肾小球肾炎患者WBC流变性和CD18表达及血清sICAM—1浓度测定及其意义

探讨ＷＢＣ流变性和细胞粘附分子（ＣＡＭｓ）与肾小球肾炎病情变化的关系。方法采用红细胞变形能力测定仪、体外。栓血小板粘附两用仪及酶联免疫吸附法（ＥＬＩＳＡ）,分别检测了４０例急性肾小球肾炎患者、４２例慢性肾小球肾炎患者和４５例健康人外周血白细胞滤过指数（ＬＥＩ）、白细胞粘附率（ＬＡＲ）、白细胞ＣＤ１８表达及血清可溶性细胞间粘附分子一１（ＳＩＣＡＭ－１）浓度的变化。结果肾小球肾炎患者ＬＦＩ,ＬＡＲｔ,白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度均明显增高,与对照组比较差异有极显著性（Ｐ均＜０．００１）,且慢性肾小球肾炎患者各指标增高较急性肾小球肾炎患者更明显（Ｐ均＜０．００１）。结论白细胞流变性异常及ＣＤ１８表达、血清ｓＩＣＡＭ－１浓度增高与肾小球肾炎病情变化有密切关系。     

氦—氖激光血液照射对急性脑梗死患者白细胞变形能？…

目的 观察Ｈｅ－Ｎｅ激光血液照射对急性脑梗死患白细胞变形能力及粘附功能地影响。方法 对３５名对照组及Ｈｅ－Ｎｅ激光治疗和常规治疗的急性脑梗死患（分别４１例和４５例）在治疗前后进行外周血白细胞滤过指数（ＬＦＩ）、白细胞粘附率（ＬＡＲ）、白细胞ＣＤ１８表达及血清可溶性细胞间粘附分子（ｓＩＣＡＭ－１）浓度的动态监测。结果 脑梗死患ＬＦＩ、ＬＡＲ、ＣＤ１８表达及血清ｓＩＣＡＭ－１浓度明显高于健康人（     

肝硬化患者血清可溶性细胞间粘附分子—1水平变化及意义

目的；探讨肝硬化患者血清可溶性细胞粘附分子－１（ｓＩＣＡＭ－１）水平变化，了解它与肝硬化患者肝功能损伤和门脉高压形成的关系。方法：用酶联免疫吸附法（ＥＬＩＳＡ）检测１７例正常人和３３例肝硬化患者血清ｓＩＣＡＭ－１。结果；肝硬化组血清ｓＩＣＡＭ－１水平显著高于对照组，且在肝功能分级中，呈现Ｃｈｉｌｄ Ｃ〉Ｃｈｉｌｄ Ｂ〉Ｃｈｉｌｄ Ａ的规律。相关分析显示肝硬化者血清ｓＩＣＡＭ－１与总胆红素及谷丙转氨     

冠心病可溶性细胞间粘附分子-1的检测及其意义

目的 检测冠心病患者可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）的变化,探讨其在冠心病发病机理、病情监测中的意义。方法 用酶联免疫吸附法检测５０例急性心肌梗死（ＡＭＩ）、５０例不稳定性心绞痛（ＵＡ）、３０例稳定性心绞痛（ＳＡ）、３０例健康者血浆ｓＩＣＡＭ－１水平。结果 （１）ＡＭＩ、ＵＡ、ＳＡ患者ｓＩＣＡＭ－１水平均较正常对照组高,且三组间亦有显著差异。（２）ＡＭＩ患者按心功能分组,各组间亦有显著差     

肠缺血—再灌注损伤对中性粒细胞和内皮细胞粘附分子表达 …

目的 研究肠缺血－再灌注过程对局部及远隔器官中性粒细胞（ＰＭＮ）和组织血管内皮细胞粘附分子表达的影响及其与脏器功能受损的关系。方法：雄性Ｗｉｓｔａｒ大白鼠，随机分为对照组、肠缺血组和再灌注组。比较肠缺血－再灌注过程中局部及远隔器官组织随过氧化物酶（ＭＰＯ）活性、ＰＭＮ上的配基ＣＤ１１ｂ／ＣＤ１８表达、细胞间粘附分子－１（ＩＣＡＭ－１）表达的变化以及主要脏器功能的改变。结果：１主要脏器功能变化异常的     

