Correlation between platelet gelsolin levels and different types of coronary heart disease

Gelsolin is an important cytoskeletal protein of platelets and studies have shown a close relationship between gelsolin and cardiovascular disease.However,the role of gelsolin in the development of coronary heart disease(CHD) is unclear.In this study,we record the distribution of gelsolin in human platelets and plasma and its association with different types of CHD.This study included 114 cases,with 33 stable angina pectoris(SAP) cases,81 acute coronary syndrome(ACS) cases—composed of 39 unstable angina pectoris(UAP) and 42 acute myocardial infarction(AMI) cases,and 31 healthy control participants.Gelsolin concentration in platelet rich plasma(PRP) and platelet poor plasma(PPP),actin filament(F-actin) and Gc-globulin of PPP were determined by enzyme-linked immunoadsorbent assay(ELISA).The fluorescence intensity of CD62p and cytoplasmic calcium([Ca2+] i) in human platelets measured by flow cytometry.We also used turbidimetry to detect the platelet aggregation rate(PAR).We analyzed the correlation between platelet gelsolin concentration and CD62p or plasma F-actin levels among each different patient group.Compared with the control group,the gelsolin level in PRP of UAP and AMI groups increased significantly(P<0.01),while the gelsolin level in PPP of all the three patient groups decreased markedly(P<0.01),and the CD62p,PAR,[Ca2+] i of platelets,F-actin and Gc-globulin of the UAP and AMI groups increased significantly(P<0.01).Compared with the SAP group,the gelsolin level in PRP,the PAR,[Ca2+] i of platelets and CD62p of other two groups increased significantly(P<0.01),F-actin of the AMI group increased markedly(P<0.01).Platelet cytoskeleton protein dynamics vary among the different types of CHD.Platelet gelsolin levels are markedly increased and accompanied by increased platelet activity,F-actin and [Ca2+] i of ACS patients,while gelsolin levels in PPP are markedly lower.Abnormally increased platelet gelsolin levels show high positive correlation with the level of platelet activity.Therefore,platelet gelsolin might be a novel molecular marker and/or a new potential therapeutic target of anti-platelet therapy of ACS.     

速度向量成像技术对代谢性疾病心功能的研究

速度向量成像技术（VVI）为近年来发展起来的比较热门的新型超声技术,是一种能够定量评价心脏功能的无创性检查,能形象、直观地显示心脏室壁运动在纵向、径向和环向上的运动特征,还能够定量、准确和快速评价心肌运动的协调性。VVI可为早期的心脏功能受损提供可靠依据,在糖尿病性心脏病、尿毒症性心脏病、甲状腺功能亢进症性心脏病这些代谢性心肌病中,根据其应变率与应变的变化,有助于心肌病的早期诊断与疗效观察。因此．本文就速度向量成像在代谢性心脏病中的心功能方面进行研究。     

重大传染病防治研究领域专利分析 ——以登革热为例

重大传染病严重危害着人类的健康,其中登革热是当今世界流行性最广的蚊媒病毒性传染病,它涉及世界100多个国家和地区,造成每年约3.9亿人感染。针对当前国际和国内登革热的研究现状,从专利分析角度,对其中的专利申请态势、技术构成、主要申请国、主要发明人等都进行了详细的阐述,并深入探究该领域的研究热点和预期的未来走向,本文有利于推进我国在登革热防治工作上的进步与发展。     

空气污染对手足口病传播的短期影响效应研究——以温州市为例

基于温州市手足口病2014—2017年周发病数据及同期空气质量数据,建立了广义加性模型,研究了空气污染对周发病数影响的短期效应.结果表明,4种空气污染物SO_2、CO、NO_2和O_3对手足口病周发病数的影响显著且存在滞后效应,滞后期均为1周.单污染物模型显示,SO_2、CO和NO_2这三种气态污染物都是手足口病发病的危险因素,在滞后1周时周平均浓度每增加1μg/m3SO_2、1 mg/m3CO、1μg/m3NO_2,手足口周发病数将分别增加2.8%、43.8%、0.9%;而O_3在滞后1周时周平均浓度每增加1μg/m3,手足口周发病数将减少0.4%.在SO_2、CO、NO_2和O_3组成的11种多污染物模型中,依据QAIC最小原则选出最优模型为双因素SO_2+CO模型.研究结果将为手足口病的防控提供科学依据.     

