1.The link between integrins and their ligands promotes the formation of focal adhesion plaque (FAP).
整合素与配体的连接可促使黏着斑(Focal adhesion plaque，FAP)的形成。
2.A number of observations strongly suggest that ligand occupy ,integrin receptor clustering and their combination trigger the aggregtion of focal adhesion kinase (FAK) in focal adhesion plaque (FAP) and autophosphorylation of FAK at Tyr397 in the N-terminal domain .
基础研究表明，整合素与其相应配基结合后，多个粘着斑激酶（focal adhesion kinase， FAK）分子聚集在粘着斑（focal adhesion plaque， FAP）处，使FAK N-端区的酪氨酸Tyr397磷酸化而被激活。
3.The ratio of TIMP-1/MMP-1 was positively correlated with plaque fibrous cap thickness, plaque area, area stenosis, and negatively with emptied plaque or lipid core size, lipid to plaque ratio.
TIMP 1/MMP 1与纤维帽厚度、面积狭窄率呈正相关 ,与脂核或无回声带面积、脂核与斑块比呈负相关。
4.The thickness of intimia-media,existence of the carotid plaque and the plaque score were compared. Results The thickness of inti-mia-media and the existence of the carotid plaque and the plaque score were significantly different among the three groups(F=(4.27),15.58,q=2.93-9.27;χ~2=12.38-34.72,P
结果各组间颈动脉内膜-中层厚度、斑块积分及斑块检出率的差异均有统计学意义(F=4.27、15.58,q=2.93~9.27;2χ=12.38~34.72,P
5.Results The mean age(62±9)of patients in the plaque group was significantly older than that of the non-plaque group(51±10,P<0.01). The proportion of accompanying hypertension(69%)and diabetes mellitus(35%)in the plaque group was also significantly higher than that in the non-plaque group(52%,P<0.05;18%,P<0.05).
结果斑块组患者的年龄[(62±9)岁]显著高于非斑块组[(51±10)岁,P<0.01)],伴有高血压(69%)及糖尿病(35%)的比例亦明显高于非斑块组(52%,18%,均P<0.05)。
6.(6) The ASI of plaque grade 0,1,2 and 3 groups were 120.07±57.66,124.10±48.34,158.59±49.82 and 204.67±47.01, respectively. The ASI of plaque grade 2 and 3 groups were significantly higher than that of plaque of grade 0 group (p
（6）0级斑块组、1级斑块组、2级斑块组和3级斑块组的ASI值依次为120.07±57.66、124.10±48.34、158.59±49.82和204.67±47.01，后两组与0级斑块组比较具有显著性差异（p＜0.01）。
7.The CCA-IMT、inner diameter of CCA、incidence rate of plaque were significantly higher in abnormal MAU group (≥30 mg/ 24h) compared with normal MAU group(P
4、UAE与CCA-IMT呈线性相关(P
8.We observed the effect on clinical symptom,and the change of intima-media thickness(IMT),inside diameter,Crouse plaque integral, peak systolic velocity(PSV),end diastolic velocity(EDV), plaque pathologic classification and carotid classification in carotid. We also observed the change of hypersensitive C-reactive protein and blood lipid.
观察患者的临床症状疗效,治疗前后颈动脉内膜-中层厚度(IMT)、内径、Crouse斑块积分、收缩期峰值流速(PSV)、舒张末期流速(EDV)、斑块超声声像病理学分型、颈动脉超声声像学分型以及高敏C反应蛋白(hs-CRP)、血脂的变化。
9.Results It was shown by quantitative real-time PCR that AU126 in subgingival plaque of aggressive periodontitis(8.72±0.44),chronic periodontitis(8.46±0.67) and plaque-induced gingivitis patients(8.47±0.47) were higher than that in normal controls(7.91±0.88)(P<0.05).
结果实时PCR定量分析显示,侵袭性牙周炎、慢性牙周炎和单纯性龈炎患者龈下菌斑中AU126(8.72±0.44、8.46±0.67、8.47±0.47)均显著多于正常对照者(7.91±0.88)(P<0.05)。
10.(5)Making the plaque cap thinner by activating MMP-1, MMP-2, MMP-3, and MMP-9 and causing the plaque vulnerability.
(5)通过活化基质金属蛋白酶-1(MMP-1)、MMP-2、MMP-3和MMP-9，导致斑块纤维帽的基质成分水解而影响斑块的稳定性；
