尿激酶型纤溶酶原激活物受体

摘要： 目的 探讨宫颈癌患者血清鳞状细胞癌抗原(SCCA)、尿激酶型纤溶酶原激活物受体(uPAR)、CD105、转化生长因子-β(TGF-β)水平及临床意义.方法 选取158例宫颈癌患者和50例宫颈上皮内瘤变(CIN)患者,分别作为宫颈癌组和CIN组,检查两组患者的血清SCCA、uPAR、CD105、TGF-β水平,分析血清SCCA、uPAR、CD105、TGF-β水平与宫颈癌患者临床特征的关系.结果 宫颈癌组患者的血清SCCA、uPAR、CD105和TGF-β水平均明显高于CIN组,差异均有统计学意义(P<0.01).TNM分期为Ⅲ～Ⅳ期、有淋巴结转移宫颈癌患者的血清SCCA水平分别高于TNM分期为Ⅰ～Ⅱ期、无淋巴结转移的患者(P<0.05),低分化宫颈癌患者的血清uPAR水平高于中高分化的患者(P<0.05),TNM分期为Ⅲ～Ⅳ期、肿瘤直径≥5 cm、低分化、有淋巴结转移宫颈癌患者的血清CD105水平分别高于TNM分期为Ⅰ～Ⅱ期、肿瘤直径<5 cm、中高分化、无淋巴结转移的患者(P<0.05),有淋巴结转移宫颈癌患者的血清TGF-β水平高于无淋巴结转移的患者(P<0.05).宫颈癌患者的血清SCCA与TGF-β水平呈正相关(r=0.431,P<0.05),血清uPAR与CD105水平呈正相关(r=0.332,P<0.05).治疗1个月后宫颈癌患者的血清SCCA、uPAR、CD105和TGF-β水平均明显低于治疗前(P<0.01).结论 宫颈癌患者的血清SC-CA、uPAR、CD105和TGF-β水平均明显升高,且其表达水平与患者的临床特征具有一定关系,值得进一步研究.

摘要： Glomerular disease refers to a class of diseases in which the lesions are mainly located in the glomerulus,and the clinical manifestations are mainly hematuria,proteinuria,edema,hypertension and renal dysfunction.In recent years,it has been found that the urokinase-type plasminogen activator (uPA) of the plasminogen activator family,urokinase-type plasminogen activator receptor (uPAR) and its soluble form have been up-regulated in the pathogenesis of certain glomerular diseases.The combination with integrin affects signaling pathways and changes the morphology and function of podocytes to promote disease progression.In this paper,the relevant research progress is summarized as follows.%肾小球疾病是指病变主要位于肾小球的一类疾病,临床表现以血尿、蛋白尿、水肿、高血压和肾功能损害为主.纤溶酶原激活物(plasminogen activator)家族在介导肾小球疾病的发病机制中具有多重作用,近年来发现纤溶酶原激活物家族之一的尿激酶型纤溶酶原激活物(urokinase-type plasminogen activator,uPA)、尿激酶型纤溶酶原激活物受体(urokinase-type plasminogen activator receptor,uPAR)及其可溶形式在某些肾小球疾病的发病过程中水平上调,并且与整合蛋白结合影响信号传导途径、改变足细胞形态与功能,促进疾病进展.该文就相关研究进展作一综述.

