尿激酶型纤溶酶原激活剂系统在喉癌中的表达及意义

目的　探讨尿激酶型纤溶酶原激活剂及其抑制剂在喉癌中的表达及与临床病理各参数及预后的关系。方法　采取免疫组化链霉卵白素生物素过氧化酶法 (labeled streptoavidin biotin peroxidase,SAB)法 ,对 10 4例喉鳞状细胞癌标本中的尿激酶型纤溶酶原激活剂 (urokinase typeplasminogenactivator,uPA)、抑制剂 (plasminogenactivatorinhibitors ,PAI)PAI 1和PAI 2表达情况进行检测。结合临床随访 ,经Kaplan Meier生存曲线、log rank检验及Cox比例风险模型分析其与临床病理参数及患者生存预后的关系。结果　uPA、PAI 1、PAI 2在喉癌组织中的表达分别为 66 3 %、70 2 %、5 0 0 %。uPA、PAI 1、PAI 2的阳性表达在颈部淋巴结转移组与非转移组中差异有显著性 ,经半定量分析P值分别为 0 0 10、0 0 2 7、0 0 3 8。单因素分析显示 :淋巴结转移及复发、肿瘤细胞分化程度、uPA和PAI 2表达是影响患者预后的因素。多因素分析提示 :淋巴结转移及复发、临床分期、uPA和PAI 2是影响患者预后的独立因素。结论　uPA在喉癌转移中起着重要的作用 ;PAI 1的作用复杂 ,可能不单纯是uPA的抑制剂 ;PAI 2可能是uPA主要抑制剂 ,由于其表达不足尚不能抑制uPA的活性     

Pulmonary thrombo-embolism in nephrotic syndrome treated with tissue plasminogen activator

We describe the case of a boy with steroid sensitive nephrotic syndrome and left pulmonary artery thrombo-embolism. Clinical presentation initially suggested sepsis and respiratory signs were minor. Treatment with tissue plasminogen activator infused into the pulmonary artery was successful. Conclusion Pulmonary thrombo-embolism should be considered in unwell children with nephrotic syndrome. Received: 6 September 1996 / Accepted: 17 December 1996     

催乳素延缓hCG诱发大鼠排卵和下调纤溶酶原激活系统在卵巢中的表达

给幼龄大鼠注射10IU PMSG,48h后注射7IU hCG,或者hCG加不同剂量的催乳素(PRL).在不同时间取出卵巢,检查输卵管中卵子数和卵巢不同细胞中组织型纤溶酶原激活因子(tPA)和抑制因子(PAI-1)mRNA含量和活性.结果表明:PRL减少hCG诱发的排卵数并有明显剂量和时间抑制曲线.当hCG注射24h后,在两组动物输卵管的卵子数无明显差异.PRL同时抑制hCG所诱发的颗粒细胞tPA表达;与少匕相反PRL还能显著刺激膜一间质细胞PAI-1mRNA表达.上述实验结果表明,PRL只暂时延缓而不是完全抑制hCG诱发的大鼠排卵.上述作用可能是通过抑制纤溶酶激活系统在卵巢中的表达引起的.     

超早期脑室穿刺引流术治疗重型脑室出血

目的 探讨重型脑室出血的治疗方法。方法 11例重型脑室出血患者，原发性脑室系统出血7例，继发性脑室系统出血4例，脑实质损伤轻微。在超早期行脑室穿刺引流加脑室内注射尿激酶溶栓治疗。结果 经治疗后11例患者预后良好8例，中残1例，死亡2例，无植物生存状态，并发脑积水3例，行脑室腹腔分流术后好转。结论 在超早期行脑室穿刺引流加脑室内注射尿激酶溶栓可以解除或缓解四脑室血肿对脑干的压迫作用，降低四脑室内压力，提高治疗效果。     

血脂康对高血压病患者血浆sICAM-1水平和PAI-1活性的影响

目的　探讨高血压病 (EH)患者血浆细胞间粘附分子 - 1(sICAM - 1)水平和纤溶酶原激活物抑制剂 - 1(PAI -1)活性的变化及血脂康对其的影响。方法　采用酶联免疫吸附法 (ELISA)、发色底物显色法分别对 71例轻至中度高血压患者应用血脂康治疗前后和正常对照组者血浆sICAM - 1水平和PAI- 1活性进行检测。结果　EH患者血浆sICAM - 1水平和PAI- 1活性明显高于正常对照组 (P <0 .0 1及P <0 .0 5 ) ,经血脂康治疗 8周后其浓度明显下降(P <0 .0 1及P <0 .0 5 )。结论　EH病人血浆sICAM - 1水平和PAI- 1活性较正常人明显升高 ,血脂康在有效调脂的同时能降低EH患者血sICAM - 1浓度和PAI- 1活性 ,减少高血压并发症发生。     

t-PA用于青光眼滤过术的临床随机对照研究

目的　研究组织型纤溶酶原激活剂 (t PA)在青光眼滤过术中的作用。方法　采用随机对照的临床验证方法 ,将 76例 ( 86眼 )难治性青光眼分为用药组 42例 ( 4 4眼 )和对照组 3 4例 ( 4 2眼 )。用药组术中及术后均应用t PA ;对照组未用t PA。术后随访 18～ 48个月 (平均 3 6个月 )。采用寿命表分析法统计。结果　用药组与对照组手术成功率及功能性滤过泡的累计百分率差异有显著性 (P <0 0 5 )。而眼毒性作用的发生率无显著性差异 (P >0 0 5 )。结论　t PA是安全有效的治疗滤过性手术失败的药物。至少可以在术后 3年内将眼压维持在正常水平     

