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（     

创伤后多脏器功能衰竭患者细胞粘附分子和补体激活成分水平的变化及意义

目的：探讨创伤后多器官功能衰竭（ＭＯＦ）患者血浆粘附分子和补体活化成分水平的变化及意义。方法：采用酶联免疫吸附法（ＥＬＩＳＡ）检测３６例创伤后ＭＯＦ患者及３１例创伤患者和３５例健康人外周血白细胞ＣＤ１８的变化、血浆可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）,可溶性血管细胞间粘附分子－１（ｓＶＣＡＭ－１）和血浆补体活化片段（ｓＣ５ｂ－９）浓度的变化。结果：ＭＯＦ患者白细胞ＣＤ１８的表达、ｓＩＣＡＭ－     

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。     

急性髓系白血病细胞侵袭能力与粘附分子表达关系探讨

目的：探讨白血病细胞浸润及转移与粘附分子表达的关系。方法：用免疫组织化学ＡＰＡＡＰ、免疫印迹方法研究５０例急性髓系白血病（ＡＭＬ）骨髓和（或）外周血白血病细胞粘附分子ＶＬＡ４（ＣＤ４９ｄ）、ＬＦＡ１（ＣＤ１１ａ）的表达。结果：发现ＡＭＬ浸润组ＣＤ４９ｄ、ＣＤ１１ａ表达较非浸润组显著增高（Ｐ＜０．００５）。结论：ＡＭＬ白血病细胞可能通过ＣＤ４９ｄ／ＶＣＡＭ－１，ＣＤ１１ａ／ＩＣＡＭ－１粘附机制与血管内皮细胞粘附而浸润组织。外周血白血病细胞与骨髓白血病细胞ＣＤ４９ｄ、ＣＤ１１ａ表达无显著差别，说明骨髓白血病细胞ＣＤ４９ｄ、ＣＤ１１ａ表达高低不是其从骨髓释出的唯一因素。     

过敏性鼻炎患者血清sICAM—1水平测定及其意义

目的：了解过敏性鼻炎患者血清中可溶性细胞间粘附分子（ｓＩＣＡＭ）－１水平及意义。方法：采用抗体夹心ＥＬＩＳＡ法对３１例过敏性鼻炎患者血清ｓＩＣＡＭ－１水平进行测定。结果：过敏性鼻炎患者血清中ｓＩＣＡＭ－１水平与正常对照组比较明显增高（Ｐ〈０．００１）。结论：ｓＩＣＡＭ－１参与了过敏性鼻炎发病过程,且与临床症状有一定平行关系,推测ｓＩＣＡＭ－１可能在过敏性鼻炎炎症的加重与持续发生中有一定意义。     

危重病患者血浆可溶性内皮细胞白细胞粘附分子─1含量的变化

探讨可溶性内皮细胞白细胞粘附分子１（ｓＥＬＡＭ１）含量变化在危重病患者病情变化和判断预后中的意义。用酶联免疫吸附测定（ＥＬＩＳＡ）法测定了４０例危重病患者ｓＥＬＡＭ１含量。发现严重肺感染、肺原性心脏病伴发多器官功能衰竭、急性呼吸窘迫综合征及多器官功能失常综合征患者血浆ｓＥＬＡＭ１含量均较正常对照组显著增高（Ｐ均＜０．００１）；死亡组血浆ｓＥＬＡＭ１含量较存活组亦明显增高（Ｐ＜０．００１）；血浆ｓＥＬＡＭ１水平与ＰａＯ２呈显著负相关（ｒ＝０．６７，Ｐ＜０．００５）；综合治疗可使血浆ｓＥＬＡＭ１水平降低。结果提示：Ｅ选择素粘附分子参与了上述各种危重病的病理生理过程，且与临床预后有关，可作为判断病情及预后的良好指标     