摘要： 目的 采用新合成的尿激酶型纤溶酶原激活物受体(uPAR)衍生肽(RERF肽),探讨其对白血病耐药细胞K562/ADM耐药性的逆转作用及其机制.方法 应用MTT法观察RERF肽对K562/ADM细胞生长增殖影响及非细胞毒素剂量对耐药逆转作用.应用实时荧光定量PCR (qPCR)检测RERF肽作用后K562/ADM细胞中uPA、uPAR和MDR1基因的表达;Western blot检测RERF肽作用后K562/ADM细胞中uPA、uPAR和P-gp蛋白的表达.结果 ADM单独作用K562/ADM细胞24、48、72 h,IC50分别为92.48±0.27、30.99±0.19、28.06±0.12tg/mL;ADM与非细胞毒性剂量的RERF肽共同作用K562/ADM细胞24、48、72 h,IC50分别降低为83.83±0.29、18.52±0.17、16.38±0.13 μg/mL.联合用药48 h后K562/ADM细胞其uPA、uPAR、MDRl mRNA与uPA、uPAR和p-gP蛋白的表达量明显降低(P＜0.05).结论 RERF肽可部分逆转K562/ADM细胞对ADM的耐药性,提高ADM的敏感性.RERF肽有可能通过uPA/uPAR途径下调MDR1基因,降低P-gp的表达,从而逆转白血病耐药.%Objective To investigate its effect of the newly synthesized uPAR-derived peptide (RERF peptide) on leukemic K562/ADM and its mechanism.Methods The effect of RERF peptide on the proliferation of K562/ADM cells was observed by MTT assay.The reversal effect of non-cytotoxic dose of RERF peptide on drug resistance of adriamycin resistant K562/ADM cells was observed.The relative expression of uPA,uPAR and MDR1 gene in K562/ADM cells was detected by qPCR.And the expression of uPA,uPAR and P-gp protein in K562/ADM cells were detected by a western blot analysis.Results The IC50 values of K562/ADM cells were 92.48±0.27,30.99±0.19,28.06±0.12 μg/mL respectively at 24 h,48 h,and 72 h after ADM administration.The IC50 decreased to 83.83±0.29,18.52±0.17,16.38±0.13 μg/mL respectively at 24 h,48 h and 72 h after ADM combined with non-cytotoxic doses of RERF peptide.The expression of uPA,uPAR,MDR1 mRNA and p-gp protein in K562/ADM cells after treatment 48 h were significantly decreased (P ＜ 0.05).Conclusion RERF peptide could partially reverse the drug resistance of ADM in K562/ADM cells and improve the sensitivity of ADM.RERF peptide could reverse the resistance by affecting MDR1 gene via the uPA/uPAR pathway and decrease the express of P-gp.

