G-CSF联合化疗动员外周血干细胞过程中某些生物因子的动态变化

目的　探讨IL 8、可溶性血管细胞粘附分子 1 (sVCAM 1 )及可溶性细胞间粘附分子 1(sICAM 1 )在自体造血干细胞动员过程中的变化及其意义。方法　采用酶联免疫吸附实验方法动态分析患者造血干细胞动员过程中血浆IL 8、sICAM 1及sVCAM 1水平的变化 ;通过免疫荧光标记和流式细胞仪检测CD3 4+细胞 ;体外半固体培养CFU GM集落及血细胞计数法观察白细胞和血小板数量变化。结果　①在动员过程中 ,外周血IL 8[(2 4 7.4± 84.2 ) μg L]、sICAM 1 [(530 .3± 2 86 .1 ) μg L]及sVCAM 1[(575 .3± 350 .4) μg L]含量均较动员前和正常人显著升高 (P <0 .0 1 ) ;②患者外周血中IL 8、sVCAM 1水平与CD3 4+细胞和CFU GM集落数呈正相关 (P <0 .0 0 1 )。结论　在自体干细胞动员过程中 ,血浆IL 8和sVCAM 1的含量与患者CD3 4+细胞数和CFU GM集落形成有显著的相关性 ,分析这些生物因子的变化具有临床实用价值     

急性心肌梗死患者溶栓治疗前后血清sICAM-1、sVCAM-1、IL-6及IL-8的动态观察

目的探讨急性心肌梗死 (AMI)溶栓治疗前后血清可溶性细胞间粘附分子 1(sICAM 1)、可溶性血管细胞粘附分子 1(sVCAM 1)、白细胞介素 6 (IL 6 )、白细胞介素 8(IL 8)的动态变化。方法采用ELISA法观察 2 6例经尿激酶溶栓治疗及 2 2例常规治疗的AMI患者治疗前及治疗后 1、2、5、7、14天血清sICAM 1、sVCAM 1、IL 6、IL 8的动态变化并进行比较分析。结果治疗前两组间sICAM 1、sVCAM 1、IL 6、IL 8无差异 ,治疗后各指标变化趋势相似 ,但溶栓组sVCAM 1在治疗后第 5、7、14天显著高于对照组 (P <0 .0 1) ;而sICAM 1在第 5、7天明显低于对照组 (P <0 .0 1) ,IL 6在治疗后第 1、2、7天显著低于对照组 (P <0 .0 1) ,IL 8在治疗后第 1、7天明显低于对照组 (P <0 .0 1)。结论sICAM 1、sVCAM 1、IL 6、IL 8均可作为溶栓监测指标 ,其动态改变及作用影响AMI的发生、发展变化。溶栓治疗可减轻AMI的病理损伤 ,缩短病程。     

Elevated soluble CD40 ligand is related to the endothelial adhesion molecules in patients with acute coronary syndrome

BACKGROUND: Increasing evidence indicates that the CD40-CD40L interaction plays a pivotal role in the inflammatory regulation of atherosclerosis. Adhesion molecules especially the vascular adhesion molecules also play an important role in the pathogenesis of atherosclerosis which act as markers of inflammation. These inflammatory factors render vulnerability to the atherosclerotic plaque by triggering the fissure, rupture, and subsequent thrombosis, leading to the clinical scenario of unstable angina and acute myocardial infarction. METHODS: The difference of sCD40L concentration in different subtype of coronary heart disease and its relationship with vascular adhesion molecules was investigated. Enzyme-linked Immunosorbent Assay (EIA) was used to measure the serum sCD40L, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1). RESULTS: The sCD40L concentration was significantly higher in patients with acute coronary syndrome (ACS) (3.17+/-2.84 ng/ml) than in controls (1.19+/-1.05 ng/ml, p<0.01) and in patients with stable coronary heart disease (1.61+/-1.46 ng/ml, p<0.05). The sCD40L concentration was positively correlated with sICAM-1 (r=0.413, p<0.01), triglycerides (TG) (r=0.23, p<0.05), apoB (r=0.248, p<0.05), and HDL-cholesterol (r=-0.253, p<0.05). CONCLUSIONS: The sCD40L concentration was increased in acute coronary syndrome, suggesting the possible relation of CD40L to the pathogenesis. The serum CD40L concentration was positively correlated with adhesion molecule and was negatively associated with serum high-density lipoprotein cholesterol (HDL-C).     

