缺血—再灌注状态白细胞粘附性变化及针刺的作用

本文利用缺血－再灌注动物模型，研究了白细胞粘附性的变化以及针刺对缺血及再灌注状态下白细胞粘附性的改善作用。实验结果表明：不同切变率（１５、３０、６０、１５０、３００ｓ￣（－１））作用于白细胞，随切变率的增大，白细胞粘附率逐渐下降，较之对照组，缺血组及缺血再灌注组白细胞粘附率均有所下降，切变率为１５０ｓ￣（－１）时，对照组为０．６５±０．３２，缺血组为０．４９±０．２７，缺血再灌注组为０．３８±０．３６；醒脑开窍针刺法对缺血及再灌注组白细胞粘附性均有明显改善作用。     

前列腺素E1治疗急性肺损伤研究进展

前列腺素Ｅ１具有降低肺毛细血管通透性，抑制肺内血小板聚集，抑制白细胞在肺内聚集及影响血浆ＴＸＢ２浓度等一系列作用，对治疗急性肺损伤有一定的效果，但临床应用亦有降低体循环血压和增加肺内分流等副作用。     

重组sICAM-1对PMA刺激的白细胞与\=肺微血管内皮细胞粘附的影响

目的:探讨重组sICAM-1对大鼠白细胞与肺微血管内皮细胞粘附的影响。方法:采用原代培养的大鼠肺微血管内皮细胞及⁹⁹Tm-HMPAO标记的白细胞,观察不同浓度的sICAM-1、CA7(sICAM-1的单抗)以及sICAM-1·CA7(sICAM-1的二聚体)对PMA刺激的大鼠白细胞与肺微血管内皮细胞粘附的影响。结果:sICAM-1与CA7即使在100mg/L也不能抑制白细胞与肺微血管内皮细胞的粘附,而其二聚体在20mg/L和40mg/L即可抑制42%和50%的细胞粘附(P＜0.05)。结论:sICAM-1对细胞粘附的抑制作用很弱,可能与其单体形式有关。     

由人肺中分离树突状细胞(文摘)

作者建立了一种纯化人肺中树突状细胞(DC)的方法。这种DC有两个特征:能紧密粘附于塑料表面,也不表达T、B、NK及单核细胞的表面标志。由酶消化肺组织所获白细胞包含有DC、淋巴细胞和大量的肺巨噬细胞(PM)。将白细胞粘附90min,洗去非粘附的     

急、慢性缺氧对大鼠微循环白细胞流变性的影响

目的：研究急、慢性缺氧对大鼠肠系膜微循环白细胞流变学行为的影响。方法：活性显微镜结合计算机图象处理系统研究白细胞的流变学行为。结果：急性缺氧白细胞粘附显著增加，白细胞－内皮细胞接触时间（TLECT）延长，而慢性缺氧白细胞粘附显著减少，沿壁滚动减少，TLECT显著缩短。结果：1．急性缺氧引起肠系膜微循环白细胞流变性显著性改变，严重影响微循环的正常灌流，是导致血管内皮损伤的重要机制。2．与急性相比，慢性缺氧大微循环白细胞的流变行为有明显不同，这对促进动物习服适应可能有重要作用。3．急、慢性缺氧下白细胞流变性的显著性差异可能与白细胞功能的改变及局部微环境的变化有关。     

烧伤大鼠粒细胞与内皮细胞粘附力学特性的研究

本文以大鼠作为烧伤的实验动物模型，以微管吸吮技术研究了烧伤情况下粒细胸（ＰＭＮ）与肺毛细血管内皮细胞（ＰＣＥＣ）的粘附力学特性．作者首先测定了ＰＭＮ与ＰＣＥＣ间的粘附力Ｆａ，进而在实验条件下定义了相对粘附应力Ｓ１．实验结果表明：在烧伤后２４小时内，粒细胞与肺毛细血管内皮细胞间的粘附力及相对粘附应力均显著升高，且在烧伤后１小时达到最大值。结合烧伤早期的病理变化，作者对实验结果进行了一定的分析和讨论．     

