进展性缺血性卒中患者白细胞流变特性及分子流变特性研究

目的:探讨白细胞流变特性和分子流变特性的改变在进展性缺血性卒中(PIS)发病中的作用。方法:128例首次发病的缺血性卒中患者(起病在24h内)作为研究对象,PIS的诊断根据神经功能缺损评分(SSS评分)的增加来判断,并对患者入院时白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、肿瘤坏死因子(TNF)、可溶性细胞间黏附分子-1(sICAM-1)、血管内皮细胞黏附分子-1(sVCAM-1)浓度及白细胞聚集性(LA)、白细胞黏附功能(LAF)进行检测。结果:128例脑梗死患者中有35例(27.3%)发展为PIS,PIS患者入院时IL-1、IL-6、TNF、sVCAM-1、sICAM-1浓度及LA、LAF明显高于无进展的脑梗死患者(P<0.01)。LA和LAF均与IL-1、IL-6、TNF、sICAM-1、sVCAM-1正相关。经多元Logistic回归分析发现:IL-1、IL-6、TNF、sVCAM-1、sICAM-1、LA、LAF是PIS独立的危险因素。结论:脑梗死患者存在白细胞流变特性及分子流变特性的异常,这种异常在PIS的发病过程中可能发挥重要作用。     

可溶性细胞间黏附分子-1、血管细胞黏附分子-1与急性脑梗死关系的研究

急性脑梗死(acute cerebral infarction,ACI)后会引发颅内炎性反应。研究显示,缺血区内大量白细胞(WBC)黏附于血管内皮细胞表面并外渗。炎性介质细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)与这一过程密切相关,而外周血可溶性ICAM-1(sICAM-1)、VCAM-1(sVCAM-1)主要来源于细胞表面模型ICAM-1、VCAM-1,其血浆水平的增高是内皮细胞和WBC损害或激活的标志。作者观察了38例ACI、33例恢复期脑梗死(remissonstages cerebral infarction,RSCI)患者血浆sICAM-1、     

脑梗死患者血清E2与可溶性细胞间黏附分子-1白介素-6的关系研究

目的探讨可溶性细胞间黏附分子1(sICAM-1)、白细胞介素6(IL-6)及血清雌二醇(E2)在脑梗死患者中的表达情况以及sICAM-1、IL-6与E2的关系。方法选取2011-01—2014-06 92例脑梗死患者为研究对象(观察组);急性期52例,缓解期40例;根据体积大小分为3组,小梗死灶组42例,梗死灶体积5cm3;中梗死灶组28例,梗死灶体积5~10cm3;大梗死灶组22例,梗死灶体积10cm3。选择70例健康人为对照组。检测受试者血清E2、sICAM-1、IL-6水平,并对脑梗死患者血清E2、sICAM-1、IL-6表达与年龄、病情、梗死灶大小、BMI进行相关性分析。结果观察组血清sICAM-1和IL-6水平均高于对照组(P0.01);观察组血清E2水平低于对照组(P0.01);随着脑梗死病情的加重,血清sICAM-1和IL-6水平均呈上升趋势(P0.01),血清E2水平呈下降趋势(P0.01);随着脑梗死体积的增加,血清sICAM-1和IL-6水平均呈上升趋势(P0.01),血清E2水平呈下降趋势;sICAM-1和IL-6的表达与脑梗死病情、梗死灶大小均呈正相关(P0.05);E2的表达与脑梗病情、梗死灶大小均呈负相关(P0.05);E2的表达与sICAM-1和IL-6的表达均呈负相关(P0.05),sICAM-1和IL-6的表达呈正相关(P0.05)。结论 sICAM-1、IL-6在脑梗死患者血清中高表达,E2在脑梗死患者血清中低表达,上述指标与脑梗死发病及病情进展密切相关。     

脑梗死患者急性期可溶性粘附分子的变化及临床意义

目的:为了解脑梗死患者急性期可溶性粘附分子的变化及临床意义。方法:采用双抗体夹心ELIsA法测定76例脑梗死患者血清sICAM-1、sVCAM-1、sE-selectine,并与52例TIA患者和40例健康老年人对照比较。结果:脑梗死患者24小时内血清sICAM-1、sVCAM-1、sE-selectine水平明显高于TIA和健康对照组(P<0.01)。大梗死灶组血清sICAM-1、sVCAM-1、sE-selectine水平明显高于中梗死灶组和小梗死灶组。脑梗死患者血清sICAM-1、sVCAM-1、sE-selectine水平在脑梗死发生24小时至7天呈现上升趋势,7天至14天呈下降趋势。结论:sICAM-1、sVCAM-1、sEselectine与急性脑梗死密切相关,参与了缺血后脑组织损伤的病理过程。在脑梗死急性期阻断粘附分子的表达可能有助于减轻缺血性脑损伤。     