uPA及PAI-1在卵巢上皮性肿瘤组织中的表达和活性

目的:探讨卵巢上皮性肿瘤组织中尿激酶型纤溶酶原激活物(uPA)及其抑制物1(PAI-1)的表达与活性及其临床意义。方法:免疫组化SABC法检测35例恶性卵巢上皮性肿瘤及12例良性卵巢上皮性肿瘤组织uPA和PAI-1蛋白质的表达,发色底物法检测肿瘤组织uPA活性。结果:恶性卵巢上皮性肿瘤uPA、PAI-1的表达明显高于良性卵巢上皮性肿瘤,恶性卵巢上皮性肿瘤中PA活性明显高于良性卵巢上皮性肿瘤(P<0·01);在组织学分型中随恶性卵巢上皮性肿瘤分化程度的降低uPA、PAI-1的表达逐渐升高(P<0·01),uPA活性逐渐升高(P<0·05);在临床分期晚的病例中uPA、PAI-1的表达及uPA活性较临床分期早的病例高(PAP<0·05;PAIP<0·01;uPA活性P<0·05)。结论:uPA、PAI-1与卵巢恶性上皮性肿瘤的分化、转移及浸润有关,可能做为恶性卵巢上皮性肿瘤诊治的靶点。     

原发性高血压血管内皮损伤与血栓前状态的研究

目的探讨内皮损伤的分子标志物与原发性高血压发生血栓性疾病的关系。方法应用酶联免疫吸附法(ELISA)分别测定98例原发性高血压患者和36例健康对照者血浆血栓调节蛋白(TM)、血管性血友病因子(VWF)、纤溶酶原激活剂抑制物-1(PAI-1)的水平变化。结果与正常对照组比较,1、2、3级高血压组VWF、PAI-1水平显著增高(P<0.05),23、级高血压组TM水平显著增高(P<0.05),与1级高血压组比较,2、3级高血压组TM、VWF、PAI-1水平显著增高(P<0.05)。结论原发性高血压病患者存在的血管内皮损伤、抗凝作用减弱、血小板粘附与聚集、纤溶活性的下降,可能是其并发心、脑血管血栓性并发症的原因之一。     

Lesion-associated accumulation of uPAR/CD87- expressing infiltrating granulocytes, activated microglial cells/macrophages and upregulation by endothelial cells following TBI and FCI in humans

Urokinase-type plasminogen activator receptor (uPAR/CD87) together with its ligand, urokinase-type plasminogen activator (uPA), constitutes a proteolytic system associated with tissue remodelling and leucocyte infiltration. uPAR is a member of the glycosyl phosphatidyl inositol (GPI) anchored protein family. The functional role of uPAR comprises fibrinolysis by conversion of plasminogen to plasmin. In addition, uPAR promotes cell adhesion, migration, proliferation, re-organization of the actin cytoskeleton, and angiogenesis. Furthermore, uPAR is involved in prevention of scar formation and is chemoattractant to macrophages and leucocytes. In order to investigate the pathophysiological role of uPAR following human CNS injury we examined necrotic brain lesions resulting from traumatic brain injury (TBI; n = 28) and focal cerebral infarctions (FCI; n = 17) by immunohistochemistry. Numbers of uPAR+ cells and uPAR+ blood vessels were counted. Following brain damage, uPAR+ cells increased significantly within 12 h, reached a maximum after 3-4 days and remained elevated until later stages. uPAR was expressed by infiltrating granulocytes, activated microglia/macrophages and endothelial cells. Numbers of uPAR+ vessels increased in parallel subsiding earlier following FCI than post TBI. The restricted, lesion-associated accumulation of uPAR+ cells in the brain parenchyma and upregulated expression by endothelial cells suggests a crucial role for the influx of inflammatory cells and blood-brain barrier (BBB) disturbance. Through a failure in BBB function, uPAR participates in formation of brain oedema and thus contributes to secondary brain damage. In conclusion, the study defines the localization, kinetic course and cellular source of uPAR as a potential pharmacological target following human TBI and FCI.     

纤溶酶原激活物抑制物-1与不稳定心绞痛的关系

目的:探讨纤溶酶原激活物抑制物-1(PAI-1)血浆抗原水平及其基因启动子-844G→A多态性与不稳定心绞痛(UAP)的关系。方法:UAP患者121例(UAP组)和冠状动脉造影正常者108例(对照组),以ELISA法测定其血浆PAI-1抗原水平。PCR扩增特定DNA片段,XhoI酶切和琼脂糖电泳确定基因型。结果:UAP组血浆PAI-1抗原水平为(68.15±45.29)μg/L,显著高于对照组的(53.39±20.62)μg/L(P<0.01)。血浆PAI-1抗原水平与冠状动脉病变支数呈正相关(r=0.139熏P<0.05),与血糖(Glu)、总胆固醇(TC)、低密度脂蛋白(LDL)正相关,r分别为0.147,0.151,0.144(P<0.05)。AA、AG、GG3种基因型在2组间分布差别无统计学意义,但A等位基因与较高的血浆PAI-1抗原水平有关。UAP组AA及AG基因型者血浆PAI-1抗原水平显著高于对照组。结论:PAI-1基因启动子-844G→A基因多态性与UAP无关,但A等位基因携带者存在较高的PAI-1血浆抗原水平。