Increased levels of markers of vascular inflammation in patients with coronary heart disease

Elevated levels of soluble cell adhesion molecules (sCAMs), inflammatory cytokines and C-reactive protein (CRP) have been associated with atherosclerotic disease states. The aim of the present study was to evaluate whether circulating levels of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), E- and P-selectin were significantly elevated in patients with coronary heart disease (CHD) compared with healthy controls, and to study possible associations between these sCAMs, tumour necrosis factor alpha (TNFalpha). interleukin-6 (IL-6), CRP and major CHD risk factors. The study included 193 patients in various stages of CHD and 193 matched controls. To evaluate any possible influence of acute phase reaction, reinvestigation was performed after 6 months. After adjustment for major CHD risk factors, sVCAM-1, sICAM-1, P-selectin, IL-6 and CRP remained significantly elevated in the CHD patients (p for all <0.001). In multivariate analysis sVCAM-1 was predicted by age (p=0.015), sICAM-1 by smoking (p<0.001) and total cholesterol (p=0.026), E-selectin by body mass index (BMI) (p=0.004) and P-selectin by male gender (p=0.015). TNFalpha significantly predicted sICAM-1 and E-selectin levels, while IL-6 predicted CRP but none of the sCAMs measured. This might indicate that TNFalpha, but not IL-6, plays a major role in the regulation of sCAM levels in vivo.     

Increased levels of markers of vascular inflammation in patients with coronary heart disease

Elevated levels of soluble cell adhesion molecules (sCAMs), inflammatory cytokines and C-reactive protein (CRP) have been associated with atherosclerotic disease states. The aim of the present study was to evaluate whether circulating levels of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), E- and P-selectin were significantly elevated in patients with coronary heart disease (CHD) compared with healthy controls, and to study possible associations between these sCAMs, tumour necrosis factor &#102 (TNF &#102 ), interleukin-6 (IL-6), CRP and major CHD risk factors. The study included 193 patients in various stages of CHD and 193 matched controls. To evaluate any possible influence of acute phase reaction, reinvestigation was performed after 6 months. After adjustment for major CHD risk factors, sVCAM-1, sICAM-1, P-selectin, IL-6 and CRP remained significantly elevated in the CHD patients (p for all < 0.001). In multivariate analysis sVCAM-1 was predicted by age (p = 0.015), sICAM-1 by smoking (p < 0.001) and total cholesterol (p = 0.026), E-selectin by body mass index (BMI) (p = 0.004) and P-selectin by male gender (p = 0.015). TNF &#102 significantly predicted sICAM-1 and E-selectin levels, while IL-6 predicted CRP but none of the sCAMs measured. This might indicate that TNF &#102, but not IL-6, plays a major role in the regulation of sCAM levels in vivo .     

Soluble L-selectin level is a marker for coronary artery disease in type 2 diabetic patients

OBJECTIVE: To investigate whether the fall in soluble L-selectin (sL-selectin) level constitutes a marker for myocardial ischemia. RESEARCH DESIGN AND METHODS: The levels of soluble forms of adhesion molecules, i.e., intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin), P-selectin (sP-selectin), and L-selectin (sL-selectin), were compared in type 2 diabetic patients without inflammatory syndrome but with symptomatic coronary artery disease (CAD) (group 1, n = 11), with silent ischemic disorders and proven coronary stenoses (group 2, n = 11), with silent myocardial ischemia (SMI) and normal coronary angiography (group 3, n = 10), and without proven SMI (group 4, n = 13). These levels were compared with those of 22 control subjects. RESULTS: The sL-selectin level was significantly lower in groups 1, 2, or 3 with symptomatic CAD or with SMI as compared with the control group (P = 0.0004). Group 4 without myocardial ischemia did not significantly differ from the control subjects (P = 0.6). In type 2 diabetic patients, after controlling for HbA1c, a partial correlation between sL-selectin and the CAD status was significant (P = 0.001). sICAM-1 and sP- or sE-selectin did not differ significantly between type 2 diabetic patients and control subjects or among the different groups of patients. The sVCAM-1 level in type 2 diabetic patients was significantly higher than in the control subjects (P = 0.001), but there were no significant intergroup differences (P = 0.4). CONCLUSIONS: In type 2 diabetic patients, sVCAM-1 is increased with regard to glycemic control, whatever the CAD status. In type 2 diabetic patients with symptomatic CAD or SMI associated with coronary stenoses, sL-selectin is significantly decreased. A marked fall in sL-selectin might constitute a marker for silent CAD in type 2 diabetic patients.     

Metabolic syndrome aggravates the increased endothelial activation and low-grade inflammation in subjects with familial low HDL

BACKGROUND: Inhibition of cytokine-induced expression of adhesion molecules is one of the atheroprotective mechanisms of high-density lipoprotein (HDL). AIM: We investigated whether increased endothelial activation and low-grade inflammation are present in Finnish subjects with familial low HDL, and which factors contribute to the inflammatory parameters. METHOD: High-sensitivity C-reactive protein (hsCRP), soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and sE-selectin were measured in 91 subjects with low HDL-cholesterol from 41 low-HDL families and in 112 normolipidemic controls with comparable age- and gender distribution. Presence of the features of the metabolic syndrome (MetS) was recorded. RESULTS: sVCAM-1, sICAM-1, sE-selectin, and hsCRP were significantly higher in low-HDL subjects than in the controls (sVCAM-1: 560+/-147 ng/mL versus 496+/-95 ng/mL, P = 0.001; sICAM-1: 247+/-60 ng/mL versus 215+/-47 ng/mL, P<0.001; sE-selectin: 52+/-20 ng/mL versus 44+/-16 ng/mL, P = 0.022; and hsCRP: 1.73+/-2.05 mg/L versus 0.85+/-1.10 mg/L, P<0.001). Low-HDL subjects had increased body mass index (BMI) and waist, and elevated insulin and triglyceride levels. Adhesion molecules and hsCRP increased according to the number of the features of the MetS. CONCLUSIONS: The presence of the MetS in subjects with familial low HDL-cholesterol aggravates the low-grade inflammation and endothelial activation, and ultimately may add to the higher susceptibility for atherosclerotic disease in these individuals.     