肺炎衣原体与脑梗死的关系研究

目的 探讨肺炎衣原体(Cpn)与脑梗死之间的关系. 方法 选取自2005年9月至2007年10月珠江医院神经内科收治的脑血栓患者(150例)、腔隙性脑梗死患者(52例)、脑出血伴梗死患者(62例)、高血压合并高血脂患者(52例)以及健康对照者52例,分别应用微量免疫荧光法(Micro-IFA)检测Cpn特异性抗体IgG、IgM和双抗体夹心酶联免疫吸附法(ELISA)检测各组患者血清中自介素-6(IL-6)和可溶性黏附分子1(sICAM-1)的水平. 结果 五组患者的Cpn感染率差异有统计学意义(P<0.001),Cpn特异性抗体IgG与脑梗死有关,脑血栓组患者血清IL-6与sICAM-1水平呈明显正相关(r=0.356,P=0.000),Cpn IgG滴度与IL-6水平呈正相关(r=0.204,P=0.022),但与sICAM-1无明显相关性. 结论 Cpn感染可能通过影响IL-6、sICAM-1水平作用于血管内膜,促进白细胞内皮黏附参与脑梗死的病理过程.     

脑缺血患者微栓子检测与黏附分子的相关性研究

目的研究脑缺血患者微栓子与黏附分子的相关性。方法选择108例研究对象,其中68例为发病72h内颈内动脉或大脑中动脉区域脑梗死或短暂性脑缺血发作患者,经TCD检测微栓子信号(microembolic sig-nals,MES)分为MES阳性组(19例)和MES阴性组(49例);对照组40例,无脑梗死或脑缺血发作病史,且无明显颅内外动脉狭窄。均用双抗体夹心酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)测定血清可溶性细胞间黏附分子-1(soluble intercellular adhesion molecule-1sICAM-1)、可溶性血管细胞黏附分子-1(soluble vascularcell adhesion molecule-1,sVCAM-1)水平。结果MES阳性组sICAM-1、sVCAM-1水平高于MES阴性组(P<0.05);MES阳性组、MES阴性组sICAM-1、sVCAM-1水平明显高于对照组(P<0.01)。结论黏附分子参与了脑缺血的损伤过程,且与动脉粥样硬化(artherosclerosis,AS)斑块的不稳定性相关。微栓子和黏附分子是...     

奥扎格雷钠对急性脑梗死患者血清IL-6和sICAM-1的影响

目的 探讨奥扎格雷钠对急性脑梗死(ACI)患者血清白介素-6(IL-6)和可溶性细胞间黏附分子-1(sICAM-1)的影响.方法 80例ACI患者随机分为治疗组和对照组.2组均给予常规治疗,治疗组加用奥扎格雷钠治疗,对照组加用维脑路通,采用双抗体酶联免疫吸附法(ELISA)分析.结果 2组治疗后血清IL-6和sICAM-1水平均降低,治疗组下降更明显.结论 血清sICAM-1及IL-6水平升高可能是脑梗死发病的危险因素,奥扎格雷钠对急性脑梗死患者血清中异常升高的IL-6和sICAM-1有降低作用.     

进展性脑梗死患者血浆t-PA及PAI-1水平的变化及临床意义

目的探讨血浆中组织型纤溶酶原激活物(t-PA)及其抑制物(PAI-1)在进展性脑梗死发病中的作用。方法采用发色底物显色法测定100例急性脑梗死患者不同时期血浆t-PA及PAI-1水平变化,并根据神经功能缺损(SSS)评分判断是否发展为进展性脑梗死。60例健康体检者作为对照组。结果100例急性脑梗死患者中有38例(38.0%)于7d内发展为进展性脑梗死,与无进展脑梗死患者比较,其发病后第1d、3d、7d、14d外周血t-PA水平显著降低,而PAI-1水平则明显升高(均P<0.01);第21d与正常对照组无明显差异(P>0.05)。结论急性脑梗死患者血浆t-PA降低及PAI-1增高与进展性缺血性脑梗死密切相关,是进展性缺血性脑梗死发病过程中的重要因素之一。     

脑出血患者血清细胞间黏附分子-1与血管细胞黏附分子-1含量变化

目的观察脑出血患者1d、3d、7d、14d血清中可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sV-CAM-1)含量变化,探讨临床意义。方法采用双抗夹心酶联免疫吸附法(ELISA)测定血清中sICAM-1、sVCAM-1含量。结果脑出血患者sICAM-1、sVCAM-1含量第1d开始升高,与对照组比较差异无统计学意义(P>0.05);第3d、7d含量显著升高,与对照组相比差异有统计学意义(P<0.01);第14d含量开始下降,与对照组相比差异有统计学意义(P<0.01);重型脑出血组与轻型脑出血组比较,第3d、7d差异均有统计学意义(P<0.05,P<0.01)。结论ICAM-1、VCAM-1参与脑血肿周围脑组织炎症反应及继发性脑组织损伤。     

