肿瘤坏死因子在急性脑梗塞患者血清中的变化

肿瘤坏死因子在急性脑梗塞患者血清中的变化罗南萍杨道理于金萍孙文杰陈世敏肿瘤坏死因子（ＴＮＦ）是由激活的巨噬细胞产生的一种多肽细胞因子。ＴＮＦ可作用于血管内皮细胞（ＶＢＣ），导致血管损伤和血栓的形成［１］。ＴＮＦ对免疫应答的多种调节效应在一定程度上引起...     

急性脑梗塞患者血清肿瘤坏死因子增高

采用放射免疫法测定４５例急性脑梗塞患者血清肿瘤坏死因子（ＴＮＦ）含量，并与３０例脑动脉硬化患者及２７例健康体检者进行比较。结果表明脑梗塞患者ＴＮＦ水平明显增高，脑梗塞组ＴＮＦ为７．１９±１．６７ｎｇ／ｍｌ，脑动脉硬化组为２．３０±１．０６ｎｇ／ｍｌ，正常对照组为１．４１±０．２３ｎｇ／ｍｌ。脑梗塞组与脑动脉硬化组比较有显著性差异（Ｐ＜０．００１）；与正常对照组比较有极显著性差异（Ｐ＜０．００１）。重型脑梗塞患者血清ＴＮＦ含量亦较轻型患者显著增高。重型ＴＮＦ含量为１１．３２±１．４３ｎｇ／ｍｌ，轻型为６．９０±１．５０ｎｇ／ｍｌ（Ｐ＜０．０５）。提示ＴＮＦ参与脑梗塞的发生、发展全过程，脑梗塞患者血清ＴＮＦ含量测定可作为判断患者病情、治疗及预后的一项免疫学指标。     

急性脑梗塞患者血清肿瘤坏死因子α测定

采用放射免疫法测定６２例急性脑梗塞患者血清肿瘤坏死因子α含量，并与２０名正常对照者比较。结果发现患者组血清ＴＮＦα明显高于对照组、提示在脑梗塞发病过程中存在ＴＮＦα介导的免疫反应。     

脑梗塞患者血清肿瘤坏死因子测定及意义

脑梗塞患者血清肿瘤坏死因子测定及意义杜颂伟陈祖舜杜同信作者单位：２１０００６南京市第一医院神经内科我们通过观察脑梗塞患者外周血肿瘤坏死因子（ＴＮＦ）水平在不同梗塞时期及不同梗塞灶大小时的变化。探讨其在脑梗塞发病中的作用及临床意义。１对象与方法１．１研...     

脑梗塞患者血与脑脊液肿瘤坏死因子含量变化的研究

检测了４２例急性脑梗塞患者血浆与脑脊液（ＣＳＦ）肿瘤坏死因子（ＴＮＦ）水平。结果发现：脑梗塞急性期患者血浆与ＣＳＦＴＮＦ含量显著高于对照组，ＴＮＦ水平与梗塞灶的大小明显相关。提示ＴＮＦ参与了急性脑缺血的炎性反应过程，抑制炎性反应的治疗可能具有潜在的临床价值。     

急性脑血管病患者血清肿瘤坏死因子α的变化

采用放射免疫法，检测了６２例脑梗塞和５３例脑出血急性期患者血清肿瘤坏死因子α（ＴＮＦ－α）的含量。结果发现，两患者组ＴＮＦ－α均明显高于对照组（Ｐ＜０．００１）。提示在脑梗塞和脑出血的发病过程中，都存在着ＴＮＦ－α介导的免疫反应。     

癫痫患者血清肿瘤坏死因子—α水平变化

采用双抗体夹心ＥＬＩＳＡ法对３８例正常对照和５２例癫痫患者血清肿瘤坏死因子－α水平进行检测。结果显示癫痫组血清ＴＮＦ－α水平显著高于对照组，血清ＴＮＦ－α水平变化与癫痫患者性别，年龄，病程及发作类型无关，抗癫痫药物对血清ＴＮＦ－α水平无明显影响。     

偏头患者血清和脑脊液肿瘤坏死因子α水平变化

近年来发现偏头痛患者存在免疫功能异常 ,并发现肿瘤坏死因子 (ＴＮＦ α)与偏头痛关系密切。对偏头痛患者血中ＴＮＦ α的研究国内外有少量报道 ,而对脑脊液 (ＣＳＦ)中ＴＮＦ α水平如何未见报道 ,我们对偏头痛患者血清和ＣＳＦ中ＴＮＦ α的水平同时进行研究 ,以探讨ＴＮＦ α在偏头痛中的作用机制。对象和方法 :偏头痛发作组 2 1例 ,男 4例 ,女 17例 ,年龄 9～ 46岁 ,平均 2 7岁 ;间歇组 16例 ,男 3例 ,女 13例 ,年龄11～ 42岁 ,平均 2 5岁 ;对照组 19例 ,男 6例 ,女 13例 ,年龄 5～ 48岁 ,平均 2 6岁。所选对象均未应用免疫抑制剂和免…     