糖尿病视网膜病变病人血清OX-LDL和CAMS浓度变化及意义

目的探讨糖尿病视网膜病变（DR）与血清氧化低密度脂蛋白（OX-LDL）和细胞黏附分子（CAMS）浓度变化的关系及临床意义。方法采用酶联免疫吸附测定法检测62例DR病人血清CAMS和OX-LDL浓度的变化,并与82例非DR（NDR）糖尿病病人及68例对照组进行比较,对32例增殖型DR（PDR）病人与30例非增殖型DR（NPDR）病人的血清CAMS和OX-LDL浓度进行比较。结果 DR病人血清OX-LDL和可溶性细胞间黏附分子-1（sICAM-1）、可溶性血管细胞间黏附分子-1（sVCAM-1）水平明显高于对照组和NDR病人（F=356.942-408.695,q=5.589-38.488,P〈0.001）;PDR病人血清OX-LDL和sICAM-1、sVCAM-1明显高于NPDR病人（t=6.156-15.078,P〈0.001）。DR病人血清OX-LDL与sICAM-1、sVCAM-1水平呈明显的正相关（r=0.524、0.660,P〈0.01）。结论血清OX-LDL与sICAM-1、sVCAM-1浓度变化参与了DR的发生与发展,且与病情严重程度有关。     

替罗非班应用于急诊经皮冠状动脉介入治疗对急性心肌梗死患者心肌灌注和内皮功能的影响

目的探讨急诊经皮冠状动脉介入治疗（PCI）术中冠状动脉内应用替罗非班对急性心肌梗死（AMI）患者冠状动脉血流和内皮功能的影响。 方法选择2013年1月至2015年6月在泰安市中心医院心内科接受急诊PCI治疗的AMI患者共114例,用随机数字表法分为替罗非班组（58例）及对照组（56例）。替罗非班组冠状动脉内注射替罗非班10 μg / kg,继之以0.075 μg·kg^-1·min^-1静脉滴注24至48 h,对照组不应用替罗非班。根据冠状动脉造影图像观察两组患者TIMI血流分级情况,并应用酶联免疫吸附法检测两组PCI治疗术前及术后24 h、72 h的可溶性细胞黏附因子1（sICAM-1）、可溶性血管细胞黏附分子1（sVCAM-1）、内皮损伤标志物血管性血友病因子（vWF）、炎症反应标志物超敏C反应蛋白（hs-CRP）水平并予以分析。 结果替罗非班组心肌梗死溶栓治疗（TIMI）3级血流比例显著高于对照组,差异有统计学意义（79.3% vs. 50%,χ² = 10.747,P = 0.001）。对照组与替罗非班组患者治疗前的sICAM-1、sVCAM-1、vWF、hs-CRP水平比较,差异均无统计学意义（P均> 0.05）,替罗非班组患者治疗后24 h的sICAM-1[（24.2 ± 2.3）μg / L vs.（37.1 ± 3.3）μg / L]、sVCAM-1[（26.2 ± 2.9）μg / L vs.（43.1 ± 3.8）μg / L]、vWF[（514 ± 135）U / L vs.（588 ± 126）U/L]水平均低于对照组（P均< 0.05）,替罗非班组患者治疗后72 h的sICAM-1[（22.4 ± 1.8）μg / L（32.4 ± 2.5）μg / L]、sVCAM-1[（23.7 ± 2.2）μg/L vs.（38.9 ± 2.6）μg /L]、vWF[（586 ± 145）U / L vs. （678 ± 144）U / L]、hs-CRP[（7.2 ± 2.7）mg / L vs.（8.5 ± 3.5）mg/L]水平均明显低于对照组（P均< 0.05）。 结论AMI患者急诊PCI冠状动脉内注射替罗非班可显著改善靶血管前向血流TIMI分级和血管内皮功能。     