摘要： 目的 探讨小干扰RNA(siRNA)沉默尿激酶型纤溶酶原激活物受体(uPAR)和组织蛋白酶B(CB)基因对肝癌细胞迁移的影响及其机制.方法 培养肝癌SMMC-7721细胞后,用荧光标记的低、中、高浓度的siRNA转染肝癌细胞,在荧光显微镜下计算siRNA转染效率,筛选出最佳siRNA转染浓度.将肝癌细胞分成空白对照组、阴性对照组(LC组)、uPAR-siRNA转染组(si-uPAR组)、CB-siRNA转染组(si-CB组)和uPAR-siRNA/CB-siRNA联合转染组(si-UC组).si-uPAR组、si-CB组、si-UC组细胞分别加入uPAR-siRNA、CB-siRNA、uPAR-siRNA/CB-siRNA转染试剂复合物进行转染,LC组仅加入转染试剂,空白对照组不进行干预.转染72 h后通过细胞划痕实验检测癌细胞迁移能力;转染48 h后,用流式细胞术分析细胞周期,实时荧光定量PCR法检测各组肝癌细胞整合素α6和基质金属蛋白酶9(MMP9)基因表达水平.结果 24 h后,用荧光标记的低浓度的siRNA转染肝癌细胞其转染效率在85％以上,细胞状态良好.与空白对照组及LC组相比,si-uPAR组、si-CB组、si-UC组细胞的迁移能力均下降、G0/G1期细胞比例增加、整合素α6及MMP9 mRNA表达水平均降低(均P<0.05);与si-uPAR组、si-CB组相比,si-UC组细胞的迁移能力均下降、G0/G1期细胞比例增加、整合素α6及MMP9 mRNA表达水平均降低(均P<0.05).结论 siRNA沉默uPAR或CB基因均可抑制肝癌细胞的迁移,且联合沉默抑制效果更明显,其可能通过抑制整合素α6和MMP9 mRNA的表达、诱导细胞G0/G1期阻滞而发挥作用.%Objective To explore the effect of small interfering RNA(siRNA) silencing urokinase-type plasminogen activator receptor(uPAR) and cathepsin B(CB) genes on the migration of hepatocellular carcinoma(HCC) cells and its mechanism. Methods HCC SMMC-7721 cells were cultured,then were transfected with fluorescent labeled siRNA of low,moderate and high concentrations. The transfection efficiency of siRNA was calculated under fluorescence microscope and the optimal transfection concentration of siRNA was screened out. The HCC cells were divided into blank control group,negative control group(LC group),uPAR-siRNA transfection group ( si-uPAR group) ,CB-siRNA transfection group( si-CB group) and uPAR-siRNA/CB-siRNA combined transfection group( Si-UC group) . The cells in the si-uPAR group,si-CB group and si-UC group were transfected by the compounds of uPAR-siRNA/transfection reagent, CB-siRNA/transfection reagent and uPAR-siRNA/CB-siRNA/transfection reagent respectively. The LC group was treated only by transfection reagent,and no treatment was performed in the blank control group. After 72h of transfection, the migration ability of HCC cells was detected by cell scratch assay. After 48h of transfection,the cell cycle was analyzed by flow cytometry. And the expression levels of integrinα6 mRNA and matrix metalloprotein 9 ( MMP9 ) mRNA were detected by real-time quantitative PCR assay. Results After 24 h of transfection with fluorescent labeled siRNA of low concentration,the transfection efficiency of HCC cells was more than 85％,and the cells were in good condition. Compared to the blank control group and LC group,the migration ability of the cells significantly decreased,the proportion of the cells at G0/G1 phase increased and the expression levels of integrin α 6 mRNA and MMP9 mRNA were lower in the si-uPAR group,si-CB group and si-UC group(all P<0. 05). Compared to the si-uPAR group and si-CB group,the migration ability of the cells significantly decreased,the proportion of the cells at G0/G1 phase increased and the expression levels of integrin α 6 mRNA and MMP9 mRNA were lower in the si-UC group(all P<0. 05). Conclusion Either uPAR or CB gene silencing by siRNA can inhibit the migration of HCC cells,and the combined silencing is more effective. The main mechanism might be related to inhibiting integrinα6 mRNA and MMP9 mRNA expressions and inducing cell arrest at G0/G1 phase.

摘要： 目的 探讨血清尿激酶型纤溶酶原激活物受体(uPAR)水平与胆道闭锁(BA)患者术后肝硬度值的相关性.方法 选取2014年1月-2016年12月本院择期行Kasai术的BA儿童患者48例作为研究对象(BA组).本院同期健康体检儿童40例作为对照(正常组).根据血清总胆红素值(TB),将BA组分成有黄疸组(n=20)和无黄疸组(n=28).应用酶联免疫吸附法测定血清uPAR水平,应用瞬时弹性成像(TE)测量肝硬度值.结果 BA组血清uPAR水平和肝硬度值均显著高于正常组患者(P＜0.001),患有黄疸的BA组血清uPAR水平和肝硬度值显著高于无黄疸组(P＜0.001).血清uPAR水平和肝硬度值及肝功能指标总胆红素(TB)、ALT、AST及碱性磷酸酶(ALP)呈正相关(P＜0.001).结论 BA患者术后血清uPAR水平与肝硬度值及肝功能密切相关,可考虑作为肝纤维化进程的非侵入性检测指标.