急性脑梗死患者血清肿瘤坏死因子及循环内皮细胞含量变化的对比研究

目的　研究急性脑梗死 (ACI)患者血清肿瘤坏死因子 (TNF)及循环内皮细胞 (CEC)含量的变化 ,探讨 TNF与 CEC的关系及其临床意义。方法　采用放射免疫分析法检测 6 0例 ACI患者血清 TNF- α和 CEC的含量 ,并与 2 0例健康人作对照。结果　 (1)脑梗死患者急性期血清 TNF- α和 CEC含量明显高于恢复期 (P<0 .0 1)。恢复期血清 TNF- α及 CEC则高于正常水平 (P<0 .0 1)。 (2 )脑梗死急性期血清 TNF- α和 CEC升高的程度与梗死灶大小密切相关 (P<0 .0 1)。 (3)急性期血清 TNF- α与 CEC呈正相关 (r=0 .6 9,P<0 .0 1)。结论　 ACI患者血清TNF- α及 CEC含量升高 ,提示 TNF- α及血管内皮细胞的损伤共同参与脑梗死的发生发展过程。保护血管内皮细胞 ,降低 TNF- α的水平 ,对于缺血性脑血管病的防治将具有重要意义。     

急性脑梗死患者早期血清肿瘤坏死因子样弱凋亡诱导剂水平与脑白质病变的相关性

目的 探讨急性脑梗死患者早期血清可溶性肿瘤坏死因子样弱凋亡诱导剂(Soluble tumor nec-rosis factor like weak apoptosis inducer,sTWEAK)水平与脑白质病变(White matter lesions,WMLs)的相关性.方法 收集2018年2月-2019年12月...     

血清肿瘤坏死因子-α对急性缺血性脑卒中患者预后的影响

目的通过观察急性缺血性脑卒中患者血清肿瘤坏死因子-α水平的动态变化,探讨其对急性缺血性脑卒中患者预后的影响及在发病机制中的临床意义。方法采用双抗体夹心酶联免疫吸附法,连续检测55例急性缺血性脑卒中患者发病第1、3、7和28天血清肿瘤坏死因子-α水平,并与23例短暂性脑缺血发作患者和30例正常对照者进行比较,根据梗死灶体积及临床神经功能缺损程度评价患者预后。结果急性缺血性脑卒中组患者于发病第1天血清肿瘤坏死因子-α水平即开始升高（P〈0.05）,第3天达峰值水平（P〈0.01）,然后逐渐下降,至第28天时仍高于对照组和短暂性脑缺血发作组（P〈0.05）;梗死灶体积越大、临床神经功能缺损程度评分越高者,血清肿瘤坏死因子-α水平越高,与其他各组相比差异有统计学意义（P〈0.05或P〈0.01）;恢复良好者血清肿瘤坏死因子-α水平高于无改善者（P〈0.05）。短暂性脑缺血发作组患者血清肿瘤坏死因子-α水平与正常对照组之间差异无统计学意义（P〉0.05）。结论血清肿瘤坏死因子-α水平的动态变化与急性缺血性脑卒中的发生、发展有关,在发作期间对患者进行动态观察有助于评价脑损害程度和预后。     

急性脑梗死患者同型半胱氨酸与炎症因子的相关性分析

目的研究急性脑梗死患者肿瘤坏死因子-α（TNF-α）及白介素-6（IL-6）与同型半胱氨酸（Hcy）之间的相关性,以探讨其与急性脑梗死发生的关系。方法收集158例急性脑梗死患者（ACI组）、122例健康人（对照组）血液标本,采用循环酶法检测血浆同型半胱氨酸（Hcy）水平,用ELISA法即酶联免疫吸附法测定血清肿瘤坏死因子-α（TNF-α）,白介素-6（IL-6）水平。结果 ACI组Hcy、TNF-α和IL-6的水平均较对照组显著升高（P均〈0.05）。ACI组Hcy与TNF-α、IL-6水平存在显著性正相关（r=0.346,P〈0.05）,TNF-α与IL-6水平之间也存在显著性正相关（r=0.382,P〈0.05）。结论 Hcy、TNF-α、IL-6水平与急性脑梗死的发生密切相关,三者联合检测对急性脑梗死的预防、早期诊断及治疗和预后均有重要价值。     