可溶性细胞间粘附分子—1和白细胞介素—8与病毒性肝炎关 …

为探讨可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）和白细胞介素－８（ＩＬ－８）在慢性及重型病毒性肝炎发病过程中的意义，用酶联免疫吸附试验同期检测了６７例肝炎患者及１６例健康献血员血清ｓＩＣＡＭ－１和ＩＬ－８的水平。     

内毒素条件下中性粒细胞／血管内皮细胞膜表面CD18／ICA…

应用细胞酶联免疫吸附测定法（ＲＬＩＳＡ）测定内纱刺激条件下，中性粒细胞（ＰＭＮ）和增益脐静脉内皮细胞（ＶＥＣ）膜表面主要粘附分子的表达，前者检测ＣＤ１８，后者检测作为ＣＤ１８配体的细胞间粘附分子－－１（ＩＣＡＭ－１）。结果表明：内毒素可迅速导致ＰＭＮ膜表面ＣＤ１８的表达，半小时内达表达高峰，增另刺激时间不能持续其表达水平，ＶＥＣ在内毒素刺激诱导３ｈ后，ＩＣＡＭ－１的表达在一定基础表达水平上开始持续     

急性冠状动脉综合征患者血清细胞粘附分子的变化

目的：观察急性冠状动脉综合征患者血清可溶性细胞粘附分子－１（ＩＣＡＭ－１、血管细胞粘附分子－１（ＶＣＡＭ－１）、Ｅ－选择素（Ｅ－Ｓ）和血管性血友病因子（ＶＷＦ）的变化以及急性心肌梗死（ＡＭＩ）患者成功再灌注后上述指标的动态变化。方法急性冠状动脉综合征组３７例中ＡＭＩ２１例，随机主动脉腔内成形术或溶栓治疗，于再灌注治疗前和治疗后１２、２４、４８和７２小时各抽血１次，心绞痛患者１６例和正常对照组４０例     

ICAM—1／LFA—1和HLA—DR在蕈样肉芽肿中的表达及其意义

目的：为探讨粘附分子在蕈样肉芽肿（ＭＦ）病理形成机制中的作用。方法：采用免疫组化技术，检测了１６例ＭＦ皮损部位ＩＣＡＭ－１／ＬＦＡ－１和ＨＬＡ－ＤＲ的表达。结果：ＩＡＣＭ－１／ＬＦＡ－１和ＨＬＡ－ＤＲ在ＭＦ表皮和／或毛囊上皮角朊细胞 不同程度的表达，其中ＩＣＡＭ－１的表达与ＭＦ亲表皮性明显相关。结论Ｌ：ＩＣＡＭ／１ＬＦＡ－１在ＭＦ亲表皮性形成过程中可能起着重要作用。     

LPS对心脏微血管内皮细胞ICAM-1表达的影响及rHDL的调控作用

目的：观察 ＰＬＳ作用下心脏微血管内皮（ＣＭＥＣｓ）细胞间粘附分子 （ＩＣＡＭ）－１的表达情况及ｒＨＤＬ的调控作用,为ＣＨＤ的防治提供实验依据。方 法：利用培养的血管内皮细胞,采用流式细胞仪检测正常细胞、ＬＰＳ作用和ＬＰＳ与 ｒＨＤＬ协同作用下０、１、２、６、１２小时不同时相点 ＩＣＡＭ－１表达阳性细胞数及荧光 强度。结果：ＬＰＳ和ＣＭＥＣｓ共同孵育下,随时间延长ＩＣＡＭ－１表达的阳性细胞数 和荧光强度上升,ｒＨＤＬ有抑制ＩＣＡＭ－１表达作用。结论：ＰＬＳ可以刺激ＣＭＥＣｓ 表达ＩＣＡＭ－１,ｒＨＤＬ对血管内波细胞的损伤有保护作用。     