摘要： 目的 研究黑素瘤组织中乙醛脱氢酶1(aldehyde dehydrogenase 1,ALDH1)、上皮性钙黏附蛋白(E-cadherin,E-cad)及尿激酶型纤溶酶原激活物受体(urokinase-type plasminogen activator receptor,uPAR)的表达及与临床病理特征的关系.方法 选择50例黑素瘤和50例色素痣患者的病变组织作为研究对象,采用免疫组化法检测病变组织中的ALDH1、E-cad及uPAR的表达情况,分析这3种蛋白表达与患者临床组织病理特征、肿瘤分期的关系.结果 黑素瘤组织中ALDH1和uPAR表达阳性率分别为82.00％(41/50)和86.00％(43/50),均显著高于色素痣组(P90％.浸润深度Ⅳ～Ⅴ的黑素瘤患者E-cad表达阳性率显著低于浸润深度Ⅰ～Ⅲ的患者(P<0.05),黑素瘤患者E-cad表达阳性率与其他临床特征无相关性.结论 黑素瘤在发生和进展过程中ALDH1、uPAR表达上调,E-cad表达下调,E-cad表达下调与肿瘤程度有关.%Objective To study the expression of aldehyde dehydrogenase 1(ALDH1), E-cadherin(E-cad) and urokinase-type plasminogen activator receptor(uPAR) in melanoma tissues and their relationship with clinicopathological features. Methods A total of 50 lesions of melanoma and 50 lesions of nevus were selected as the research objects, and the expression of ALDH1, E-cad and uPAR were detected by immunohistochemical method, then the correlations between the expression of the three kinds of proteins, clinicopathological features, and tumor staging were analyzed. Results ALDH1 and uPAR positive expression rate of melanoma tissues were 82.00％ (41/50) and 86.00％ (43/50) respectively, which were significantly higher than that of pigmented nevus group (P<0.05); melanoma tissue E-cad positive expression rate was 38.00％ (19/50), which was significantly lower than that of pigmented nevus group (P<0.05). ALDH1, uPAR expression wasn't related to age, gender, tumor thickness, depth of invasion, lymph node metastasis and pathological classification, but for the melanoma tissues which tumor invasion depth over 4mm, depth of invasion ranged IV ～ V and lymph node metastasis occurred, the positive expression rate of ALDH1 and uPAR was above 90％. The positive expression rate of E-cad was significantly lower in patients with infiltrative depth ranged IV ～ V than that in patients with invasive depth ranged I ～ III (P<0.05), and the positive expression rate of E-cad was not associated with other clinical features. Conclusion The expression of ALDH1 and uPAR was up-regulated and the expression of E-cad was down-regulated during the development and progression of melanoma. The down-regulation of E-cad expression was related to the degree of tumor.

摘要： 目的 观察乙酰肝素酶(HPA)及其相关因子mRNA在白血病细胞中的表达,研究白血病细胞表面止血平衡改变.方法 选取白血病患者40例(研究组),缺铁性贫血患者20例(对照组).采用半定量反转录聚合酶链反应(RT-PCR)方法测定受试者骨髓单个核细胞组织因子(TF)、尿激酶型纤溶酶原激活物受体(uPAR)、HPA mRNA的含量.结果 研究组骨髓中单个核细胞TF、uPAR、HPAmRNA的表达与对照组相比均升高(均P＜0.05),35例初发白血病患者中急性髓系白血病(AML)组(23例)骨髓中单个核细胞TF、uPAR、HPA mRNA高于慢性粒细胞白血病(CML)组(4例)、慢性淋巴细胞白血病(CLL)组(3例)、急性淋巴细胞白血病(ALL)组(5例)(对照组、AML组、CML组、ALL组、CLL组TF分别为0.66±0.03、2.56±0.37、1.33±0.06、1.93±0.08、1.23±0.07,uPAR分别为0.53士0.02、1.89±0.26、0.92±0.15、1.44±0.01、1.19±0.16,HPA分别为2.37±0.24、1.42±0.13、1.68±0.09、1.54±0.12,均P＜0.05).结论 白血病细胞中HPA、TF、uPAR mRNA表达增高;不同类型白血病表达水平不同.提示TF、uPAR、HPA可能影响白血病细胞表面止血平衡,不同类型白血病细胞表面止血平衡改变不同.%Objective To explore whether the expression of heparanase (HPA) and other coagulation proteins on blast membrane could determine the hemostatic balance on the surface of leukemia cells.Methods 40 patients with leukemia (study group) and 20 patients with iron deficiency anemia (control group) were analyzed,the levels of TF,uPAR,HPA mRNA were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).Results The levels of TF,uPAR,HPA mRNA in study group were higher than those in the control group (P ＜ 0.05).The levels of TF,uPAR,HPA mRNA in acute myeloid leukemia (AML) group (23 cases) were significantly higher than those in the acute lymphoblastic leukemia (ALL) (5 cases),chronic myelocytic leukemia (CML) (4 cases),chronic lymphocytic leukemia (CLL) groups (3 cases) (in control,AML,CML,ALL,CLL groups,TF levels were 0.66±0.03,2.56±0.37,1.33±0.06,1.93± 0.08,1.23±0.07,uPAR were 0.53±0.02,1.89±0.26,0.92±0.15,1.44±0.01,1.19±0.16,HPA were 2.37±0.24,1.42±0.13,1.68±0.09,1.54±0.12,respectively,all P ＜ 0.05).Conclusions The TF,uPAR and HPA predominate in leukemia cells.The expression of coagulation proteins on blast membrane may determine the hemostatic balance on the surface of leukemia cells,and the hemostatic balance on the blast surface may contribute to thombohemorrhagic syndrome manifestations in leukemic patients.