急性脑梗死患者血清血管内皮生长因子的测定

目的　探讨急性脑梗死与血管内皮生长因子 (VEGF)的关系。方法　对 3 0例急性脑梗死患者和 40例健康人血清血管内皮生长因子含量进行测定。患者采血时间为病后第 2天或第 3、4天 ,取均数与对照组比较。结果　 3 0例急性脑梗死患者血清 VEGF含量为 (2 95 .0 4± 3 5 .73 ) pg/ ml,对照组为 (13 7.71± 11.5 3 ) pg/ m l,两组比较差异显著。结论　急性脑梗死患者血清 VEGF升高 ,提示 VEGF是脑梗死急性期的自我保护机制之一。     

阿托伐他汀对急性脑梗死患者血清内脂素水平的影响

目的 观察急性脑梗死患者血清内脂素水平的变化,并进一步探讨阿托伐他汀治疗对其有无影响.方法 随机选取86例急性脑梗死患者和52名正常对照者,检测其血清内脂素水平有无差异,并分析其与临床各指标的联系.86例急性脑梗死患者再进一步随机分为常规治疗组和阿托伐他汀治疗组.每组43例.常规治疗组给予常规治疗,阿托伐他汀治疗组在常规治疗的基础上,给予阿托伐他汀20 mg/d,治疗2周,检测2组治疗前后血清内脂索水平的变化.结果 与对照组相比,急性脑梗死患者血清内脂素水平明显增高(78.52±16.41 ng/mL、42.83±13.45 ng/mL).差异有统计学意义(P<0.01).非条件Logistic回归分析显示,血清高内脂素水平是急性脑梗死患者发病的独立危险因子(OR 1.652,95%CI 1.032～2.256;P=0.014).相关性分析表明.急性脑梗死患者血清内脂素与梗死面积、空腹血糖、收缩压和三脂酰甘油呈正相关,与高密度脂蛋白呈负相关.治疗2周后,阿托伐他汀治疗组的血清内脂素水平较治疗前明显下降(62.14±14.37 ng/mL、78.52±16.41ng/mL).差异有统计学意义(P<0.01);而常规治疗组的血清内脂素水平与治疗前相比,差异无统计学意义(P>0.05).结论 阿托伐他汀具有降低急性脑梗死患者血清内脂素的作用.     

早期血清中高敏C-反应蛋白含量水平与急性脑梗死患者脑水肿严重程度的关系

目的 探讨早期血清中高敏C-反应蛋白(HS-CRP)不同含量水平与急性脑梗死(ACI)患者脑水肿严重程度的关系.方法 采用微粒化增强免疫固定试验测定152例ACI者人院第2天血清HS-CRP含量水平,并与30例健康人(对照组)作对照.同时观察人院第2天血清中HS-CRP不同含量水平者人院第1、3、5、7天双侧大脑半球脑电阻抗扰动系数.结果 ACI早期血清中HS-CRP含量水平明显高于对照组(P＜0.01);入院第2天血清中HS-CRP不同含量水平第1天各组间患侧、健侧电阻抗扰动系数比较无明显差异(P＜0.05),人院第3天较第1天患侧、健侧电阻抗扰动系数均明显升高(P＜0.05),P＜0.01).但HS-CRP含量水平越高,患侧、健侧电阻抗扰动系数升高越明显(P＜0.05);第7天较第3天患侧电阻抗扰动系数均明显降低(P＜0.01),但HS-CRP含量水平越低,患侧电阻抗扰动系数降低越明显(P＜0.01).结论 ACI患者早期血清中HS-CRP含量水平明显升高.其早期含量水平越高,脑水肿形成后越严重;含量水平越低,脑水肿形成后越轻,且消退越明显.     

急性脑梗死患者血清缺血修饰蛋白表达水平与神经功能缺损程度及预后的关系

目的 探讨急性脑梗死患者血清缺血修饰蛋白（Ischemia-modified albumin,IMA)表达水平与神经功能缺损程度及预后的关系。方法 选择2016年1月～2017年12月在本院神经内科住院的急性脑梗死患者84例作为脑梗死组,同期选择本院健康体检的健康人群80例作为对照组,用美国国立卫生研究院卒中量表（NIHSS)对神经功能缺损程度进行评分,用Modified Rankin量表（MRS）进行预后评价,检测血清中IMA水平,分析其与脑梗死患者预后的关系。结果 与对照组比较,脑梗死组血清中IMA水平增高(P<0.05);随着神经功能缺损程度的加重,脑梗死患者血清中IMA水平增高,预后不良脑梗死患者血清中IMA水平高于预后良好患者(P<0.05);用四分位数法将脑梗死患者血清IMA水平从低到高分组显示,随IMA水平的增加,脑梗死患者预后不良率逐渐增高,脑梗死患者预后不良的风险也增加(P<0.05)。结论 急性脑梗死患者血清中IMA水平显著升高, 其水平与神经功能缺损程度及预后密切相关。     

Changes in tumor necrosis factor alpha and myeloper-oxidase in mouse models of local cerebral infarction induced by photochemical method