2型糖尿病患者血清sICAM-1和sVCAM-1的检测与大血管病变的关系

目的　探讨 2型糖尿病患者血清可溶性细胞间黏附分子 1(solubleintercellaradhesionmolecule 1,sICAM 1)和可溶性血管细胞黏附分子 1(solublevascularcelladhesionmolecule 1,sVCAM 1)与大血管病变的关系。方法　测定 76例 2型糖尿病患者及 4 8例健康对照者血清sICAM 1和sVCAM 1水平 ,76例 2型糖尿病患者分为大血管病变组 (2 8例 )与无大血管病变组 (48例 ) ,比较三组间sICAM 1和sVCAM 1的水平。并对糖尿病组中颈总动脉内膜厚度 (intima mediathickness,IMT)与sICAM 1和sVCAM 1作单因素相关分析。结果　 2型糖尿病患者中无大血管病变组及有大血管病变组的血清sICAM 1和sVCAM 1水平分别高于健康对照者 (P <0 .0 5 ,P <0 .0 1) ,有大血管病变者又高于无大血管病变者 (P <0 .0 5 )。糖尿病组中颈总动脉IMT分别与sICAM 1和sVCAM 1呈正相关 (r =0 .2 0 2 ,P <0 .0 5 ;r =0 .35 8,P <0 .0 1)。结论　 2型糖尿病患者血清sICAM 1和sVCAM 1水平的升高 ,表明了体内存在血管内皮细胞功能紊乱和白细胞的激活 ,并参与了大血管病变的发生发展过程 ,可作为病情监测的血清学指标     

不稳定性心绞痛患者血清Vaspin水平及与血管内皮细胞黏附分子的相关性

目的 观察不稳定性心绞痛（UA）患者血清内脏脂肪组织来源的丝氨酸蛋白酶抑制剂（visceral adipose tissue derived serine protease inhibitor, Vaspin）水平,并探讨血清Vaspin与可溶性血管细胞黏附分子1（sVCAM 1）、可溶性细胞间黏附分子1（sICAM 1）之间的相关性。方法 采用定量夹心酶联免疫检测技术对90例不稳定性心绞痛患者（UA组）、90例稳定性心绞痛（SA）患者（SA组）及80例健康对照者（对照组）血清Vaspin、sVCAM 1、sICAM 1水平的变化进行检测,同时常规检测其他临床生物化学指标。在UA组,采用Pearson相关检验对血清Vaspin与sVCAM 1、sICAM 1、高敏C反应蛋白（hs CRP）及其他生物化学指标进行相关性分析。结果 UA组血清sVCAM 1、sICAM 1水平显著高于SA组（分别P＜0.01）及对照组（均P＜0.01）。UA组血清Vaspin水平与sVCAM 1（r＝0.354,P=0.001）、sICAM 1（r＝0.287,P=0.006）、hs CRP（r＝0.3111,P=0.003）水平呈显著负相关。结论 不稳定性心绞痛患者血清Vaspin水平显著降低,并与sVCAM 1、sICAM 1、hs CRP呈负相关,提示血清Vaspin与血管内皮损伤、冠心病严重程度密切相关,可能为不稳定性心绞痛患者重要的生物标志物。     

急性心肌梗死患者黏附分子及相关因素的研究

目的探讨急性心肌梗死(AMI)患者发病早期至1周内血清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(sVCAM-1)、D-二聚体(D-D)、血小板第4因子(PF4)的动态变化及其相互关系.方法测定40例AMI患者发病24小时和1周时的血清sICAM-1、sVCAM-1、D-D、PF4并与健康对照组30例比较.结果AMI患者于发病24小时及1周时sICAM-1、sVCAM-1、DD、PF4[发病24小时分别(420.97±128.83)μg/L,(51.44±14.83)μg/L,(357.93±147.09)μg/L和(6.10±1.54)mg/L;发病1周时分别为(404.96±115.22)μg/L,(48.01±17.24)μg/L,(381.12±163.00)μg/L和(6.33±2.19)mg/L]均明显高于对照组[分别为(180.70±32.07)μg/L,(13.31±12.81)μg/L,(84.00±26.99)μg/L和(3.07±1.34)mg/L,P均<0.01].AMI组于发病24小时及1周时sICAM1与sVCAM-1均具有正相关性(P均<0.01),PF4与sICAM1、sVCAM-1、D-D间亦具有正相关性(P均<0.01),而D-D与sICAM-1、sVCAM-1间均无相关性(P均>0.05).结论AMI从发病早期至1周内sICAM-1、sVCAM-1持续升高,表明炎症参与心肌细胞损伤过程,早期应用抗黏附分子抗体和药物可防止AMI病情进展.     