进展性缺血性脑卒中患者超敏C反应蛋白的水平变化

目的观察进展性缺血性脑卒中患者血清超敏C反应蛋白(hsCRP)变化规律,探讨超敏C反应蛋白在进展性缺血性脑卒中发病中的作用和临床意义。方法分别于患者入院第1d、第3d、第7d和第14d分别检测缺血性脑卒中患者hsCRP水平,比较进展组与非进展组的差异,分析hsCRP动态水平与缺血性脑卒中患者病情的关系。结果进展组第1d、第3d和第7d血清hsCRP水平高于非进展组,差异有显著统计学意义。结论血清hsCRP水平可作为进展性缺血性脑卒中的预测指标。     

Association of soluble intercellular adhesion molecule 1 with neurological deterioration of ischemic stroke: The Chongqing Stroke Study

BACKGROUND: Adhesion molecules play important roles in the pathophysiology of ischemic stroke. The aim of the present study was to investigate whether serum levels of soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cellular adhesion molecule 1 (sVCAM-1) and soluble E-selectin were associated with neurological deterioration of ischemic stroke. METHODS: 238 consecutive patients with ischemic stroke examined within 24 h from onset were enrolled into the study. The stroke severity was daily assessed with the NIH Stroke Scale (NIHSS) within the first week after admission. Serum levels of sICAM-1, sVCAM-1 and sE-selectin after admission were measured using enzyme-linked immunosorbent assay. Multivariate logistic regression was used to analyze the association of serum levels of sICAM-1, sVCAM-1 and sE-selectin on admission with the neurological deterioration of ischemic stroke, adjusted for potential confounders. RESULTS: 52 (21.8%) out of 238 stroke patients suffered from neurological deterioration. Serum levels of sICAM-1 on admission of stroke patients were significantly higher than those of healthy controls. Compared with patients without deterioration, patients with neurological deterioration had higher levels of sICAM-1, but not of sVCAM-1 and sE-selectin. On multivariate logistic regression, the serum level of sICAM-1 on admission was associated with neurological deterioration of stroke (OR 2.92, 95% CI 1.41-6.05). Other variables associated with neurological deterioration were fasting serum glucose (OR 1.65, 95% CI 1.24-2.20), baseline fibrinogen (OR 1.31, 95% CI 1.13-1.52) and NIHSS score (OR 1.23, 95% CI 1.15-1.32). CONCLUSIONS: The serum level of sICAM-1 on admission is associated with neurological deterioration of ischemic stroke.     

Soluble adhesion molecules and functional outcome after ischemic stroke: A Mendelian randomization study

ObjectivesWe employed Mendelian randomization to determine whether genetically predicted circulating levels of endothelial-derived adhesion molecules (soluble intercellular adhesion molecule-1 [sICAM-1]), soluble vascular-leukocyte adhesion molecule-1 [sVCAM-1], and soluble-endothelial-leukocyte adhesion molecule [sE-selectin]) were associated with functional outcome after ischemic stroke.MethodsIndependent genetic variants robustly associated with soluble adhesion molecules, located at or close to the coding gene (cis), were used as genetic instruments. The functional outcome was evaluated using the 3-month modified Rankin Scale (mRS) score after ischemic stroke. A poor functional outcome was defined as mRS ≥ 3 at 3 months. We extracted summary data for functional outcome after ischemic stroke from the Genetics of Ischaemic Stroke Functional Outcome network (n = 6,021).ResultsGenetically elevated sICAM-1 (OR 1.28, 95% CI 1.05-1.56) and sE-selectin (OR 2.69, 95% CI 1.23-5.86) levels were related with poor post-stroke outcome. However, we found no evidence that genetically elevated sVCAM-1 were associated with post-stroke outcome (OR 1.36, 95% CI 0.39-4.66).ConclusionsWe found that genetically elevated higher sICAM-1 and sE-selectin levels are associated with poor post-stroke outcome. Further studies are warranted to evaluate the potential of ICAM-1 and E-selectin to be drug targets for post-stroke recovery.     

