论文部分内容阅读
背景:随着对急性脑梗死病理生理机制的深入探讨,发现炎症反应在中枢神经系统缺血性损伤中占有重要地位,其中肿瘤坏死因子α,白细胞介素1β和可溶性细胞间黏附分子1正成为研究的热点。目的:研究缺血性脑卒中患者血清中炎性细胞因子水平与病程,病情严重程度的关系。设计:以患者和健康人为研究对象,病例-对照研究。单位:武汉大学医院的神经内科。对象:2001-01/2003-12武汉大学人民医院神经内科住院和门诊缺血性脑卒中患者50例,其中男23例,女27例,平均年龄(60.26±8.77)岁。对照组40例为同期门诊体检的健康人,其中男18例,女22例,平均年龄(61.05±8.09)岁。干预:采用双抗体夹心酶联免疫吸附法测定血清肿瘤坏死因子α,白细胞介素1β,可溶性细胞间黏附分子1水平。主要观察指标:缺血性脑卒中患者病程不同时期、不同梗死体积、不同神经功能缺损程度血清中肿瘤坏死因子α,白细胞介素1β,可溶性细胞间黏附分子1水平。结果:急性期、恢复期脑梗死患者血清肿瘤坏死因子α,白细胞介素1β和可溶性细胞间黏附分子1水平较对照组显著增高(P<0.01),急性期又较恢复期高(P<0.05),增高程度与神经功能缺损程度及梗死体积大小密切相关,且血清中肿瘤坏死因子α含量与白细胞介素1β和可溶性细胞间黏附分子1也相关。结论:肿瘤坏死因?
BACKGROUND: In-depth discussion of the pathophysiological mechanism of acute cerebral infarction found that inflammatory response plays an important role in ischemic injury of the central nervous system. Tumor necrosis factor-α, interleukin-1β and soluble intercellular adhesion molecule 1 are becoming Hot research. Objective: To study the relationship between the level of inflammatory cytokines and the course of disease and the severity of the disease in the serum of patients with ischemic stroke. Design: Patients and healthy people for the study, case-control study. Unit: Department of Neurology, Wuhan University Hospital. PARTICIPANTS: Fifty patients with inpatient and outpatient ischemic stroke were enrolled in Department of Neurology, Wuhan University People’s Hospital from January 2001 to December 2003, including 23 males and 27 females, with an average age of (60.26 ± 8.77) years. Forty patients in the control group were healthy people in the same period, including 18 males and 22 females, with an average age of (61.05 ± 8.09) years. Intervention: Serum levels of tumor necrosis factor alpha, interleukin 1 beta and soluble intercellular adhesion molecule-1 were measured by double antibody sandwich enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Tumor necrosis factor alpha, interleukin 1 beta, soluble intercellular adhesion molecule-1 levels in serum of patients with ischemic stroke at different stages of disease, different infarct volume, different degrees of neurological deficits. Results: Serum levels of tumor necrosis factor alpha, interleukin 1 beta and soluble intercellular adhesion molecule-1 in acute phase and convalescent cerebral infarction group were significantly higher than those in control group (P <0.01) ). The degree of increase was closely related to the degree of neurological deficit and the size of infarct volume. The level of TNF-α in serum was also correlated with interleukin-1β and soluble intercellular adhesion molecule-1. Conclusion: The cause of tumor necrosis?