氦－氖激光血液照射对急性脑梗死患者白细胞变形能力及粘附功能的影响

目的　观察He Ne激光血液照射对急性脑梗死患者白细胞变形能力及粘附功能的影响。方法　对 3 5名健康对照组及He Ne激光治疗和常规治疗的急性脑梗死患者 (分别 41例和 45例 )在治疗前后进行外周血白细胞滤过指数 (LFI)、白细胞粘附率 (LAR)、白细胞CD18表达及血清可溶性细胞间粘附分子 1(sICAM 1)浓度的动态监测。结果　脑梗死患者LFI、LAR、CD18表达及血清sICAM 1浓度明显高于健康人 ( P <0 .0 0 1) ;随着治疗后病情的好转 ,各组治疗前及治疗后 7、14、2 1d ,患者LFI、LAR、CD18表达和sICAM 1浓度均逐渐降低 ,其变化有统计学差异 (P <0 .0 1) ;激光治疗组与常规治疗组比较 ,治疗前各指标间差异无显著性 ,治疗后 14、2 1d激光治疗组各项指标均低于对应时点的常规治疗组 (P <0 .0 1或P<0 .0 0 1)。结论　He Ne激光血液照射可改善脑梗死患者白细胞变形能力 ,降低白细胞粘附功能并使白细胞粘附分子表达减少 ,这可能是其治疗急性脑梗死的作用机制之一。     

Prognostic Value of Serum Von Willebrand Factor,but Not Soluble ICAM and VCAM,for Mortality and Cardiovascular Events is Independent of Residual Renal Function in Peritoneal Dialysis Patients

♦ Objective: We explored associations between markers of endothelial dysfunction and outcome events, and whether those associations were independent of residual renal function (RRF) in patients on peritoneal dialysis.♦ Methods: The study enrolled 261 incident patients and 68 healthy control subjects who were followed till death, censoring, or study end. Demographics, biochemistry, markers of inflammation (C-reactive protein) and endothelial dysfunction [soluble intercellular adhesion molecule 1 (sICAM), soluble vascular adhesion molecule 1 (sVCAM), and von Willebrand factor (vWf)] were examined at baseline. Outcome events included all-cause death and fatal and nonfatal cardiovascular (CV) events.♦ Results: Mean levels of vWf, sICAM, and sVCAM were significantly higher in patients than in healthy control subjects. Levels of sICAM and sVCAM, but not vWf, were significantly correlated with RRF. Levels of sICAM and vWf both predicted all-cause mortality and fatal and nonfatal CV events after adjustment for recognizable CV risk factors. The association between sICAM and outcome events disappeared after further adjustment for RRF. However, RRF did not change the predictive role of vWf for outcome events. Compared with the lowest vWf quartile (6.6% - 73.9%), the highest vWf quartile (240.9% - 1161%) predicted the highest risk for fatal and nonfatal CV events (adjusted hazard ratio: 2.05; 95% confidence interval: 1.15 to 3.64; p = 0.014). We observed no associations between sVCAM and RRF, or sVCAM and any outcome event.♦ Conclusions: The prognostic value of vWf, but not sICAM, is independent of RRF in predicting mortality and CV events.     