糖皮质激素受体阻断对大鼠白细胞粘附的作用

目的明确ＧＲ阻断后对白细胞粘附的作用及可能的作用机制。方法１．在体实验。观察肠系膜微循环白细胞贴壁粘附数。 ２．高体实验。（１）ＰＭＮ与玻璃珠粘附;ＰＭＮ粘附率（％）粘附：ＰＭＮ粘附率（％）＝粘附前ＰＭＮ计数一洗脱液ＰＭＮ计数（３）ＰＭＮ粘附 粘附前ＰＭＮ计数分子ＣＤ１８：ＥＬＩＳＩＡ检测;（４）ＣＤ１８表达和ＰＭＮ与ＩＣＡＭ－１包被磁珠粘附的关系：ＰＭＮ与ＩＣＡＭ－１包被磁珠粘附,同时测定ＣＤ１８表达。结果１．在体实验。对照组仅有少量白细胞贴壁粘附（２．５０±２．１７）,阻断ＧＲ后白细胞贴壁粘附±Ｄｅｘ组的粘附率与ＴＮＦ组相比无显著差异（Ｐ＞０．０５）,Ｄｅｘ±ＴＮＦ组的粘附率与ＴＮＦ组相比有下降趋势．但差异不显著。ＴＮＦ＋Ｄｅｘ＋ＲＵ４８６组的粘附率与ＴＮＦ组和对照组相比均有差异（分别是 Ｐ＜０． ０５,Ｐ＜０． ０１）。 ２． ＰＭＮ与 ＥＣ粘附： ＴＮＦ组与ＴＮＦ＋Ｄｅｘ组结果同ＰＭＮ与玻璃珠粘附。Ｄｅｘ＋ＴＮＦ组的粘附率与ＴＮＦ组相比差异显著（Ｐ＜０．０５）。ＴＮＦ＋Ｄｅｘ＋ＲＵ４８６组的粘附率与对照组相差十分显著（Ｐ＜０．０１）,与ＴＮＦ组相比,两者无明显差异。３．ＰＭＮ与ＩＣＡＭ－１包被磁珠粘附：ＴＮＦ     

慢性喘息型支气管炎患者sELAM－1测定及意义

慢性喘息型支气管炎患者ｓＥＬＡＭ－１测定及意义齐法莲，杨道理，陈英剑，孙文杰，张波（济南军区总医院免疫科，济南２５００３１）内皮白细胞粘附分子－１（ＥＬＡＭ－１）属于粘附分子的选择素家族，在炎症过程中是介导内皮细胞与白细胞等粘附的重要分子［１］。呼吸...     

细胞因子对心脏微血管内皮细胞与淋巴细胞粘附的影响

目的：观察细胞因子对心脏微血管内皮细胞表面细胞间粘附分子－１（ｉｎｔｅｒｃｅｌｕｌａｒａｄｈｅｓｉｏｎｍｏｌｅｃｕｌｅ－１，ＩＣＡＭ－１）的表达的调控，及对内皮细胞与激活淋巴细胞粘附的影响。方法：体外培养大鼠心脏微血管内皮细胞，以肿瘤坏死因子（ｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ－α，ＴＮＦ－α）、白细胞介素－６（ｉｎｔｅｒｌｅｕｋｉｎ６，ＩＬ－６）和白细胞介素－１（ｉｎｔｅｒｌｅｕｋｉｎ１β，ＩＬ－１β）诱导。采用免疫组织化学染色法观察内皮细胞表面ＩＣＡＭ－１表达；采用粘附试验和抗ＩＣＡＭ－１或抗ＬＦＡ－１单克隆抗体阻断抑制试验。结果：ＴＮＦ－α、ＩＬ－６和ＩＬ－１β诱导内皮细胞１８～２４ｈ，均可使内皮细胞与淋巴细胞的粘附率显著增加，ＴＮＦ－α和ＩＬ－１β的诱导还可使内皮细胞表面ＩＣＡＭ－１分子表达明显增强，表现为ＩＣＡＭ－１表达阳性细胞数增多，着色加深。用１０～２０ｍｇ／Ｌ抗ＩＣＡＭ－１或抗ＬＦＡ－１单克隆抗体均可部分抑制内皮细胞与淋巴细胞的粘附。结论：ＴＮＦ－α和ＩＬ－１β可以有效地激活心脏微血管内皮细胞，通过诱导内皮细胞ＩＣＡＭ－１表达增多，促进内皮细胞与淋巴细胞的粘附     