血清可溶性L—选择素,sICAM—1,HBV DNA拷贝数及肝功能损害的相关性研究

目的 探讨Ｌ－ｓｅｌｅｃｔｉｎ（Ｌ－选择素）和ＩＣＡＭ－１（细胞间粘附分子－１）在乙型肝炎病毒感染造成肝功能损害过程中的作用。方法 定量检测４２例乙型肝炎病人血清ＨＢＶ ＤＮＡ拷贝数、可溶性Ｌ－选择素（ｓＬ－ｓｅｌｅｃｔｉｎ）、可溶性细胞产粘附分子－１（ｓＩＣＡＭ－１）及肝功能相关生化指标,并对结果进行统计分析。结果 ２２例ＤＮＡ阴性和２０例ＤＮＡ阳性病人血清ｓＬ－ｓｅｌｅｃｔｉｎ和ｓＩＣＡＭ－１水平均明显高于对照组（Ｐ〈０．０５）,但ＤＮＡ阴性组和阳性组之间的ｓＬ－ｓｅｌｅｃｔｉｎ和ｓＩＣＡＭ－１水平均无显著差异（Ｐ〉０．０５）;ＤＮＡ拷贝数与ｓＩＣＡＭ－１水平呈负相关（ｒ＝－０．５０１,Ｐ〈０．０５）;ＤＮＡ拷贝数与肝功能损害呈负相关;４２例乙肝病人的ｓＬ－ｓｅｌｅｃｔｉｎ和ｓＩＣＡＭ－１水平均与肝功能损害     

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。     

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     

冠心病患者细胞间粘附分子-1、P-选择素和von Willebrand因子的表达

探讨细胞间粘附分子－１（ＩＣＡＭ－１）、Ｐ－选择素（Ｐ－ｓｅｌｅｃｔｉｎ）．ｖｏｎＷｉｌｌｅｂｒａｎｄ因子（ｖＷＦ）在冠心病中的表达特点和临床意义。方法用酶联免疫吸附法（ＥＬＩＳＡ）检测２８例稳定性心绞痛患者（ＳＡ）、２３例不稳定性心绞痛患者（ＵＡ）和２０例心肌梗死患者（ＡＭＩ）血中ＩＣＡＭ－１、Ｐ－ｓｅｌｅｃｔｉｎ、ｖＷＦ的表达。结果冠心病患者血中ＩＣＡＭ－１、Ｐ－ｓｅｌｅｃｔｉｎ和ｖＷＦ的表达较正常组增高,且在ＵＡ组中的表达高于ＳＡ组,ＡＭＩ组的表达高于ＵＡ组。除Ｐ－ｓｅｌｅｃｔｉｎ在ＳＡ组与正常组间差别不显著外,其余均差异显著（Ｐ＜０．０１）。ＩＣＡＭ－１和ｖＷＦ在ＳＡ、ＵＡ及ＡＭＩ组均呈正相关。结论ＩＣＡＭ－１、Ｐ－ｓｅｌｅｃｔｉｎ和ｖＷＦ在不同类型冠心病患者有不同的增加,表明它们与冠心病的发生、发展及临床严重程度密切相关。     

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。     

急性脑梗死患者黏附分子CD18与CD54的表达水平与临床意义

目的探讨黏附分子CD18、CD54的表达与急性脑梗死（ACI）之间的关系及临床意义。方法采用流式细胞术（FCM）对68例ACI患者不同的发病时程、部位、面积及治疗前后黏附分子CD18、CD54表达情况进行检测与分析,同时检测健康对照30倒。结果ACI时黏附分子CD18、CD54表达明显上调,与健康对照组比较差异有统计学意义（P〈0．05）,黏附子CD18、CD54水平与ACI面积、部位关系不大（P〉0．05）;ACI患者在7d内黏附分子CD18、CD54均呈较高水平的表达,治疗10d后表达降低。比较治疗前后黏附分子CD18、CD54水平差异有统计学意义（P〈0．05）。结论黏附分子CD18、CD54参与ACI发生、发展的病理过程,有望成为新的ACI诊断、监测病情及评估预后的辅助诊断指标。     

Synthetic fibronectin peptides suppress arthritis in rats by interrupting leukocyte adhesion and recruitment.