摘要： 探讨血清抗磷脂酶A2受体(PLA2R)抗体、可溶性尿激酶型纤溶酶原激活物受体(suPAR)和尿液血管生成素样蛋白-4(Angpt14)在特发性膜性肾病(IMN)诊断中的临床意义.

摘要： 目的:检测上皮-间质细胞转化(EMT)在慢性阻塞性肺疾病(COPD)患者小气道中的表达,并探讨尿激酶型纤溶酶原激活物受体(uPAR)在COPD患者小气道上皮细胞EMT发生中的调控作用.rn 方法:(1)通过免疫组织化学方法检测25例正常不吸烟对照,25例正常吸烟对照,18例COPD患者小气道上皮uPAR、上皮细胞标志物E-cadherin及间质细胞标志物vimentin蛋白表达情况;(2)通过spearman等级相关分析观察小气道上皮细胞uPAR、vimentin表达与肺功能参数FEVl％相关性,及uPAR与vimentin蛋白表达相关性分析;(3)体外培养人小气道上皮细胞(HSAEpiC),香烟烟雾提取物(CSE)干预后观察uPAR及EMT相关标志物的表达变化;通过uPAR基因沉默观察uPAR对小气道上皮细胞EMT的调控作用rn .结果:(1)同对照不吸烟组、对照吸烟组比较,uPAR及间质细胞标志物vimentin在COPD患者小气道上皮细胞中表达明显升高;对照吸烟组uPAR及vimentin表达较对照不吸烟组明显升高(P＜0.01);(2)COPD患者小气道上皮uPAR(r=0.564,P＜0.01)、vimentin(r=0.461,P＜0.01)表达与COPD严重程度肺功能指标FEVl％呈负相关;小气道上皮uPAR与vimentin蛋白表达呈正相关(r=0.701,P＜0.01);(3)Real-time PCR、western blot结果显示CSE干预HSAEpiC细胞后,uPAR及间质细胞标志物N-cadherin、α-SMA表达明显升高,上皮细胞标志物E-cadherin、α-catenin表达明显降低;shRNA干扰CSE诱导HSAEpiC细胞uPAR表达后,上皮细胞标志物E-cadherin、α-catenin表达降低及间质细胞标志物N-cadherin、α-SMA表达升高明显被抑制.rn 结论:uPAR及EMT在COPD患者小气道上皮细胞中表达明显并呈正相关,体外实验证实uPAR能调控小气道上皮细胞EMT的发生.