CD45McAb通过LFA－1和ICAM－1诱导外周血单个核细胞粘附反应

ＣＤ４５ＭｃＡｂ通过ＬＦＡ－１和ＩＣＡＭ－１诱导外周血单个核细胞粘附反应〔英〕／ＬｏｒｅｎｚＨＭ…／／ＣｅｌｌＩｍｍｕｎｏｌ。─１９９３，１４７．─１１０～１２８ＣＤ４５是白细胞的共同抗原，是唯一表达于所有白细胞表面的一种含量最丰富的跨膜蛋白质，但是...     

山莨菪碱对急性失血性休克家兔白细胞变形能力的影响

观察了急性失血性休克家兔白细胞变形能力的变化及山莨菪碱对其的影响。结果显示，休克时白细胞滤过指数明显高于休克前（Ｐ＜０．００１），且随休克时间的延长，滤过指数逐渐增高。应用山莨菪碱治疗后，白细胞滤过指数明显低于对照组和休克时，差异有显著性意义（ｐ＜０．００１），与休克前相比无明显差异（Ｐ＞０．０５）。本文结果提示，山莨菪碱具有明显改善白细胞变形能力的作用。     

高血压患者白细胞变形性的初步观察

对２５例高血压患者和２０例正常血压者血液流变学指标检测的结果表明：高血压组白细胞滤过指数（ＩＦ）明显大于正常血压组（Ｐ＜０．０１），低切变率全血粘度与平均动脉压呈正相关（ｒ＝０．６２７４，Ｐ＜０．０１）。提示：高血压病程中全血粘度升高与白细胞变形性（ＬＤ）降低有关，高血压微血管病变可能是导致ＬＤ降低的机制之一。     

可溶性血管细胞粘附分子1(sVCAM-1)在紫癜性肾炎发病中的作用探讨

目的:探讨血管细胞粘附分子-1(VCAM-1)在过敏性紫癜性肾炎(HSPN)发病中的作用,并观察其与白介素-6(IL-6)、免疫球蛋白E(IgE)在HSPN发病中的关系。方法:采用酶联免疫吸附法(ELISA)检测27例过敏性紫癜、35例紫癜性肾炎患儿(其中急性期16例,恢复期10例)及20例健康对照儿童的血清sVCAM-1、IL-6、IgE水平。结果:①紫癜性肾炎组较单纯过敏性紫癜组、正常对照组血清sVCAM-1均明显升高,且急性期高于恢复期及正常对照组,差异均有显著性意义(P均<0.001),肾炎组、单纯组分别与对照组比较,血清IL-6、IgE水平升高,差异有显著性意义(P<0.01),恢复期较正常对照组血清sVCAM-1、IL-6水平无很大变化,差异无显著性意义(P均>0.05)。②紫癜性肾炎组、单纯过敏性紫癜组sVCAM-1水平随血清IL-6、IgE水平升高而增加(相关系数分别为0.35、0.38,P均<0.01)。结论:sVCAM-1参与了过敏性紫癜、紫癜性肾炎的发病过程,且可反映其病情程度。     

学习障碍儿童微量元素测定及营养素摄入的分析

目的旨在对儿童学习障碍(LD)的可能发病机制以及促进学习障碍儿童学习成绩提高的膳食指导提供一定的线索,探讨了微量元素与营养素对儿童学习障碍的影响。方法测定LD组与对照组儿童各50名血清Zn、Cu、Fe、Pb含量,并对两组儿童膳食进调查分析。结果LD组儿童血清Zn、Cu、Fe显著低于对照组(P<0.01),而血清Pb显著高于对照组(P<0.01);摄入营养素Zn、Cu、Fe、V itB1、DHA、AA、EPA显著低于对照组(P<0.01),两组儿童维生素C、蛋白质以及钙摄入的差异无统计学意义。结论儿童学习障碍的发生可能与饮食结构失调有关,应重视LD儿童饮食结构的调整,增加富含Zn、Cu、Fe、V itB1、DHA、AA、EPA食物的摄入。     