In an experimental model of arthritis, increased leukocyte adhesion is associated with the evolution of acute and chronic synovial inflammation. Whereas peripheral blood mononuclear cells (PBMC) from control animals bind minimally to fibronectin matrices, PBMC from animals receiving arthropathic doses of bacterial cell walls demonstrate increased integrin mRNA expression and enhanced adhesion. To determine whether this augmented adhesion was causal in the development of synovial pathology, peptides synthesized from several fibronectin domains which inhibited leukocyte adhesion in vitro were administered to arthritic animals either as free peptides or coupled to a carrier molecule. Not only were peptides containing either the RGD or CS-1 cell-binding domains inhibitory to chronic synovial pathology (articular index = 10.5 +/- 0.3 for untreated animals compared to 1.25 +/- 0.25 for RGD and 2.5 +/- 0.7 for CS-1), but three peptides synthesized from the carboxy-terminal 33-kD heparin-binding domain of fibronectin were also found to significantly inhibit leukocyte recruitment and the evolution of arthritis. Based on these data, which are the first to explore the therapeutic potential of heparin-binding fibronectin peptides in chronic inflammation, it appears that antagonism of cellular adhesion and recruitment by fibronectin peptides may provide an important mechanism for modulating the multi-step adhesion process and attenuating aberrant inflammatory responses.     

恶性肿瘤患者化疗前后外周血免疫学指标的检测及其临床意义

目的观察恶性肿瘤患者化疗前后外周血免疫学指标的变化,并探讨其临床意义。方法应用流式细胞仪检测103例恶性肿瘤患者静脉化疗前、后外周血T淋巴细胞亚群(CD3+、CD4+、CD8+)、B淋巴细胞(CD19+)及NK细胞(CD3-/CD16+56+)的表达率。结果所有患者化疗后CD3+、CD4+、CD4+/CD8+表达高于化疗前(P<0.05),其中化疗有效组(30例),差异有显著性意义(P<0.01),化疗无效组(40例),差异无统计学意义(P>0.05);化疗前后CD19+的变化无统计学差异(P>0.05);化疗后NK细胞降低明显,有统计学差异(P<0.05)。结论有效的化疗能够改善恶性肿瘤患者的T淋巴细胞免疫功能。     

Chromosomal location of the genes encoding the leukocyte adhesion receptors LFA-1, Mac-1 and p150,95. Identification of a gene cluster involved in cell adhesion

The adhesion receptors Mac-1, LFA-1, and p150,95 are cell surface alpha/beta heterodimers that play a key role in leukocyte adhesion processes. The genes for Mac-1, LFA-1, and p150,95 alpha subunits have been located to chromosome 16 by means of Southern blot analysis using a series of somatic cell hybrids. Chromosomal in situ hybridization has demonstrated that the genes for the three alpha subunits map to the short arm of chromosome 16, between bands p11 and p13.1, defining a cluster of genes involved in leukocyte adhesion. The gene encoding the LFA-1/Mac-1/p150,95 beta subunit, and defective in leukocyte adhesion deficiency, has been located on chromosome 21, band q22. The leukocyte adhesion receptor alpha and beta subunits are mapped to chromosomal regions that have been shown to be involved in cytogenetic rearrangements in certain patients with acute myelomonocytic leukemia and the blast phase of chronic myelogenous leukemia, respectively.     

Estradiol enhances leukocyte binding to tumor necrosis factor (TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercellular adhesion molecule type 1, and vascular cell adhesion molecule type 1.

Adhesion of leukocytes to endothelial cells is a critical step in the development of acute and chronic inflammatory lesions. We report here that estradiol treatment of cultured human umbilical vein endothelial cells stimulated up to a twofold increase in TNF-induced adhesion of both polymorphonuclear leukocytes and PMA-activated peripheral blood mononuclear cells. This effect was more evident (threefold increase) when endothelial cells were cultured on the basement membrane glycoprotein laminin. Progesterone, but not testosterone, had a similar stimulatory effect. Estradiol also promoted a slight increase in interferon gamma-stimulated endothelial cell adherence for peripheral blood mononuclear cells, but no effect of estradiol was observed when adhesion of leukocytes to endothelial cells was stimulated with IL-1 or IL-4. The estradiol-induced increase in leukocyte binding to human umbilical vein endothelial cells was partially blocked by antibodies to the adhesion molecules E-selectin, intercellular adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule type 1 (VCAM-1). Indirect immunofluorescence techniques showed that estradiol produces an increase in TNF-induced cell surface expression of these molecules. Northern blot analysis demonstrated a transient increase in TNF-induced expression of mRNA for E-selectin, ICAM-1, and VCAM-1 in endothelial cells treated with estradiol. Our data demonstrate that estradiol has important regulatory functions in promoting leukocyte-endothelial cell interactions that might contribute to the observed predominance in females of some autoimmune inflammatory diseases.     

