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91.
目的:探讨抗人热休克蛋白60或抗分枝杆菌热休克蛋白65抗体是否能够预测因急性心源性胸痛入院的患者一年预后不良。设计:前瞻性观察研究。地点:教学医院。患者:连续588例急诊收治的疑似急性心源性胸痛患者。主要观察指标:测定入院后晨起血样的抗人热休克蛋白60和抗分枝杆菌热休克蛋白65效价。出院后终点为冠心病死亡、非致死性心肌梗死、冠状动脉搭桥术、经皮穿刺腔内冠状动脉成形术、血管造影或因心脏缺血性胸痛加重再次入院。 相似文献
92.
羟甲芬太尼(I)是一个新的高强度高选择性阿片μ受体激动剂。本文用cis-A-N-[1-(2-羟基-2-苯乙基)-3-甲基-4-哌啶基]-苯胺(II)或cis-N-[1-(苯甲酰甲基)-3-甲基-4-哌啶基]-苯胺(III)作为前体合成了[11C]-羟甲芬太尼,以便用正电子发射断层扫描(PET)来观察μ受体。通过水解cis-A-羟甲芬太尼(I)和cis-N-[1-(苯甲酰甲基)-3-甲基-4-哌啶]-N-苯基丙酰胺(cis-IV)的4-N-丙酰基分别获得II和III。溴乙烷的格氏试剂与回旋加速器产生的[11C]-二氧化碳反应后继而直接加入邻苯二甲酸二酰氯和2,6-二叔丁基吡啶生成同位素标记中间体[11C]-丙酰氯。[11C]-丙酰氯与OH-前体(II)反应后再经HPLC分离纯化直接得[11C]-羟甲芬太尼;[11C]-丙酰氯与酮-前体(III)反应后,再用硼氢化钠甲醇溶液处理,然后进行HPLC分离纯化得[11C]-羟甲芬太尼。两种方法均可获得ll.1~14.8GBq/μmol的特异性放射化学纯[11C]-羟甲芬太尼。总共耗时为40~50min(EOB)。 相似文献
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目的 探讨常年性变应性鼻炎 (PAR)患者细胞免疫功能状态及微波凝固治疗的作用机制。方法 观察组 2 5例PAR患者分别于微波治疗前以及治疗 1个月后应用免疫组化法检测鼻粘膜上皮和外周血CD3、CD4、CD8、CD4/CD8水平。健康对照组 1 5例亦作相应检测。结果 PAR患者治疗前鼻粘膜及外周血CD3、CD4明显高于正常人 ,CD8低于正常人 ,CD4/CD8比值升高 ,与正常人比较差异有显著性 (P <0 .0 5)。微波治疗后CD4明显减少 ,CD8升高 ,CD4/CD8接近于健康对照组。结论 PAR患者存在明显的细胞免疫功能障碍 ;微波局部凝固治疗可改善PAR患者的细胞免疫状况。 相似文献
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PET for evaluation of differential myocardial perfusion dynamics after VEGF gene therapy and laser therapy in end-stage coronary artery disease. 总被引:2,自引:0,他引:2
René A Tio Eng S Tan Gillian A J Jessurun Nic Veeger Pieter L Jager Riemer H J A Slart Richard M de Jong Jan Pruim Geke A P Hospers Antoon T M Willemsen Mike J L de Jongste Ad J van Boven Dirk J van Veldhuisen Felix Zijlstra 《Journal of nuclear medicine》2004,45(9):1437-1443
The purpose of this study was to appraise the value of PET in the assessment of the effect of supposedly proangiogenic new therapies such as gene therapy with vascular endothelial growth factor (VEGF) gene and endomyocardial laser therapy. METHODS: Thirty-five patients with end-stage coronary artery disease and class III (Canadian Cardiovascular Society) angina were included. Myocardial ischemia was evaluated with dipyridamole PET scanning and exercise tolerance with bicycle ergometry. Ten patients were treated with naked plasmid DNA encoding for human VEGF165 (VEGF) and 12 patients were treated with laser therapy (direct myocardial revascularization [DMR]) using an electromechanical mapping system. Thirteen patients were treated with standard medical therapy (control). RESULTS: In both active treatment groups, angina was reduced in most subjects, except in 2 VEGF and 5 DMR patients. In the control group, no improvement in anginal classification was found, except in 3 subjects. On the PET scan, solely in the VEGF group, the stress perfusion was significantly improved (from 57 +/- 33 to 81 +/- 55 mL/min/100 g; P = 0.031). Furthermore, in the VEGF group, the number of ischemic segments was reduced from 274 +/- 41 to 234 +/- 48 segments (P = 0.004) but not in the DMR group (from 209 +/- 43 to 215 +/- 52 segments) or in the control group (from 218 +/- 18 to 213 +/- 28 segments). Bicycle exercise duration showed slight nonsignificant changes in the VEGF group (from 3.6 +/- 2.0 to 4.6 +/- 2.1 min), in the DMR group (from 5.1 +/- 1.5 to 4.7 +/- 1.3 min), and in the control group (from 3.3 +/- 1.8 to 3.5 +/- 2.3 min). CONCLUSION: PET showed that intramyocardial gene therapy with the human VEGF165 gene in contrast to laser DMR treatment effectively reduces myocardial ischemia. 相似文献
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Characterization of adhesive interactions between human endothelial cells and megakaryocytes. 总被引:3,自引:0,他引:3
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H Avraham S Cowley S Y Chi S Jiang J E Groopman 《The Journal of clinical investigation》1993,91(6):2378-2384
Cell-cell adhesion is essential for many immunological functions and is believed to be important in the regulation of hematopoiesis. Adhesive interactions between human endothelial cells and megakaryocytes were characterized in vitro using the CMK megakaryocytic cell line as well as marrow megakaryocytes. Although there was no adhesion between unactivated human umbilical vein endothelial cells (HUVEC) and megakaryocytes, treatment of HUVEC with inflammatory cytokines such as IL-1 beta, tumor necrosis factor alpha, INF-gamma, or the phorbol ester phorbol myristate acetate (PMA) resulted in a time- and dose-dependent increase in adhesion. Stimulation of marrow megakaryocytes or CMK cells with the cytokines IL-1 beta, GM-CSF, IL-6, IL-3, or PMA augmented their adhesion to endothelium. Monoclonal antibodies against the LFA-1 subunit of the leukocyte adherence complex CD18 inhibited the binding of marrow megakaryocytes or CMK cells to HUVEC. Adhesion blocking experiments also demonstrated that the VLA-4/VCAM-1 pathway was important for megakaryocyte attachment to HUVEC. Adhesion promoted maturation of megakaryocytic cells as measured by increased expression of glycoproteins GpIb and GpIIb/IIIa and by increased DNA content. These observations suggest that alterations in megakaryocyte adhesion may occur during inflammatory conditions, mediated by certain cytokines, resulting in augmented megakaryocyte maturation. 相似文献