儿童病毒性肺炎外周血细胞凋亡的研究

目的　通过对病毒性肺炎外周血细胞凋亡的研究 ,探讨病毒感染的致病机理和机体的免疫反应。方法　采集病毒性肺炎患儿急性期、恢复期新鲜外周抗凝血 ,用FACSCalibur流式细胞仪收获细胞并用CellQuest软件分析结果 ,分别得到外周血之中性粒细胞、淋巴细胞中的活细胞、早期凋亡细胞、晚期凋亡细胞、死亡细胞的百分数。肺炎组共 2 8例 ,平均年龄 (1 30± 1 16 )岁。对照组 2 4例 ,平均年龄 (1 82± 0 97)岁。计量资料以 x±s表示 ,肺炎组和对照组间做方差分析 ,肺炎急性期与恢复期间用配对t检验。结果　病毒性肺炎患儿急性期、恢复期外周血中性粒细胞、淋巴细胞中活细胞百分率较对照组明显低 ,二者之间差异有非常显著意义 (P <0 0 1)。早期凋亡细胞百分率均较对照组明显高 ,二者之间差异有显著意义 (P <0 0 5 )。而患儿急性期、恢复期比较仅淋巴细胞中活细胞、晚期凋亡细胞、死亡细胞百分率差异有显著意义 (P <0 0 5 ) ,其余各项差异均无统计学意义。结论　病毒性肺炎时外周血中性粒细胞、淋巴细胞凋亡增加 ,存活细胞减少 ,所以适当增加细胞凋亡的药物可能缩短病程。     

甘肃农村留守初中生心理健康与人格特征关系

目的:了解农村留守初中学生心理健康状况、人格特征及其关系,为开展留守儿童心理健康教育提供科学依据。方法:采用症状自评量表(SCL-90)、艾森克人格问卷儿童版(EPQ)对4所中学的886名学生进行问卷调查。比较留守与非留守儿童心理健康状况及人格特征差异,并对留守儿童心理健康及人格特征进行相关分析。结果:留守儿童在躯体化、人际关系敏感、抑郁、焦虑、恐怖、偏执、精神病性症状、总分等方面的得分均高于非留守儿童,差异有统计学意义(t=2.696,P=0.007;t=3.125,P=0.003;t=3.462,P=0.001;t=2.444,P=0.015;t=2.046,P=0.041;t=2.290,P=0.022;t=2.521,P=0.012;t=2.972,P=0.003);在人格特征方面精神质、内外向方面得分低于非留守学生(t=2.740,P=0.006、t=5.544,P=0.000),在神经质、掩饰性两方面高于非留守学生(t=2.818,P=0.005;t=3.208,P=0.001);相关分析表明,精神质与SCL-90量表中除强迫症状、恐怖两因子外其余各因子得分均呈显著相关(P0.01),内外向与人际关系敏感呈正相关(r=0.155,P0.01),与其它各因子不相关(P0.05),神经质与SCL-90各因子呈正相关(P0.01),掩饰性与各因子呈显著负相关(P0.05)。结论:留守对儿童心理健康和人格发展有不利影响,心理健康和人格特征密切相关,应对留守初中生开展心理健康铺导,并注重健全人格的塑造。     

Serum vascular endothelial growth factor in pediatric patients with community-acquired pneumonia and pleural effusion