2型糖尿病病人血清sICAM-1、sVCAM-1与颈动脉粥样硬化的相关性研究

目的探讨2型糖尿病（T2DM）病人血清细胞间黏附分子1（sICAM-1）和血管细胞黏附分子1（sVCAM-1）与颈动脉粥样硬化的关系。方法酶联免疫吸附（ELISA）法检测120例T2DM病人（T2DM组）,根据超声颈动脉内中膜厚度（IMT）检查结果将120例T2DM病人分为3个亚组：IMT正常组40例、IMT增厚组30例、IMT斑块组50例（又根据超声IMT检查结果分为2小亚组：稳定斑块组36例、不稳定斑块组14例）与58例健康体检者（对照组）血清sICAM-1、sVCAM-1水平,并进行生化指标检测。结果糖尿病组血清sICAM-1、sVCAM-1水平均显著高于对照组（均P〈0．05）。IMT增厚组、IMT斑块组血清sICAM-1、sVCAM-1水平均显著高于IMT正常组（均P〈0．05）,不稳定斑块组显著高于稳定斑块组（P〈0．05）。糖尿病组血清sICAM-1、sVCAM-1水平与三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）、糖化血红蛋白（HbAlc）、高敏C反应蛋白（Hs—CRP）均呈正相关（r=0．670、0．665、0．666、0．702、0．678、0．675、0．686、0．704,均P〈0．01）。结论T2DM病人血清sICAM—1、sVCAM-1水平与颈动脉粥样硬化程度及斑块稳定性有关,其升高与慢性高血糖、脂代谢紊乱及炎症反应相关。     

Effect of nicotine replacement and quitting smoking on circulating adhesion molecule profiles (sICAM-1, sCD44v5, sCD44v6)

BACKGROUND: Soluble ICAM-1 (sICAM-1; sCD54), sCD44v5 and sCD44v6 are circulating adhesion molecules, with immunomodulatory potential, that have been frequently attributed diagnostic, prognostic and aetiological significance in a number of inflammatory and malignant diseases. We have previously shown that systemic concentrations of these molecules are increased significantly in tobacco smokers, but reduce to within normal levels at 12 months following successful quitting. MATERIALS AND METHODS: We have been able to extend these observations by measuring levels before and 4, 8, 22 and 52 weeks after smoking cessation in subjects receiving high-dose nicotine replacement therapy (25 mg of nicotine; n = 34) or placebo patches (n = 34) for 26 weeks. Smoking cessation was confirmed by regular measurement of expired-air CO levels and by plasma cotinine analysis. RESULTS: Plasma sICAM-1, sCD44v5 and sCD44v6 concentrations all declined rapidly within 4 weeks of smoking cessation (P < 0.001 for all declines). Additionally, no differences were observed between those using nicotine replacement and those who were not for sICAM-1, sCD44v5, or sCD44v6. CONCLUSIONS: The recovery in smoking-associated adhesion molecule profiles represents an almost immediate beneficial effect of smoking cessation. Nicotine replacement therapy is an effective aid to quitting and does not affect these recoveries. The elevated levels of these important risk factors in smokers (sICAM-1, sCD44v5 and sCD44v6) are linked to noxious element(s) in tobacco smoke other than nicotine or nicotine metabolites.     

Effect of profound normovolemic hypotension and moderate hypothermia on circulating cytokines and adhesion molecules

Hypotension caused by hypovolemic, hemorrhagic shock induces disturbances in the immune system that may contribute to an increased susceptibility to sepsis. The effect of chemically induced hypotension on circulating cytokines and adhesion molecules has not been investigated yet. In 21 patients scheduled for resection of malignant choroidal melanoma of the eye the perioperative serum levels of the cytokines IL-1beta, IL-6, IL-10, TNF-alpha, and the adhesion molecules sE-Selectin and sICAM-1 were investigated. Moderate hypothermia of 32 degrees C was induced in all patients. In 14 patients profound hypotension (mean arterial blood pressure 35-40 mmHg, hypotension group) was induced by enalapril and nitroglycerin for a mean duration of 71 min. In 7 patients the tumor was not resectable, and hypotension was not induced (controls). We did not detect significant differences in serum levels of cytokines or sE-Selectin perioperatively in patients with profound hypotension compared with controls. In both groups IL-6 serum levels increased significantly and reached a maximum after rewarming (17 +/- 6 and 16 +/- 5 pg/dL, respectively, P < 0.001). IL-1beta, IL-10, and TNF-alpha did not change perioperatively in both groups. On the first postoperative day sICAM-1 serum levels were significantly increased in both groups (mean increase of 96 and 54 ng/mL, respectively, P < 0.01 and P < 0.05). We conclude from this study that profound normovolemic arterial hypotension does not seem to have effects on serum levels of circulating IL-1beta, IL-6, IL-10, TNF-alpha, and sE-Selectin. Perioperative moderate hypothermia may be the reason for the postoperative increase in sICAM-1 levels independent of the blood pressure.     