Systemic endothelial activation is greater in septic than in traumatic-hemorrhagic shock but does not correlate with endothelial activation in skin biopsies

OBJECTIVE: Sepsis and severe trauma result in endothelial activation and damage. The activated endothelium expresses adhesion receptors that control leukocyte trafficking. After activation, some adhesion molecules are also released into plasma as soluble forms. The present study was designed to compare the expression of soluble cell adhesion molecules (sCAMs) in three groups of patients: those with septic shock, severe sepsis, and traumatic-hemorrhagic shock. In addition, the endothelial expression of these adhesive molecules was examined in skin biopsies. DESIGN: Prospective observational study SETTING: Intensive care unit at a university hospital PATIENTS: The study included 15 patients with septic shock (by Bone's definition), 11 patients with severe sepsis (by Bone's definition), and 13 patients with traumatic-hemorrhagic shock. Fifteen healthy blood donors served as controls. MEASUREMENTS AND MAIN RESULTS: Measurements of sCAMs were performed on days 1, 2, and 3 of the disease. On day 1, when compared with controls, sE-selectin, sP-selectin, soluble vascular cell adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1 were markedly elevated in septic shock patients, whereas these sCAMs, except for sP-selectin, were within normal ranges in traumatic-hemorrhagic shock patients. In patients with severe sepsis, an earlier stage than septic shock in the sepsis continuum, intermediate values of sCAMs were found. In skin biopsies of septic shock patients, the endothelial cells expressed a bright staining of constitutive endothelial molecules (CD146, CD144, CD131). Inducible molecules (ICAM-1, VCAM-1, and E-selectin) were positively expressed with bright staining. The biopsies from traumatic-hemorrhagic shock patients showed a similar positive expression of endothelial molecules. CONCLUSION: The patterns of sCAMs indicate that the systemic activation of the endothelium is different in the three clinical entities, maximum in septic shock, intermediate in severe sepsis, and not different from controls in traumatic-hemorrhagic shock. Comparable endothelial activation as evidenced by skin biopsies suggests that caution is required in the interpretation of CAMs in plasma, which does not necessarily reflect the in situ activation state of endothelium.     

Transmigration of blood leukocytes into the peritoneal cavity is related to the upregulation of ICAM-1 (CD54) and Mac-1 (CD11b/CD18) adhesion molecules.

BACKGROUND: Migration of blood leukocytes into the peritoneal cavity of patients treated with peritoneal dialysis appears to be an important mechanism to prevent and fight peritonitis. To study the role of adhesion molecules in the process of leukocyte transmigration, we compared the expression of several adhesion receptors between peripheral blood monocytes and macrophages isolated from overnight dwell effluents. METHODS: The study was performed in 12, stable, infection-free patients treated with continuous ambulatory peritoneal dialysis (CAPD) and in 9 patients during peritonitis. In another set of experiments, we analyzed the expression of these molecules on blood leukocytes in 10 predialysis chronic renal failure (CRF) patients and 9 healthy controls. Peritoneal cells from an 8-hour dwell were isolated by centrifugation. Expression of adhesion receptors CD11a, CD11b, CD18, CD49d, and CD54 on blood and peritoneal leukocytes was measured using flow cytometry. RESULTS: In macrophages from the uninfected effluents, expression of both subunits of Mac-1 integrin receptor (CD11b and CD18) and intercellular adhesion molecule (ICAM)-1 receptor (CD54) was upregulated compared to peripheral blood monocytes from the same patients. The median value of mean fluorescence intensity in blood and effluent was 760.3 versus 1085.8 for CD11b (p = 0.013), 288.8 versus 448.6 for CD18 (p = 0.003), and 186.1 versus 365.7 for CD54 (p = 0.001). The same adhesion receptors were also significantly upregulated on peritoneal macrophages and neutrophils during peritonitis compared to blood leukocytes. Blood leukocytes from CAPD and CRF patients showed higher expression of CD54 and CD49d molecules compared to leukocytes from healthy controls. CONCLUSIONS: These data suggest that transmigration of blood leukocytes into the peritoneal cavity during uncomplicated dialysis and in peritonitis is related to selective upregulation of ICAM-1 (CD54) and Mac-1 (CD18/CD11b) receptors.     