This study investigated the serum vascular endothelial growth factor (VEGF) levels in children with community-acquired pneumonia. Serum VEGF levels were measured in patients with pneumonia (n=29) and in control subjects (n=27) by a sandwich enzyme-linked immunosorbent assay. The pneumonia group was classified into bronchopneumonia with pleural effusion (n=1), bronchopneumonia without pleural effusion (n=15), lobar pneumonia with pleural effusion (n=4), and lobar pneumonia without pleural effusion (n=9) groups based on the findings of chest radiographs. We also measured serum IL-6 levels and the other acute inflammatory parameters. Serum levels of VEGF in children with pneumonia were significantly higher than those in control subjects (p<0.01). Children with lobar pneumonia with or without effusion showed significantly higher levels of serum VEGF than children with bronchopneumonia. For lobar pneumonia, children with pleural effusion showed higher levels of VEGF than those without pleural effusion. Children with a positive urinary S. pneumonia antigen test also showed higher levels of VEGF than those with a negative result. Serum IL-6 levels did not show significant differences between children with pneumonia and control subjects. Serum levels of VEGF showed a positive correlation with the erythrocyte sedimentation rate in the children with pneumonia. In conclusion, VEGF may be one of the key mediators that lead to lobar pneumonia and parapneumonic effusion.     

Leukocyte adhesion in aorta and femoral artery in vivo is mediated by LFA-1

OBJECTIVE: Cytokine-induced recruitment of leukocytes is an early feature during arterial injury and atherosclerotic plaque formation. The aim of this study was to analyze the role of the beta2-integrin lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18) in cytokine-triggered firm leukocyte adhesion to arterial endothelium in vivo. MATERIAL AND METHODS: Intravital fluorescence microscopy was used to study leukocyte firm adhesion in the mouse aorta and femoral artery in response to combined local challenge with TNF-alpha and IL-1beta. RESULTS: In wild-type (WT) mice, cytokine stimulation resulted in firm adhesion of 14.6 +/- 2.8 and 11.3 +/- 1.3 leukocytes/mm along the endothelium in the aorta and femoral artery ( P < 0.05 vs. PBS-treated controls, n = 5-6). Notably, the number of firmly adherent leukocytes in aorta and femoral artery of cytokine-stimulated LFA-1-deficient animals was reduced by 54% and 92% indicating an important role of LFA-1 in leukocyte adhesion to arterial endothelium ( P < 0.05 vs. controls, n = 5-6). In addition, pretreatment of WT mice with a monoclonal antibody (mAb) directed against murine LFA-1 attenuated the leukocyte adhesive response by 60% and 86% in aorta and femoral artery, respectively ( P < 0.05 vs. control mAb-treated WT, n = 5-12). CONCLUSION: These novel data demonstrate that cytokine-induced firm leukocyte adhesion in the mouse aorta and femoral artery is LFA-1-dependent in vivo, which may implicate an important role for this beta2-integrin leukocyte extravasation in arterial injury and atherogenesis.     

Leukocyte CD15 expression and platelet activation in the coronary sinus after coronary intervention

Markers associated with coronary restenosis must be identified to develop therapeutic strategies for improving the clinical outcome. We studied whether adhesion proteins on leukocytes and platelets from coronary sinus blood were associated with restenosis after coronary intervention in patients with stable coronary artery disease. Adhesion proteins on platelets and leukocytes were measured by flow cytometry. Pre- and postinterventional leukocyte CD15 expression was significantly higher in patients with restenosis than in those without it. Increased leukocyte CD15 expression during the intervention may contribute to coronary restenosis. Inhibition of leukocyte adhesion may be useful for the prevention of restenosis.     

Leukocyte count and bronchial hyperresponsiveness

The relationship of total and differential blood leukocyte counts with bronchial methacholine response was studied in a population-based sample of 324 men. Geometric mean total leukocyte counts were significantly higher in reactors (6567 cells/mm3) than in nonreactors (5732 cells/mm3; p = 0.003). After adjusting for smoking habits, a factor contributing to both an elevation in peripheral leukocyte count and an increased level of airway responsiveness, reactor status remained significantly associated with leukocyte count. This association also persisted after controlling, with a logistic model, for atopy and common cold (marker of infection) and after excluding men with a history of asthma, chronic bronchitis, or low FEV1. Study of the differential leukocyte counts has shown that an increase was present for almost every type of leukocyte, and particularly evident for neutrophils. Whether these findings reflect an association between bronchial hyperresponsiveness and cellular inflammation needs more investigation.