Short-term hormone replacement therapy: reduced plasma levels of soluble adhesion molecules

BACKGROUND: Epidemiological data have suggested that the use of hormone replacement therapy (HRT) is associated with a decreased risk of cardiovascular disease. Vascular endothelium and adhesion molecules play an important role in the initiation and progression of atherosclerosis. MATERIAL AND METHODS: Prospective, randomized, placebo-controlled 12-week study. Sixty healthy, normotensive postmenopausal women received either micronised oestradiol 2 mg alone (n = 16, E2 group), or sequentially combined with a progestagen; E2 + P groups trimegestone 0.5 mg (E2 + T, n = 14) or dydrogesterone 10 mg (E2 + D group, n = 14) or placebo (n = 16). Data were collected at baseline and at 4 and 12 weeks. RESULTS: Twelve weeks of treatment with E2 or E2 + P was associated with a significant decrease in the plasma concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and thrombomodulin (sTM). The average decrease in these markers was about 9%. In women treated with trimegestone the decreases were larger than in those treated with dydrogesterone; for sICAM-1 (-15% vs. -2%; P < 0.0001), sVCAM-1 (-15% vs. +3%; P = 0. 003) and sTM (-9% vs. -4%; P = 0.11). Plasma levels of endothelin-1 (ET-1) decreased (by 13%) only in women treated with E2 + P. In the E2 group, flow-mediated, endothelium-dependent vasodilatation increased by 6 percentage points after 12 weeks (P = 0.07 vs. baseline, P = 0.02 vs. E2 + P, and P = 0.17 vs. placebo). CONCLUSION: Short-term treatment with E2 or E2 + trimegestone reduces plasma levels of sICAM-1, sVCAM-1 and sTM. ET-1 decreased only in the E2 + P groups. Different types of progestagens may differentially affect sICAM-1, sVCAM-1 and sTM levels, which may be relevant for the choice of type HRT.     

Inflammatory and endothelial markers in women with polycystic ovary syndrome

BACKGROUND: Women with polycystic ovary syndrome (PCOS) carry a pattern of cardiovascular risk factors. Endothelial dysfunction and chronic inflammation are early findings in the atherosclerotic process. The purpose of the study was to investigate the coexistence of active inflammation markers and endothelial dysfunction in young women with PCOS, and their relationship with metabolic and hormonal abnormalities of the syndrome. MATERIALS AND METHODS: Twenty-five young women with PCOS and 25 controls of similar age and body mass index (BMI) were studied. Endothelial function was assessed by flow-mediated dilatation (FMD) on the brachial artery and smooth muscle cells injury was excluded by nitrate-induced dilatation (NID). Plasma levels of endothelin-1 (ET-1), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and high sensitivity C-reactive protein (hsCRP) were measured. Hormonal and metabolic profiles were determined in both groups. RESULTS: Flow-mediated dilatation (FMD) was statistically lower in PCOS (P < 0.001), whereas nitrate-induced dilatation (NID) was similar within the two groups. Polycystic ovary syndrome (PCOS) had statistically higher levels of ET-1 (P = 0.03), sICAM-1 (P = 0.01), sVCAM-1 (P = 0.02) and hsCRP (P = 0.01). Furthermore FMD was statistically higher in PCOS population with hsCRP 1 mg L(-1) when compared with PCOS population with hsCRP > 1 mg L(-1) (P = 0.02). Flow-mediated dilatation (FMD) was negatively related to hsCRP (r = -0.512, P = 0.015); ET-1 was positively related to free androgen index (r = 0.27, P = 0.05) and negatively to sex hormone-binding globulin (r = -0.465, P = 0.022); sVCAM-1 was positively related to total testosterone (r = 0.431, P = 0.036); hsCRP was positively related to BMI (r = 0.647, P = 0.001), and negatively related to FMD (r = -0.512, P = 0.015), quantitative insulin sensitivity check index (QUICKI) (r = -0.499, P = 0.018), and MATSUDA index (r = -0.445, P = 0.038). CONCLUSIONS: The present study demonstrates that endothelial dysfunction coexists and is influenced by the presence of increased serum levels of inflammation and endothelial activation markers in young women with PCOS. These parameters appear to be interrelated with hyperandrogenaemia in this insulin-resistant population.     

Interaction between Chlamydia pneumoniae seropositivity, inflammation and risk factors for atherosclerosis in patients with severe coronary stenosis

OBJECTIVE: To investigate whether Chlamydia pneumoniae (Cpn) seropositivity in patients with suspected coronary artery disease (CAD) (n = 81) is associated with increases in markers of inflammation, the severity of coronary atherosclerosis, and traditional risk factors for cardiovascular events. MATERIAL AND METHODS: The severity of coronary atherosclerosis was ranked by Gensini score. Inflammation and endothelial dysfunction were evaluated using white blood cell counts and levels of high-sensitivity C-reactive protein (hs-CRP), ferritin, tumour necrosis factor-alpha (TNF-alpha), interleukins 1beta and 6 (IL-1beta, IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), E-selectin and oxidized LDL (oxLDL), and these were compared between Cpn-seropositive and seronegative individuals. RESULTS: IgA and IgG Cpn seropositivity were significantly associated with the presence of CAD (p = 0.005) and were independent predictive factors for the severity of coronary atherosclerosis (p = 0.005). Elevated levels of IL-6 (p = 0.027) and triglyceride (p = 0.038) and low levels of high-density lipoprotein cholesterol (HDL-C) (p = 0.038) were significantly predicted by Cpn IgA and IgG seropositivity. CONCLUSIONS: Seropositivity for Cpn is a risk factor for patients with significant angiographically documented coronary stenosis. Additionally, Cpn seropositivity was significantly associated with dyslipidemia and elevated IL-6, known risk factors for CAD. These observations indicate that Cpn infection may be one entry point to the causal or contributory pathways that lead to atherosclerosis and its clinical manifestations.     