摘要： 目的:检测上皮-间质细胞转化(EMT)在慢性阻塞性肺疾病(简称慢阻肺)患者小气道中的表达,并探讨尿激酶型纤溶酶原激活物受体(uPAR)在慢阻肺患者小气道上皮细胞EMT发生中的调控作用.rn 方法:通过免疫组织化学方法检测健康不吸烟对照(25例)、健康吸烟对照(25例)和慢阻肺患者(18例)小气道上皮uPAR、上皮细胞标志物E-cadherin及间质细胞标志物vimentin蛋白的表达.通过spearman等级相关分析观察小气道上皮细胞uPAR、vimentin表达与肺功能参数(FEV1占预计值％)的相关性,以及uPAR与vimentin蛋白表达的相关性.体外培养人小气道上皮细胞，烟草烟雾提取物干预后观察uPAR及EMT相关标志物表达的变化，通过uPAR基因沉默观察uPAR对小气道上皮细胞EMT的调控作用。rn 结果:与不吸烟对照组和吸烟对照组比较，uPAR及间质细胞标志物vimentin在慢阻肺患者小气道上皮细胞中表达明显升高;吸烟对照组uPAR及vimentin表达较不吸烟对照组明显升高(P<0.01)，慢阻肺患者小气道上皮uPAR和vimentin表达与慢阻肺严重程度FEV1占预计值%呈显著负相关(r值为-0.564和-0.461，均P<0.01)，小气道上皮uPAR与vimentin蛋白表达呈显著正相关(r=0.701,P<0.01);Real-time PCR和Western blot结果显示，烟草烟雾提取物干预人小气道上皮细胞后，uPAR及间质细胞标志物N-cadherin和α-SMA表达明显升高，上皮细胞标志物E-cadherin和α-catenin表达明显降低;shRNA干扰烟草烟雾提取物诱导人小气道上皮细胞uPAR表达后，上皮细胞标志物E-cadherin和α-catenin表达降低，间质细胞标志物N-cadherin和α-SMA表达升高明显被抑制。rn 结论:uPAR及EMT在慢阻肺患者小气道上皮细胞中表达明显，并呈显著正相关，体外实验证实uPAR能调控小气道上皮细胞EMT的发生。

摘要： 本发明公开一种蛇毒凝血酶原激活物及基于蛇毒凝血酶原激活物的快速止血材料，采用柱层析法将具有凝血活性的蛇毒凝血酶原激活物提取出来，通过改变层析条件和调节技术参数实现准确分离，并且可在常温下进行操作，对实验条件要求简单，容易放大生产，由于选择的层析柱可以反复使用，因此具有成本低、收率高和产品纯度高的优点，本发明的基于蛇毒凝血酶原激活物的快速止血材料，能够最大限度的保持蛇毒凝血酶原激活物的活性和稳定性；安全无毒副作用，既能快速止血又能防止二次出血和感染，可以用于事故急救、手术止血和战时创伤止血时，尤其适用于动脉大出血，能够快速止血，并且不会产生二次创伤。

摘要： 本发明涉及用于检测尿激酶纤溶酶原激活物受体(uPAR)的造影剂。更具体地，本发明涉及造影剂，其包含用可成像的部分标记的结合uPAR的肽载体。

摘要： 提供u‑PA多肽和含有所述u‑PA多肽的融合蛋白。所述u‑PA多肽经修饰成具有改变的活性和/或特异性，从而其切割补体蛋白如补体蛋白C3，因而抑制补体激活。抑制补体激活的经修饰的u‑PA多肽和融合蛋白能用于治疗由补体激活介导的或补体激活在其中发挥作用的疾病和病症。这些疾病包括缺血和再灌注失调(包括心肌梗塞和中风)、败血症、自身免疫病、糖尿病视网膜病变、年龄相关的黄斑变性、移植器官排斥、炎症性疾病以及有炎性成分的疾病。