Increased incidence of sepsis and altered monocyte functions in severely injured type A- glucose-6-phosphate dehydrogenase-deficient African American trauma patients

OBJECTIVE: To determine whether trauma patients with the common, type A- glucose-6-phosphate dehydrogenase (G6PD) deficiency have an aggravated inflammatory response, increased incidence of septic complications, and/or more profound alterations in leukocyte functions compared with nondeficient trauma patients. SETTINGS: Intensive and surgical care units of a trauma center and flow cytometry and experimental laboratories at a teaching university hospital. DESIGN: Prospective cohort clinical study with measurements on days 2 and 5 postinjury. Monocyte and neutrophil oxidant content, apoptosis, and CD11b expression and plasma cytokine levels were compared between G6PD-deficient and nondeficient patients. PATIENTS: A total of 467 male African American trauma patients were screened for the deficiency. Forty-four type A-202/376 G6PD-deficient patients were identified and enrolled in the study; 43 nondeficient patients were also enrolled and were matched by age, clinical criteria of injury severity, and type of trauma. MAIN RESULTS: After severe injury (Injury Severity Score, > or =16), 50% of the deficient and 6.2% of nondeficient patients developed sepsis with positive bacterial blood cultures. In deficient patients, the frequency of bronchial (75%) and wound infections (25%) was also increased compared with nondeficient patients (32% and 0%). The durations of systemic inflammatory response syndrome, Sepsis Syndrome, and days on antibiotics were three times longer in deficient than in nondeficient individuals. However, adult respiratory distress syndrome occurred in 37% of both groups. Anemia was more severe in the deficient than nondeficient patients from day 10 posttrauma. On day 5, the peroxide content was doubled, apoptosis was decreased, and CD11b expression was increased in monocytes from deficient patients compared with cells from nondeficient patients. On day 5, the plasma interleukin (IL)-10 concentration was significantly lower in deficient than nondeficient patients, whereas tumor necrosis factor-alpha, IL-6, and IL-8 levels were similar. After moderate injuries (Injury Severity Score, 9-16), the deficiency was not associated with adverse clinical effects, and the trauma-induced changes in leukocyte function were similar in deficient and nondeficient patients. CONCLUSIONS: The common type A- G6PD deficiency predisposes septic complications and anemia in trauma patients after severe injuries as defined by an Injury Severity Score of > or =16. This adverse clinical course is accompanied by altered monocyte functions manifested as augmented oxidative stress, a decreased apoptotic response, increased cell adhesion properties, and a diminished IL-10 response.     

Increased expression of CD11b/CD18 on phagocytes in ischaemic disease: a bridge between inflammation and coagulation

The aim of this study was to assess the expression of CD11b/CD18 integrin adhesion molecules on the phagocytes of patients with ischaemic diseases, and to evaluate the concentration of soluble adhesion molecules that are released from endothelium (sICAM-1) and from phagocytes (sL-selectin). A total of 370 patients were enrolled: 120 with coronary artery disease (CAD); 50 with peripheral artery occlusive disease (PAOD); and 200 control subjects with no clinical manifestations of ischaemic disease. CD11b/CD18 integrin was detected by flow cytometry, whereas sL-selectin and sICAM-1 concentrations were detected using a sandwich-type immunoassay. CD11b/CD18 integrin expression was found to be higher in the patients with ischaemic disease than in the control subjects ( P  < 0.001). The PAOD patients had higher values of CD11b/CD18 integrin than the CAD ones ( P  < 0.01). The concentration of soluble adhesion molecules did not show any significant differences within the three groups ( P  = NS). The high expression of CD11b/CD18 integrin in ischaemic disease patients may depend on the increased, but probably stable, cytokine network that has been demonstrated to occur in chronic ischaemic diseases: the difference observed between PAOD and CAD patients could be the consequence of higher inflammatory activation probably resulting from the greater extent of the atherosclerotic process in PAOD, or of the more localized ischaemic area in CAD patients. CD11b/CD18 can therefore be considered a marker of chronic phagocyte activation during ischaemic disease. On the other hand, sICAM and sL-selectin concentrations were found to be within the normal range; they have recently been considered as a marker for acute ischaemic events and acute inflammatory process activation. Our results confirm that in uncomplicated atherosclerosis no acute inflammatory process activation should occur.