急性冠脉综合征患者高表达的CD40L和炎症因子相关性

目的 检测急性冠脉综合征(ACS)患者CD4+T细胞CINOL的表达率、其血清可溶性CD40配体(sCD40L)和高敏C反应蛋白(hsCRP)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)的浓度,分析CD40L(sCD40L)与炎症因子的相关性,探讨CD40/CD40L在ACS发病中的作用及可能途径.方法 采用前瞻性研究方法,选取2006.10-2007.4中山大学附属第一医院急诊科、心血管医学部冠心病患者32例,包括稳定性心绞痛(SAP)7例、不稳定性心绞痛(UAP)14例、急性心肌梗死(AMI)11例.正常对照组(CON)为与患者年龄、性别相匹配的健康志愿者8例.所有受试者均排除感染、肿瘤、风湿、肝肾功能不全,未使用类固醇和免疫抑制剂等.流式细胞分析术(FCM)检测CD4+T细胞表达CD40L的阳性细胞率,ELISA法检测血清sCD40L、ICAM-1和VCAM-1浓度,免疫比浊法检测血清hsCRP浓度.所有资料使用SPSS 11.0进行统计学分析.结果 ANI、UAP、SAP、CON组CD4+T细胞中表达CD40L的阳性细胞率(%)分别为8.60±3.02、3.24±1.13、2.18±1.80、0.59±0.18,AMI组显著高于其他3组(P＜0.05),UAP组亦显著高于CON组(P＜0.05);4组血清sCD40L浓度分别为14.47±8.00、8.06±6.96、7.32±3.58、4.48±1.49(ng/mL),ANI组明显高于其他3组(P＜0.05);4组血清:hsCRP浓度分别为20.30±7.57、14.04±8.03、3.78±4.99、O.93±0.77(mg/L),AMI组显著高于其他3组(P＜0.05),UAP组亦显著高于SAP组与CON组(P＜0.05);4组血清ICAM-1浓度分别为418.09±222.19、212.86±128.43、165.04±32.12、108.62±62.27(ng/mL),AMI组显著高于其他3组(均P＜O.05),UAP组亦高于CON组(P＜0.05);4组血清VCAM-1浓度分别为5540.02±2614.65、3760.95±1915.01、4167.27±2084.48、2405.65±870.45(ng/mL),AMI组显著高于CON组(P＜0.01);AMI组CD4+T细胞中表达CD40L的阳性细胞率与VCAM-1呈明显正相关性(r=0.730,P=0.011),其血清sCD40L与hsCRP、ICAM-1、VCAN-1呈明显正相关性(r=0.677,P=0.011;r:0.901,P=0.000;r=0.714,P=0.014).结论 急性冠脉综合征患者CD4+T细胞CINOL的表达率和血清sCINOL浓度升高,且与血清hsCRP、ICAN-1、VCAM-1呈明显正相关;在ACS发生中起作用,此和hsCRP、ICAM-1、VCAN-1等有关,而CD40L/sCD40L可望作为冠心病危险性的预测因子.     

Fat distribution and endothelial function in normal-overweight menopausal women

BACKGROUND: Adipose tissue is not an inert deposit of fat; in the truncal area, it seems to be metabolically active, due to the adipokines produced locally. These substances are related to insulin resistance, inflammation and atherosclerotic damage to the vascular system. The development of ultrasound methodologies enable better estimation of fat distribution and more detailed investigation of the metabolic aspects of the fat depots and their impact on the initial stages of atherosclerosis. AIM OF THE STUDY: To investigate the influence of abdominal fat on endothelial function, the initial stages of atherosclerotic vascular damage and its relationship with inflammatory status in normal-overweight subjects [n. 162, body mass index (BMI) >25 kg/m(2) to <30 kg/m(2)]. METHODS: A total of 162 Caucasian postmenopausal women (mean age 54 +/- 4 years, menopausal age 8 +/- 4 years) were subdivided on the basis of the median value of the visceral fat distribution and associations with brachial flow-mediated vasoactivity (FMV), BMI, intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), total and LDL cholesterol investigated. RESULTS: Subjects with lower levels of visceral fat had a higher brachial FMV (7.9 +/- 4.3 vs. 5.1 +/- 3.2%, P < 0.05) and lower BMI, waist, sICAM-1, sVCAM-1, total and LDL cholesterol. In univariate analyses, abdominal visceral fat showed a direct correlation with sICAM-1 (r = 0.43, P < 0.001), and an inverse correlation with FMV (r = -0.49, P < 0.01). Moreover an indirect relationship emerged between brachial FMV and sICAM-levels (r = -0.36, P < 0.05). In a multivariate analysis the predictive variables for brachial FMV were LDL cholesterol (beta = -0.22, P < 0.05), visceral fat (beta = -0.32, P < 0.05), sICAM-1 (beta = -0.18, P < 0.05), HDL cholesterol (beta = 0.25, P < 0.05) and brachial diameter (beta = -0.27, P < 0.05). Subcutaneous fat and triglycerides were also included in the model. CONCLUSIONS: In Caucasian normal-overweight women, visceral fat thickness was directly associated with the level of soluble ICAM-1 and inversely with FMV, thereby showing its relevance to endothelial function and the inflammatory state.     