摘要： 本发明涉及鉴定尿激酶纤溶酶原激活物(uPA)抗体的方法。本发明也涉及能够结合uPA和能够减少或抑制uPA活性的抗体。此外，本发明涉及所述抗体的用途，例如治疗和药学用途。

摘要： 本发明涉及一种无水的不含精氨酸的制剂，其包括人组织尿激酶类型纤溶酶原激活物，赖氨酸，磷酸，和非离子洗涤剂，其中人组织尿激酶类型纤溶酶原激活物，赖氨酸，磷酸，和非离子洗涤剂的量分别为10－60mg，100－700mg，20－100mg，和0.2－5mg；或者为相同相对比率的量。

摘要： 本发明公开一种蛇毒凝血酶原激活物及基于蛇毒凝血酶原激活物的快速止血材料，采用柱层析法将具有凝血活性的蛇毒凝血酶原激活物提取出来，通过改变层析条件和调节技术参数实现准确分离，并且可在常温下进行操作，对实验条件要求简单，容易放大生产，由于选择的层析柱可以反复使用，因此具有成本低、收率高和产品纯度高的优点，本发明的基于蛇毒凝血酶原激活物的快速止血材料，能够最大限度的保持蛇毒凝血酶原激活物的活性和稳定性；安全无毒副作用，既能快速止血又能防止二次出血和感染，可以用于事故急救、手术止血和战时创伤止血时，尤其适用于动脉大出血，能够快速止血，并且不会产生二次创伤。

摘要： 本发明涉及蛋白裂解酶和U型纤溶酶原激活物的底物和其它可裂解部分及其使用方法。本发明一般地涉及包含可裂解部分的多肽，所述可裂解部分是选自蛋白裂解酶和U型纤溶酶原活化因子（uPA）的至少一种蛋白酶的底物，涉及可活化抗体和其它包含可裂解部分的更大的分子，所述可裂解部分是选自蛋白裂解酶和U型纤溶酶原活化因子的至少一种蛋白酶的底物，并且涉及在多种治疗、诊断和预防指征中制造和使用这些包含可裂解部分的多肽的方法，所述可裂解部分是选自蛋白裂解酶和U型纤溶酶原活化因子的至少一种蛋白酶的底物。

摘要： 本发明属临床医学领域，涉及可溶性尿激酶型纤溶酶原激活物受体(soluble urokinase plasminogen activator receptor，suPAR)可作为慢加急性肝衰竭患者临床转归的独立生物标志物。本发明提供一种血浆可溶性尿激酶型纤溶酶原激活物受体及其应用。用于可溶性尿激酶型纤溶酶原激活物受体的试剂用于制备肝癌早期诊断试剂盒中的应用。

摘要： 本申请涉及纳米晶荧光检测领域，尤其涉及一种尿激酶型纤溶酶原激活物受体荧光检测纳米晶材料及其制备方法和用途。一种尿激酶型纤溶酶原激活物受体荧光检测纳米晶材料，该纳米晶材料的纳米晶分子式如下：NaGd0.4Nd0.6F4@NaScF4：Yb。该纳米晶材料在980纳米激光器激发条件下，Nd3+离子的绿光强度随尿激酶型纤溶酶原激活物受体的浓度的增大而减弱，其关系曲线能够很好地应用于尿激酶型纤溶酶原激活物受体的近红外荧光检测。该检测方法具有无背景荧光，深穿透深度以及准确度高的优势。

摘要： 本发明涉及一种可溶性尿激酶型纤溶酶原激活物受体检测试剂盒及检测方法，检测试剂盒包括磁分离试剂、抗体试剂、校准品、质控品、浓缩清洗液和底物液。本发明提供的可溶性尿激酶型纤溶酶原激活物受体(suPAR)定量检测试剂盒，采用化学发光免疫技术和磁分离技术相结合的方法，大大提高了过敏原特异性抗体的检测灵敏度和特异性，使得检测结果更真实可信；同时优化了反应时间和反应步骤，使操作更简单。