定量蛋白质组学及其在颅内动脉瘤中的研究进展

 颅内动脉瘤（IA）是颅内动脉壁的某一部分因病变而向外突出所形成的永久性扩张,是造成蛛网膜下腔出血的首位病因。定量蛋白质组学,作为新近出现的一种崭新的研究手段,为治疗颅内动脉瘤提供了新的研究思路。通过同位素标记相对和绝对定量（iTRAQ）技术及二维液相色谱-串联质谱（2D-LC-MS/MS）法筛选动脉瘤壁差异表达蛋白质,为动脉瘤形成和破裂的分子机制研究提供了帮助。本文综述了颅内动脉瘤的研究进展以及定量蛋白质组学技术在颅内动脉瘤研究中的应用。     

阿尔茨海默症发病机制及治疗方法研究进展

 阿尔茨海默症（Alzheimer's disease,AD）是以β淀粉样蛋白斑块及神经元纤维缠结为主要病理特征的神经退行性疾病,是痴呆中最常见的一种,也是一种常见的老年人疾病。AD的发病机制可能由多种发病因素、多种通路和分子机制的相互参与引起。由于AD的发病主要同老年人有关,故研究治疗AD的方法对于提高人类健康和生活水平至关重要。虽然目前并没有一种治疗方法可以完全治愈AD,但有多种治疗策略。本文对AD的发病机制及治疗方法的研究进展进行简要综述。     

冠心病患者头发锌铜硒等微量元素测定

应用催化极谱法分析34例冠心病患者头发中铜、锌、锰、硒及铬的含量,并与30例年令相近的健康成人对照,结果冠心病患者头发中微量元素铜含量高于对照组,硒、锰及铬的含量明显低于对照组,(p值<0.01)两组间有显著性差异,认为体内微量元素铜高,低硒、低锰、低铬可能与冠心病有关。     

"鸭传染性肿头症"病毒的分离及部分特性研究

成都地区鸭场中流行一种以发病鸭头颈肿胀为特征的传染病,发病率、死亡率均可达到80％以上,各种年龄、品种均易感,危害十分严重,我们通过流行这调查、血凝和血凝抑制试验、中和试验和临床防治试验排除了鸭瘟病毒、禽流感病毒、鸭肝炎病毒、番鸭细小病毒感染的可能性,从典型病例中分离出病毒,在雏鸭上复制出与自然发病相同的病例;电镜下观察了该病毒为圆形或卵圆形,大小为50－70nm,无囊膜;对氯仿有抵抗,对鸭胚的LD50为8．67,无血凝性,初步认为本病是一种新鸭病,暂定名为“鸭传染性肿头症”。     

Molecular basis of autosomal-dominant polycystic kidney disease

Autosomal-dominant polycystic kidney disease (ADPKD) is one of the most common monogenetic diseases in humans. The discovery that mutations in the PKD1 and PKD2 genes are responsible for ADPKD has sparked extensive research efforts into the physiological and pathogenetic role of polycystin-1 and polycystin-2, the proteins encoded by these two genes. While polycystin-1 may mediate the contact among cells or between cells and the extracellular matrix, a lot of evidence suggests that polycystin-2 represents an endoplasmic reticulum-bound cation channel. Cyst development has been compared to the growth of benign tumors and this view is highlighted by the model that a somatic mutation in addition to the germline mutation is responsible for cystogenesis (two-hit model of cyst formation). Since in vitro polycystin-1 and polycystin-2 interact through their COOH termini, the two proteins possibly act in a common pathway, which controls the width of renal tubules. The loss of one protein may lead to a disruption of this pathway and to the uncontrolled expansion of tubules. Our increasing knowledge of the molecular events in ADPKD has also started to be useful in designing novel diagnostic and therapeutic strategies. Received 12 September 2001; received after revision 7 November 2001; accepted 7 November 2001     

The multifaceted Paneth cell

Paneth cells (PCs) were described over a century ago as granulated cells located at the base of small intestinal crypts, the 'crypts of Lieberkühn.' Various histochemical staining procedures were developed that identified PCs based on their distinctive granule staining pattern. Early on, PCs were proposed to perform a specialized function other than absorption of digested nutrients, the predominant task of the small intestinal epithelium. Since then, many constituents of the PC granules have been biochemically characterized. The presence of various granule-associated antimicrobial substances and their release upon microbial challenge suggest that PCs function as specialized defense cells in the small intestine. Altered resistance to microbial infection in animal models with disrupted or augmented PC function provides further support for the host defense role of PCs. Other PC components suggest that PCs may also participate in the regulation of lumenal ionic composition, crypt development, digestion, and intestinal inflammation. Received 6 June 2001; received after revision 26 July 2001; accepted 27 July 2001