血清凝集蛋白-1和可溶性细胞间黏附分子-1与急性心肌梗死患者经皮冠状动脉介入术后心肌无复流的关系

目的 观察行经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)的急性心肌梗死(acute myocardial infarction,AMI)患者术前血清凝集蛋白-1(intelectin-1,ITLN-1)和可溶性细胞间黏附分子-1(soluble intercell...     

急性心肌梗死患者血清可溶性CD40配体和纤维蛋白原的改变及其临床意义

目的 观察急性心肌梗死患者血清可溶性CD40配体(sCD40L)水平和血浆纤维蛋白原(Fg)的变化以及与临床预后的关系.方法 采用酶联免疫吸附法测定60例急性心肌梗死患者血清sCD40L水平,用全自动血凝分析仪测定血浆Fg,患者出院后随访2年,观察心血管事件.结果 急性心肌梗死患者sCD40L水平(15.36±7.32)μg/L显著高于正常对照组(5.79±2.78)μg/L(P<0.001).急性心肌梗死患者中Fg水平(4.60±1.37)g/L显著高于正常对照组(3.03±0.82)g/L(P<0.001).发生心血管事件患者的sCD40L(18.14±6.34)μg/L和Fg(4.97±1.33)g/L显著高于无心血管临床事件患者的sCD40L(14.38±6.67)μg/L和Fg(4.20±1.24)g/L(P<0.05).sCD40L水平≥14.5 μg/L或Fg≥4.4 g/L的患者的心血管事件发生增多(P<0.05).合并糖尿病的急性心肌梗死患者sCD40L水平(18.38±6.71) μg/L显著高于不合并糖尿病的急性心肌梗死患者(14.46±6.48)μg/L(P<0.05).相关性分析显示在AMI患者中sCD40L与Fg正相关(r=0.27,P<0.05),Fg与左室射血分数负相关(r=-0.319,P<0.05).结论 急性心肌梗死患者血清sCD40L水平和Fg升高,sCD40L和Fg明显升高的患者发生心血管事件的风险明显升高,糖尿病是sCD40L升高的临床危险因素,sCD40L和Fg是急性心肌梗死患者的预后指标,在急性心肌梗死的病理生理过程中起重要作用.     