Soluble adhesion molecules in muscular dystrophy

To determine whether soluble adhesion molecules are affected in muscular dystrophy, we measured serum levels of creatine kinase (CK), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), soluble (s) E-selectin, and fibrin and fibrinogen degradation products (FDP) in 25 patients with Duchenne muscular dystrophy (DMD), 7 with Becker muscular dystrophy, 7 with Fukuyama type congenital muscular dystrophy, 6 with myotonic dystrophy (MyD), and 5 with spinal muscular atrophy (SMA) type 2, and also serum sVCAM-1, sICAM-1, and sE-selectin in 9 healthy controls. The levels of sVCAM-1 in the patients with DMD were 367.0-852.0 ng/ml (552.8 +/- 23.1) and significantly elevated than those in the patients with MyD, SMA type 2, and controls. The levels of sICAM-1 and sE-selectin in the patients with muscular dystrophy were 0.2-376.0 ng/ml and 17.9-119.0 ng/ml, respectively. They were also elevated than those in the patients with SMA type 2 and controls, but not significantly. The levels of sVCAM-1 and sE-selectin in the patients with DMD significantly correlated with age. There was no correlation between the levels of soluble adhesion molecules and those of CK or FDP in any groups. These changes of soluble adhesion molecules may reflect the process of muscle destruction and endothelial cell activation in muscular dystrophy.     

Soluble adhesion molecules and angiotensin-converting enzyme in dementia

We aimed to determine plasma and cerebrospinal fluid (CSF) levels of angiotensin-converting enzyme (ACE) and the soluble forms of intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1) and platelet endothelial cell adhesion molecule-1 (sPECAM-1) as surrogate markers for endothelial cell activation in clinically diagnosed patients with Alzheimer's disease (AD, n=260), dementia with Lewy bodies (DLB, n=39) and non-demented controls (n=34). Plasma sICAM-1 and sPECAM-1 were higher and CSF sVCAM-1 were lower in AD and DLB patients than in controls (p<0.001). DLB patients had higher CSF sICAM-1, but lower CSF sVCAM-1 (p<0.001). No difference in ACE levels was found between the dementia groups and controls. In controls and AD patients CSF sICAM and sVCAM-1 strongly correlated with each other and with blood barrier permeability whereas in DLB group these correlations were weaker. The observed patterns in adhesion molecules may reflect distinctions in the pathophysiological basis of their generation in dementia patients.     

Role of sICAM-1 and sVCAM-1 as biomarkers in early and late stages of schizophrenia

Schizophrenia (SZ) is a neuroprogressive disorder presenting with biochemical, functional, and structural changes, which differ from early to late stages of the illness. We explored the differences in serum levels of soluble intercellular cell adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) between early and late stages of SZ, in regard to clinical characteristics and treatment application.Serum levels of sICAM-1 and sVCAM-1 were measured in 80 patients with SZ (40 early stage; 40 late stage), and compared with 80 healthy controls, matched by age, gender, body mass index, and smoking habits with each SZ group. Serum levels of sICAM-1 and sVCAM-1 were measured using ELISA. The severity of psychopathology was assessed using the Clinical Global Impression Scale and five-factor Positive and Negative Symptoms in Schizophrenia Scale.After adjustment for confounders, we noticed normal levels of sICAM-1 in the early stage, and elevated levels of sICAM-1 in the late stage of SZ. sVCAM-1 levels were decreased in both stages of SZ. Higher sICAM-1 levels have been related to more pronounced cognitive deficit and excitement symptoms in the early stage of SZ and to favorable characteristics of treatment application in both stages.SZ is associated with changes in the levels of adhesion molecules that vary from early to late stages of the illness. This implies that the concept of biochemical staging is applicable in SZ, at least for markers of cellular adhesion.     

Differences in levels of soluble E-selectin and VCAM-1 in malignant versus non malignant Mediterranean spotted fever

In the present study, we investigated the plasma levels of soluble adhesion molecules E-selectin, P-selectin, intercellular adhesion molecule- (ICAM- ) and vascular cell adhesion molecule-1(VCAM-1) in 24 patients with Mediterranean spotted fever (MSF), 6 of whom with a malignant form. Measurements were performed on blood samples collected before treatment (T1), then twice during treatment (T2 and T3). Before treatment, MSF patients taken as a whole presented elevated levels of sICAM-1 and sVCAM-1 and normal levels of sE-selectin and sP-selectin compared to healthy controls. We found that sICAM-1 was elevated both in mild and malignant MSF. sE-selectin and sVCAM-1 were elevated only in patients with the malignant form and allowed to discriminate the two clinical subgroups. Their levels decreased after treatment with sE-selectin reaching control values at T2 whereas sVCAM-1 remained higher over the course of the malignant form. In patients with mild MSF, sP-selectin steadily increased after treatment, whereas it did not present any modification at any of the two sampling times in patients with the malignant form. Raised plasma levels of sE-selectin and sVCAM-1 reflect endothelial activation in malignant rickettsial disease and may be sufficiently early markers to influence the therapeutic decision.