@article {= {Thomas j . DeGraba},作者DeGrabaS15 title ={炎症介质的表达和粘附分子在人类动脉粥样硬化斑块},体积={49},数量={生理4},页面= {S15——S19} = {1997}, doi = {10.1212 / WNL.49.5_Suppl_4。出版商S15} = {Wolters Kluwer健康,公司代表美国神经病学学会},文摘={机制导致颈动脉粥样硬化斑块成为症状尚不清楚。首页证据表明,炎症介质不仅有助于斑块的形成,还可能参与动脉粥样硬化病变的迅速发展,导致斑块裂隙和管腔内的血栓形成。本文回顾了现有的证据在动脉粥样硬化斑块炎症介质的作用生产和成熟。它还包括在我们实验室进行研究以确定已知的炎症通路的组件,包括细胞因子和白细胞粘附分子,优先表示在有症状和无症状的颈动脉斑块。颈动脉斑块从有症状和无症状的患者进行颈动脉内膜切除手术的损伤大于70 \ %狭窄snap-frozen并存储在-70 C {\ textdegree},直到分析。Immunofluorescent研究进行衡量内皮细胞间粘附的表情molecule-1 (ICAM-1)。ICAM-1蒙蔽的方式表达测量腔的内皮斑块表面部分的百分比。原位杂交也进行了测量信息对肿瘤坏死因子-α的表达(TNF-α)和ICAM-1斑块之间通过比较平均光密度有症状和无症状的患者。有增加内皮细胞表面表达ICAM-1高档地区(28 \ %)和低级区域(11 \ %),症状患者的斑块。还有一个更大的趋势表达ICAM-1高档地区的斑症状和无症状的高档地区的斑块。 In situ hybridization revealed increased mRNA for TNF-α and ICAM-1 in the body of the plaque, preferentially in the high-grade region of plaques from symptomatic patients. The data obtained suggest that a local increase of endothelial inflammatory mediator expression correlates with the clinical setting of thromboembolic ischemia and may play a role in conversion of atheromatous plaque to a prothrombotic state. The data also indicate that this line of investigation deserves further exploration because it may be useful in identifying new mechanisms in patients at risk for stroke and in suggesting possible novel strategies for intervention.}, issn = {0028-3878}, URL = {//www.ez-admanager.com/content/49/5_Suppl_4/S15}, eprint = {//www.ez-admanager.com/content/49/5_Suppl_4/S15.full.pdf}, journal = {Neurology} }