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2.
心脏具有重要的内分泌功能,它能感受心房和心室的压力,通过分泌多种利钠肽作用于肾脏、血管、心肌,并调节其他内分泌功能,在左室功能不全(LVD)的早期可减慢疾病的进展。近年来研究表明,氧化低密度脂蛋白自身抗体(OLAB)、脑钠肽(BNP)、高敏C-反应蛋白(CRP)在急性心肌梗死(AMI)、不稳定型心绞痛(UAP)的发病过程中可能是导致局部炎症反应和血栓形成的重要因素[1]。关于BNP检测在充血性心衰的早期诊断、不明原因呼吸困难的鉴别诊断、心衰的预后判断和治疗监测中的意义已有大量报道,许多临床试验证明了BNP也能为急性冠脉综合征(ACS)… 相似文献
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目的 研究细胞周期依赖性蛋白激酶5(cyclin dependent kinases 5,CDK5)在耐药性癫(癎)患者颞叶中的表达,探索其在耐药性癫(癎)发病机制中的作用.方法 收集耐药性癫(癎)患者术后脑组织,用荧光定量PCR、免疫组化和Western blot 3种检测方法从基因和蛋白水平分别测定CDK5在耐药性癫(癎)患者颞叶中的表达,并与对照组进行比较.结果 荧光定量PCR发现CDK5 mRAN比对照组明显增加,免疫组化检测显示这种基因的蛋白表达产物主要分布在神经元轴突和胶质细胞中,Western blot检测在相对分子质量35 000处有一蛋白条带,并且可见实验组(颞叶和海马中分别为1.4293±0.1839和2.0733±0.4738)高于对照组(颞叶和海马中分别为0.9680±0.4147和1.403±0.6163,P<0.05).结论 CDK5在耐药性癫(癎)患者颞叶中表达增强,提示他们可能参与了耐药性癫(癎)的形成. 相似文献
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宫腔镜电切术治疗宫颈肌瘤的临床应用 总被引:1,自引:0,他引:1
目的 :探讨应用宫腔镜电切术治疗宫颈肌瘤的临床应用价值。方法 :用宫腔镜电切术切除宫颈肌瘤3 7例 ,其中有蒂宫颈肌瘤 2 1例 ,无蒂内突型宫颈肌瘤 16例 ,术后随访 3~ 3 1个月。结果 :平均手术时间2 0 7min ,术中平均出血 2 0 5ml ,一次性治愈率达 10 0 % ,无 1例子宫穿孔、低钠血症、周围脏器损伤、感染及宫颈管粘连等并发症发生。结论 :治疗宫颈肌瘤首选宫腔镜电切术 ,它具有治愈率高、创伤小、恢复快、并发症少的特点。 相似文献
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目的:观察残杀威对德国小蠊的药效。方法:采用果酱瓶药膜法和现场试验评价效果。结果残杀威对德国小蠊敏感品系的平均KT50为13.86min,现场品系8个调查点的KT50为11.25—38.02min,对抗氯菊酯品系KT50为16.06-23.37min,72h死亡率均为100%;现场试验,4周后的杀灭率仍达90.58%。结论:残杀威对德国小蠊现场品系为一般击倒;对抗氯菊酯品系尚未形成交互抗性,其水乳剂防制舰艇蜚蠊效果满意。 相似文献
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胸腺移植的方法和应用 总被引:1,自引:0,他引:1
目的:回顾胸腺移植的方法和应用,展望胸腺移植的发展。
资料来源:应用计算机检索Pubmed数据库1968—01/2005—10相关胸腺移植方面的文章,检索词为“thymus,transplantation”,限定文章语言种类为English;计算机检索CNKI 1990-01/2005—10相关胸腺移植方面的文章,限定文章语言种类为中文。
资料选择:对资料的摘要进行阅读初审,纳入标准:①有关胸腺移植的各种方法的原理及实施方案。②胸腺移植的临床应用和动物实验。排除标准:综述文献、重复研究、Meta分析类文章。
资料提炼:共纳入符合标准的文章20篇,多为胸腺移植的临床应用和动物实验方面的文章。
资料综合:自1968年胸腺移植被用于治疗DiGeorge综合征以来,它已经被很多学者应用于临床和基础医学研究中。胸腺移植的方法很多,主要包括胸腺细胞移植、胸腺组织块移植、带血管的胸腺移植和胸腺与其他脏器联合移植等。胸腺移植最初被用来治疗免疫性疾病,随后其对各种恶性肿瘤的治疗作用也得到证实。近年来,胸腺移植对器官移植耐受的诱导作用引起人们的重视,有关这方面的研究已取得很多进展。
结论:随着基因工程技术和免疫学研究的不断前进:胸腺移植将会更好地服务于基础和临床研究。 相似文献
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川芎嗪及复方丹参注射液辅助治疗妊娠高血压综合征60例临床分析 总被引:17,自引:0,他引:17
目的 比较川芎嗪注射液及复方丹参注射液在辅助治疗妊娠高血压综合征(PHI)中的作用,探讨两药在改善微循环及胎儿宫内缺氧方面的差异,进一步指导临床用药。方法 选取2001年6月~2002年6月在我院住院治疗的60例PHI患者,平均分为2组,在有效镇静、解痉、降压、低流量吸氧等治疗的基础上,分别给予静脉滴注川芎嗪注射液及复方丹参注射液治疗1个疗程。结果 川芎嗪组抑制纤溶、改善微循环的效果显著;复方丹参组主要降低血液粘稠度、降低胆圊醇及血酯。结论 川芎嗪及复方丹参对PHI有肯定的治疗作用,由于两药的临床作用不同,需有针对性用药。 相似文献
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J. W. P. GOVERS-RIEMSLAG M. SMID J. A. COOPER† K. A. BAUER‡ R. D. ROSENBERG‡ C. E. HACK§ K. HAMULYAK¶ H. M. H. SPRONK G. J. MILLER† H. TEN CATE 《Journal of thrombosis and haemostasis》2007,5(9):1896-1903
BACKGROUND: The plasma kallikrein-kinin system (PKKS) has been implicated in cardiovascular disease, but activation of the PKKS has not been directly probed in individuals at risk of coronary heart disease (CHD) or stroke. OBJECTIVE: To determine the involvement of the PKKS, including factor XI, in cardiovascular disease occurring in a nested case-control study from the Second Northwick Park Heart Study (NPHS-II). METHODS AND RESULTS: After a median follow-up of 10.7 years, 287 cases of CHD and stroke had been recorded and 542 age-matched controls were selected. When FXIIa-C1 esterase inhibitor (C1-inhibitor) concentrations were divided into tertiles (lowest tertile as reference), the odds ratios (ORs) at 95% CIs for CHD were 0.52 (0.34-0.80) in the middle tertile and 0.73 (0.49-1.09) in the highest tertile (P = 0.01 for the overall difference; P = 0.01 for CHD and stroke combined). For kallikrein-C1-inhibitor complexes, the ORs for stroke were 0.29 (0.12-0.72) and 0.67 (0.30-1.52) in the middle and high tertiles, respectively (P = 0.02). FXIIa-C1-inhibitor and kallikrein-C1-inhibitor complexes were negatively related to smoking and fibrinogen (P < 0.005). FXIa-inhibitor complexes correlated strongly with FXIIa-inhibitor complexes. CONCLUSIONS: Lower levels of inhibitory complexes of the PKKS enzymes and particularly of FXIIa contribute to the risk of CHD and stroke in middle-aged men. This observation supports the involvement of the PKKS in atherothrombosis. 相似文献