干燥综合征患者白细胞跨内皮细胞转运途径和细胞粘附分子途径相关基因表达

目的分析干燥综合征患者白细胞跨内皮细胞转运及细胞黏附分子途径相关基因的表达情况及其意义。方法取3例干燥综合征患者及3例正常对照者的外周血单个核细胞,提取总RNA,反转录至cDNA后与寡核苷酸芯片杂交。采用图像分析软件对芯片图像进行数据提取,以Cy5/Cy3的比值数据分析处理。结果干燥综合征组与对照组外周血单个核细胞中的白细胞跨内皮细胞转运途径及细胞黏附分子途径相关基因表达差异最为显著(P<0.01),以上途径中VCAM1、PECAM1、ICAM1、ITGAL、SELE这5个基因表达上调,JAM1、JAM2、JAM3、SELL、CD226、CD99这6个基因表达下调。结论干燥综合征患者在白细胞跨内皮细胞转运途径及细胞黏附分子途径相关基因的表达差异最为显著,这些基因将为研究疾病的发病机制及新的治疗靶向提供重要依据。     

A new member of the immunoglobulin superfamily that has a cytoplasmic region homologous to the leukocyte common antigen

A human gene (LAR) that hybridizes to mouse leukocyte common antigen cDNA under relaxed hybridization conditions was isolated. The LAR gene is expressed in a broad range of cells, including T lymphocytes, kidney, and prostate cells. The structure of the protein encoded by the LAR gene was deduced by determining the nucleotide sequences of a 7.7-kb LAR cDNA. The putative LAR protein is composed of a 1,234 amino acid extracellular region, a 24 amino acid transmembrane segment, and a 623 amino acid cytoplasmic region. The cytoplasmic region contains two homologous domains that have extensive sequence similarity to the cytoplasmic region of the leukocyte common antigens. The NH2-terminal region of the extracellular segment of the LAR protein contains three tandem Ig-like domains and nine non-Ig-like domains. Among the known Ig-like proteins, the LAR protein has the highest degree of similarity to neural-cell adhesion molecule. The non-Ig-like domains of the LAR protein are also similar to the non-Ig-like domains of neural-cell adhesion molecule.     

Circulating levels and liver tissue distribution of intercellular adhesion molecule-1 during β-interferon therapy of hepatitis C virus-associated chronic active liver disease

Summary Intercellular adhesion molecule-1, an immunoglobulin supergene family member, is known to account for important steps in cell activation and the immune response. By a non-isotopic slot-dot immunoblotting assay, we measured circulating levels of intercellular adhesion molecule-1 in 26 patients with hepatitis C virus-associated chronic active liver disease before and after β-interferon therapy, in 6 patients with non-A, non-B acute self-limiting hepatitis and in 13 healthy subjects. Circulating intercellular adhesion molecule-1 was found in 10 of 13 (77%) normal controls at low concentrations which were not statistically different from those measured in patients with hepatitis C virus-associated chronic active liver disease responsive to β-interferon, whereas significantly higher levels were found in unresponsive patients. Higher serum intercellular adhesion molecule-1 levels were found in 4 of 10 (40%) β-interferon-responsive patients compared with 13 of 16 (18%) unresponsive patients. Intercellular adhesion molecule-1 levels persisted after discontinuation of β-interferon treatment and did not correlate with hepatocytolysis (as indicated by alanine aminotransferase serum activity) either in chronic active liver disease or acute hepatitis. However, a good correlation was found between intercellular adhesion molecule-1 and its expression on liver cells, thus emphasizing that induced circulating levels may reflect the state of activation at the sites of the inflammatory process. These data strongly support the view that intercellular adhesion molecule-1 plays an important role in liver cell damage in hepatitis C virus-associated acute and chronic liver disease, and that its circulating levels may be a good prognostic parameter of responsiveness to β-interferon therapy.