complex. But the signaling events that regulate p34 cdc2 in irradiated cells remain unclear. This note demonstrates that PI3 kinase family inhibitor wortmannin (wort) and PARP specific inhibitor 3_AB can reduce the G 2 arrest induced by 2Gy γ_ray. Immunoprecipitation studies demonstrate that wort and 3_AB can facilitate dephosphorylation of p34 cdc2 in G 2 phase arrest induced by radiation. These findings suggest that wort sensitive pathway and PARP may be involved in initiating the signal transduction of G 2 phase arrest caused by IR.     

心功能自动检测系统的设计

给出了微型计算机无创检测心脏期、舒张期及心输出量的整体方案，检测信号为导纳心动微分信号、心电信号、心音信号及颈动脉波信号。