脑缺血再灌注损伤的炎症反应机理研究进展

脑缺血再灌注损伤过程包含一系列复杂的病理生理变化,各因素之间又相互影响.本文就近年来备受关注的炎症反应机理做一综述.     

蚓激酶与奥扎格雷钠合用治疗脑梗死60例临床观察

蚓激酶是从中药蚯蚓中提取的一组蛋白水解酶,可以使纤维蛋白原降低,K PTT延长,全血黏度降低。奥扎格雷钠为一种高效、选择性血栓素合成酶抑制剂,具有抗血小板聚集和扩张血管作用。二者合用治疗脑梗死,具有很好的临床效果。1.临床资料1.1病例选择病例选择均为2001年5月至2002年5月在沧州市中心医院住院的急性脑梗死患者60例,均经头颅CT证实。分为治疗组30例,男性15例,女性15例,年龄45岁至70岁之间。对照组30例,男性17例,女性13例,年龄45岁至68岁之间。二组病人病情程度、发病和给药时间基本相同,经统计学计算具有可比性。1.2治疗方法治疗…     

大鼠肺炎链球菌脑膜炎病理机制及干预措施的初步研究

细菌性脑膜炎是儿科常见的中枢神经系统感染性疾病，肺炎链球菌脑膜炎是我国最常见的化脓性脑膜炎之一，也是导致神经系统后遗症的主要病原菌。基质金属蛋白酶(metalloproteinase，MMP)系(MMPs)是一组锌依赖的蛋白水解酶，具有降解多种细胞外基质成分的功能，生理状态下，MMPs主要参与组织发育、伤口愈合、骨生长及血管生成等；病理条件下，MMPs则能促进许多疾病的发生、发展，如肿瘤的侵袭和转移，动脉粥样硬化及多发性硬化、阿尔茨海默病、恶性胶质瘤等中枢神经系统疾病。     

术后病人疼痛护理

1疼痛的病理生理机制 感觉神经系统内部存在着疼痛的知觉感受器，痛信号传导神经及疼痛中枢整合释放痛信号的感受器，痛信号传导神经及疼痛中枢整合释放痛信号的组织结构，痛觉感觉器即游离神经末梢遍及全身，这种感受器能感受机械性刺激及某些化学物质刺激，如缓激肽5-羟色胺、蛋白水解酶等，这些刺激神经纤维传至感觉神经、然后尚脊髓丘脑束传至大脑感觉中枢，经分辨及处理整合后形成痛沉。     

基础医学

20060701高原地区健康老年人同型半胱氨酸水平与血管内皮细胞功能的相关性/阿祥仁…∥中华老年医学杂志·-2006,25(2)·-123~124老年组50例,非老年组50例,血清同型半胱氨酸(Hcy)分别为17·7±4·3和14·2±5·4(μmol/L,ELISA法),P<0·01。老年组血清中Hcy与可溶性血管内皮细胞     

菌斑蛋白水解酶的分离纯化及活性测定

为了解人牙根面菌斑中蛋白水解酶的种类和活性。采用ＳｅｐｈａｄｅｘＧ－２００层析技术和荧光分光光度法对收集和菌斑中的蛋白水解酶进行了分离纯化及活性测定。结果发现，亮氨酸氨肽酶和甘氨酰脯氨酸二肽酶和胰酶样蛋白酶存在于根面菌斑中，且均有一定的活性。     

氟对大鼠软骨丝氨酸蛋白水解酶活性的影响

目的；研究慢氟中毒大鼠软丝氨酸蛋白水解酶（ＳＰＥ）活性的变化。方法：用不同饲料喂养大白鼠，测定软骨中的ＳＰＥ活力。结果：偏食大鼠在饮用含２００ｐｐｍ的氟化钠水１０周后，股骨头软骨和肋软骨中ＳＰＥ蛋白水解酶活力仅显著高于正常膳食和饮氟水组；而与单纯偏食组比较无显著差异。两个偏食组动物软骨中ＤＮＡ含量高于两个正常膳食组，但饮氟水未能使软骨中的ＤＮＡ含量改变。结论：高氟可能提高营养不良鼠软骨中的ＳＰＥ活     

高苯丙氨酸对神经元Rho GTPases基因体外表达的研究

采用实时荧光定量聚合酶链反应(RT-PCR)方法,观察高苯丙氨酸对神经元Rho GTPases主要家族成员Racl、Cdc42、RhoA mRNA体外表达的影响,并进一步研究脑源性神经营养因子(BDNF)对它们的作用,探寻高苯丙氨酸导致神经损伤的可能机制及BDNF在体外对神经损伤的保护机制。     

小儿支气管哮喘与血小板活化因子乙酰水解酶的相关性研究

为探讨血浆血小板活化因子乙酰水解酶(PAF-AH)基因多态性与我国哮喘儿童的相关性及其多态性与血浆PAF-AH酶活性的关系,我们于2001年10月至2003年3月。应用等位基因特异性聚合酶链式反应(AS—PCR)技术,对哮喘发作期儿童PAF-AH第9外显子上G994-T基因位点的突变进行了检测,同时应用酶水解底物显色法检测血浆PAF-AH活性。现报告如下。     

Relationship between polymorphisms of genes encoding microsomal epoxide hydrolase and glutathione S-transferase P1 and chronic obstructive pulmonary disease

Background Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). However, only 10% -20% of chronic heavy cigarette smokers develop symptomatic disease. COPD is most likely the result of complex interactions between environmental and genetic factors. Genetic susceptibility to COPD might depend on the variations in enzyme activities that detoxify cigarette smoke products, such as microsomal epoxide hydrolase (mEH) and glutathione Stransferase (GST). In this study, we investigated the relationship between polymorphisms in the genes encoding mEH and glutathione S-transferase P1 (GSTP1) and COPD in a Chinese population.Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to find mEH polymorphism in exon 3 (Tyr113→His), exon 4 (His139→Arg) and GSTP1 polymorphism in exon 5 (Ile105→Val) in 100 COPD patients and 100 age- and sex-matched healthy controls.Results The proportion of mEH exon 3 heterozygotes was significantly higher in patients with COPD than that in the control subjects (42% vs 32% ). The odds ratio (OR) adjusted by age, sex, body mass index (BMI) and cigarette years was 2.96 (95% CI 1.24 - 7. 09). There was no marked difference in very slow activity genotype versus other genotypes between COPD patients and the controls. When COPD patients were non-smokers, the OR of very slow activity genotype versus other genotypes was more than 1.00; and when COPD patients were smokers ( current smokers and exsmokers), the OR was less than 1.00. There was no significant difference in GSTP1 polymorphism adjusted by age, sex, BMI and smoking between COPD patients and the controls.Conclusions mEH exon 3 heterozygotes might be associated with susceptibility to COPD in China.The interaction might exist between mEH genotype and smoke. The gene polymorphism for GSTP1 might not be associated with susceptibility to COPD in the Chinese population.