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Objective: To investigate the anti-inflammatory effect of erythropoietin (EPO) pretreatment on cardiomyocytes exposed to hypoxialreoxygenation injury (H/R) and explore the possible mechanism.
Methods: The cultured neonatal rats' ventricular cardiomyocytes were divided randomly into 4 groups, control group (C group), EPO pretreatment group (E group), EPO and pyrrolidine dithiocarbamate (PDTC) pretreatment group (EP group) and PDTC pretreatment group (P group). After 24 hours' pretreatment, the cardiomyocytes were exposed to H/R. After pretreatment and H/R, the expression of tumor necrosis factor- α (TNF- α ) gene in all the groups was detected by RT-PCR and Western blot. The nuclear factor- κ B (NF- κB) activity was detected by electrophoretic mobility shift assay (EMSA) and the inhibitor- κB α (Ⅰ- κB α) protein level was detected by Western blot.
Results: The decrement of Ⅰ- κB a protein and the increasing NF- KB activity were found in cardiomyocytes pretreated with EPO before H/R compared to other groups (t=3.321, 4.183, P〈0.01). However, after H/R, NF- κB activity and expression of TNF- α gene were significantly reduced, Ⅰ- κB a protein expression was increased in cardiomyocytes of E group compared to other groups (t=-3.425, 3.687, 3.454, P〈0.01). All theses changes caused by EPO pretreatment were eliminated by the intervention of PDTC (an antagonist to NF- κB) during pretreatment.
Conclusions: EPO pretreatment can inhibit the activation of NF- κB and upregulation of TNF- α gene in cardiomyocytes exposed to H/R through a negative feedback of NF- κB signaling pathway, and thus produces the anti-inflammatory effect. This might be one of the ways EPO produces the anti-inflammatory effect. 相似文献
Methods: The cultured neonatal rats' ventricular cardiomyocytes were divided randomly into 4 groups, control group (C group), EPO pretreatment group (E group), EPO and pyrrolidine dithiocarbamate (PDTC) pretreatment group (EP group) and PDTC pretreatment group (P group). After 24 hours' pretreatment, the cardiomyocytes were exposed to H/R. After pretreatment and H/R, the expression of tumor necrosis factor- α (TNF- α ) gene in all the groups was detected by RT-PCR and Western blot. The nuclear factor- κ B (NF- κB) activity was detected by electrophoretic mobility shift assay (EMSA) and the inhibitor- κB α (Ⅰ- κB α) protein level was detected by Western blot.
Results: The decrement of Ⅰ- κB a protein and the increasing NF- KB activity were found in cardiomyocytes pretreated with EPO before H/R compared to other groups (t=3.321, 4.183, P〈0.01). However, after H/R, NF- κB activity and expression of TNF- α gene were significantly reduced, Ⅰ- κB a protein expression was increased in cardiomyocytes of E group compared to other groups (t=-3.425, 3.687, 3.454, P〈0.01). All theses changes caused by EPO pretreatment were eliminated by the intervention of PDTC (an antagonist to NF- κB) during pretreatment.
Conclusions: EPO pretreatment can inhibit the activation of NF- κB and upregulation of TNF- α gene in cardiomyocytes exposed to H/R through a negative feedback of NF- κB signaling pathway, and thus produces the anti-inflammatory effect. This might be one of the ways EPO produces the anti-inflammatory effect. 相似文献