连续性高容量血液滤过对多器官功能障碍综合征患者血清炎性介质水平及血管内皮功能的影响研究

目的 探讨连续性高容量血液滤过(CHVHF)对多器官功能障碍综合征(MODS)患者血清炎性介质水平及血管内皮功能的影响.方法 选择2013年5月至2014年6月湖北省恩施自治州民族医院收治的80例MODS患者作为研究对象.采用随机数字表法将80例MODS患者分为研究组(n=40)与对照组(n=40).所有患者均有明确的原发疾病,且出现MODS,均符合《MODS诊断标准、病情严重度评分及预后评估系统和中西医结合证型诊断》中关于MODS的诊断标准.本研究纳入标准:年龄为35～68岁,符合MODS诊断标准,且首次行CHVHF治疗.排除标准:妊娠期妇女、接受免疫抑制治疗者及慢性肾功能衰竭者.对照组患者采用间歇性血液透析(IHD)及常规治疗方案,研究组患者在对照组治疗方案基础上进行CHVHF治疗.检测两组患者靶器官功能、血清炎性介质水平、血管内皮功能指标及治疗效果,并进行统计学分析.本研究遵循的程序符合湖北省恩施自治州民族医院医院人体试验委员会所制定的伦理学标准,得到该委员会批准,征得受试对象的知情同意,并与之签署临床研究知情同意书.两组受试对象性别构成比、年龄、原发病类型、急性生理和慢性健康状况评分系统(APACHE)Ⅱ评分、MODS评分、治疗时间等临床资料比较,差异均无统计学意义(P＞0.05).结果 ①治疗前,研究组与对照组MODS患者血清淀粉酶、丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、肌酐及尿素氮水平比较,差异均无统计学意义(P＞0.05).治疗后,研究组患者血清淀粉酶、ALT、AST、肌酐及尿素氮水平与治疗前相比,均显著减低,并且差异均有统计学意义[血清淀粉酶水平:(156.7±17.4) U/L与(316.3±45.3) U/L,t=20.671,P=0.000;血清ALT水平:(62.1±7.8) U/L与(88.3±9.3) U/L,t=13.598,P=0.000;血清AST水平:(58.7±6.9) U/L与(108.4±12.4) U/L,t=22.209,P=0.000;血清肌酐水平:(125.2±15.5) μmol/L与(321.4±54.2) μmol/L,t=21.997,P=0.000;血清尿素氮水平:(12.1±1.5)mmol/L与(25.3±3.2) mmol/L,t=23.488,P=0.000].治疗后,对照组患者血清中上述5种靶器官功能指标与治疗前相比,亦均显著减低,并且差异亦均有统计学意义[血清淀粉酶水平:(241.1±30.4)U/L与(312.2±43.3) U/L,t=8.501,P=0.008;血清ALT水平:(87.7±9.3) U/L与(98.3±10.3) U/L,t=4.853,P=0.036;血清AST水平:(87.7±9.1)U/L与(107.6±13.1) U/L,t=7.878,P=0.010;血清肌酐水平:(189.7±23.4)μmol/L与(318.6±55.2) μmol/L,t=13.597,P=0.000;血清尿素氮水平:(18.6±2.3) mmol/L与(25.3±3.3) mmol/L,t=10.559,P=0.000].治疗后,研究组患者血清淀粉酶、ALT、AST、肌酐及尿素氮水平均显著低于对照组,并且差异均有统计学意义(t=15.218、17.645、16.029、14.506、14.796,P=0.000).②治疗前,研究组与对照组MODS患者血清降钙素原(CRP)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6与-8水平比较,差异均无统计学意义(P＞0.05).治疗后,研究组患者血清CRP、TNF-a、IL-6与-8水平治疗前均显著降低,并且差异均有统计学意义[血清CRP水平:(11.3±1.6) mg/L与(25.1±3.2)mg/L,t=24.035,P=0.000;血清TNF-α水平:(326.3±41.2) ng/L与(468.0±52.0) ng/L,t=13.502,P=0.000;血清IL-6水平:(64.1±6.8) ng/L与(123.2±22.1) ng/L,t=16.186,P=0.000;血清IL-8水平:(121.3±10.1) ng/L与(196.3±23.1) ng/L,t=18.781,P=0.000].治疗后,对照组患者血清中上述4种炎性介质水平与治疗前相比,亦均显著减低,并且差异亦均有统计学意义[血清CRP水平:(18.8±2.4)mg/L与(25.1±3.3)mg/L,t=9.731,P=0.000;血清TNF-α水平:(368.2±42,4)ng/L与(461.6±52.1) ng/L,t=12.865,P=0.000;血清IL-6水平:(78.1±7.3) ng/L与(123.1±21.1) ng/L,t=12.712,P=0.000;血清IL-8水平:(135.4±9.3) ng/L与(195.3±22.4) ng/L,t=15.572,P=0.000].治疗后,研究组患者血清中CRP、TNF-α、IL-6与-8水平均显著低于对照组,并且差异有统计学意义(t=11.619、4.486、8.850、6.489,P=0.000、0.035、0.005、0.022).③治疗前,研究组与对照组MODS患者血清可溶性细胞间黏附分子(sICAM)-1、可溶性血管细胞黏附分子(sVCAM)-1、血管性假血友病因子(vWF)及基质金属蛋白酶(MMP)-9水平比较,差异均无统计学意义(P＞0.05).治疗后,研究组患者血清sICAM-1、sVCAM-1、vWF及MMP-9水平与治疗前相比,均显著减低,并且差异均有统计学意义[血清sICAM-1水平:(203.4±32.3) μg/L与(445.3±56.2) μg/L,t=22.579,P=0.000;血清sVCAM-1水平:(325.5±35.2) μg/L与(436.4±48.2)μg/L,t=11.734,P=0.000;血清vWF水平:(263.4±34.5) μg/L与(512.4±60.2)μg/L,t=22.682,P=0.000;血清MMP-9水平:(104.5±16.6) μg/L与(148.3±26.5) μg/L,t=8.859,P=0.008].治疗后,对照组患者血清中上述4种内皮损伤因子水平与治疗前相比,亦均显著减低,并且差异均有统计学意义[血清sICAM-1水平:(313.5±45.7)μg/L与(442.2±55.3)μg/L,t=11.344,P=0.000;血清sVCAM-1水平:(389.6±35.6) μg/L与(435.9±47.6) μg/L,t=8.804,P=0.007;血清vWF水平:(341.3±41.3) μg/L与(508.6±59.3) μg/L,t=14.628,P=0.000;血清MMP-9水平:(126.1±21.6) μg/L与(147.6±25.6) μg/L,t=4.063,P=0.035].治疗后,研究组患者血清sICAM-1、sVCAM-1、vWF及MMP-9水平均显著低于对照组,并且差异有统计学意义(t=12.433、8.084、9.141、5.014,P=0.000、0.008、0.000、0.032).④研究组患者病情好转或痊愈率为80.0％(32/40),显著高于对照组的60.0％(24/40),并且差异有统计学意义(x2=4.713,P＜0.05).结论 CHVHF治疗有助于改善MODS患者靶器官功能,减低患者血清中炎性介质水平与内皮损伤因子水平,进而保护血管内皮功能,提高治疗效果.但因本研究纳入样本量较小,CHVHF治疗MODS的作用机制及确切疗效,尚有待更多的基础、临床研究予以证实.