BACKGROUND: Lots of evidences have demonstrated that acute inflammatory reaction plays an important role in cerebral ischemia and cerebral ischemia/reperfusion injury. Tumor necrosis factor (TNF), as one of important inflammatory cytokines, also participates in the injury. OBJECTIVE: To observe the changes in TNF-α expression and myeloperoxidase (MPO) activity of mouse models of local cerebral infarction induced by photochemical method, and analyze the correlation of TNF-α expression and MPO activity. DESIGN: Randomized controlled experiment. SETTING: Laboratory of Cerebral Microcirculation, Taishan Medical College. MATERIALS: Sixty involved male adult Kunming mice were provided by the Experimental Animal Center of Shandong University. TNF-α primary antibody, kits for enzyme-linked immunosorbent assay(ELISA) and streptavidin-biotin complex immunohistochemical dyeing kit were purchased from Boster Company(Wuhan). MPO kit was purchased from Jiancheng Bioengineering Institute (Nanjing). Cold light source was developed by Hengfa Co.,Ltd.( LG-150, Xuzhou). METHODS: This experiment was carried out in the Laboratory of Cerebral Microcirculation of Taishan Medical College between July 2004 and July 2005. The involved 60 Kunming mice were randomized into 3 groups: normal control group (n =6), sham-operation group (n =6) and model group (n =48). Mice in the model group were observed at 30 minutes, 1, 3, 6, 12, 24, 48 and 72 hours after illumination, separately, 6 mice at each time point. In the model group, mice models of local cerebral infarction were developed as follows: The mice were anesthetized to expose left skulls. Taking 2 mm left to sagittal suture and 2 mm posterior to coronal suture as center, a field with diameter of 3 mm for illumination was set. The optical fiber detecting head of cold light source was vertically close to exposed skull. The mice were injected with rose Bengal for 5 minutes, and then cold light source was open for 10 minutes. Illumination was omitted in the sham-operation group. Mice in the control group were not modeled. At postoperative 6 hours, TNF-α expression in infracted-side cortex was detected with immunohistochemical method and ELISA, and MPO activity in infracted-side cortex with chromatometry. MPO activity could reflect the infiltration degree of neutrophils in tissue. Stronger activity indicated severer infiltration. Single-factor analysis of variance was used for comparison among groups, q test for pairwise comparison and correlative analysis for detecting the inter-parameter correlation. MAIN OUTCOME MEASURES: Changes in TNF-α expression and MPO activity of left cortex of mice in each group. RESULTS: Sixty mice were involved in the final analysis. After cerebral infarction, TNF-α positive cells were neurons and glial cells mainly, distributing in and around the infarct region. TNF-α expression in cortex of mice of sham-operation group was （615.7±16.1） ng/L, and that of model group increased to （792.2±17.8） ng/L at 3 hours after illumination, and reached peak [（921.9±23.9） ng/L] at 6 hours after illumination, and decreased to （848.0±30.6） ng/L at 12 hours after illumination and recovered to the normal level [（625.3±14.3） ng/L] at 72 hours after illumination. MPO activity of sham-operation group was （7.151±0.433） nkat/g, and that of model group increased to （10.469±0.600） nkat/g at 3 hours after illumination, reached the peak [（15.486±0.650） nkat/g] at 12 hours after illumination, decreased to （11.052±0.617） nkat/g at 24 hours after illumination and recovered to the normal level [（7.418±0.617） nkat/g] at 72 hours after illumination. Change of MPO activity lagged behind that of TNF-α, and correlative analysis showed that the both were positively correlated（r =0.953, P < 0.01）. CONCLUSION: In the acute stage of cerebral infarction of mice induced by photochemical method, TNF-α expression in infarcted-side cortex is closely related with infiltration of neutrophils. TNF-α induces inflammatory cells to intrude into ischemic brain tissue, and participates in the inflammatory reaction process at the early stage of cerebral ischemia.     

急性脑梗死及并发肺部感染患者血清C反应蛋白水平的变化

目的 探讨急性脑梗死及其并发肺部感染患者血清C反应蛋白（CRP）水平的变化及其意义。方法 采用免疫散射比浊法测定20例健康体检者（对照组）和55例脑梗死患者（按梗死面积分为大、中、小3组）血清CRP含量,中等面积梗死患者据是否合并肺部感染分组,于入院7d后复测CRP。结果 CRP含量为大面积梗死组〉中面积梗死组〉小面积梗死组〉对照组,组间差异均具显著性（P〈0．05～0．01）。中面积梗死组,1周后并发感染者较入院1d时CRP含量增高,未并发感染者降低（均为P〈O．01）;中面积梗死者,入院时CRP含量虽无显著性差异（P〉0．05）,1周后感染者较未感染者CRP含量显著升高（P〈0．01）。结论 血清CRP含量反映脑梗死严重程度,动态观察对了解有无合并感染的病情变化有帮助。