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目的检测重症肺炎患儿血清降钙素原(PCT)、超敏C反应蛋白(hs-CRP)、铜蓝蛋白(CER)水平,并分析其与心肌损害发生率的关系。方法对医院2015年4月~2018年9月收治的212例重症肺炎患儿的资料进行回顾,检测其基线血清PCT、hs-CRP和CER水平。计算心肌损害发生率,对比心肌损害发生者和未发生者基线血清PCT、hs-CRP和CER水平。采用Logistic回归分析探讨上述血清因子与重症肺炎患儿心肌损害的关系,并绘制受试者工作特征曲线(ROC)探讨基线血清PCT、hs-CRP、CER水平及三者联合对心肌损害的预测效能。结果本组患儿心肌损害发生率为11.79%,发生时间为(7.15±2.08)d;心肌损害发生者基线血清PCT、hs-CRP和CER水平均高于未发生组(P<0.05);发生者年龄<3岁、并发呼吸衰竭、低蛋白血症、低氧血症、低钾血症、发病至入院时间>7d、发病至入院时间3~7d、基线PCT升高>50%、基线hs-CRP升高>50%、基线CER升高>50%构成比均高于未发生者(P<0.05),经Logistic回归分析证实均为心肌损害的危险因素;基线PCT、hs-CRP、CER水平预测心肌损害的Cut-off值分别为8.45pg/L、12.50mg/mL、402.47mg/L,三者联合预测心肌损害的灵敏度、特异度、AUC分别为92.00%、97.86%、0.896,均高于单独预测。结论重症肺炎患儿并心肌损害发生风险高,发生者基线PCT、hs-CRP、CER水平较高,年龄<3岁、并发呼吸衰竭等均是其危险因素,且基线PCT、hs-CRP、CER水平联合预测心肌损害的效能较高。  相似文献   
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Aim: Patients with Wilson disease show complex clinical features. Accurate diagnosis at the initial clinical manifestation is important for patients to receive effective treatment with anti‐copper agents. In this study, we assessed whether the international scoring system for the diagnosis of Wilson disease is a reliable tool for screening Japanese patients with primary copper toxicosis requiring anti‐copper treatment. Methods: Twenty‐three Japanese patients suspected of Wilson disease were enrolled in this study. We performed long‐range polymerase chain reaction to detect ATP7B mutations in this series. Finally, we retrospectively assessed the reliability of using a diagnostic score of 4 or more points as the cut‐off for this scoring system. Results: Ten patients were homozygous or compound heterozygous for ATP7B mutations including a novel mutation of 3837 bp deletion including 3 exons. The mutation would have been missed by the traditional analysis. Six patients were heterozygous for ATP7B mutations. Three of these six patients had additional diagnostic points. The other three patients were diagnosed as carriers of a mutant gene based on their low scores. One of the seven patients free from ATP7B mutation was affected by copper toxicosis. Though the score was 3 points based on increased urinary copper and copper‐positive cirrhosis, anti‐copper treatment promptly improved liver failure, which was likely due to idiopathic copper toxicosis. Conclusion: The international scoring system for diagnosis of Wilson disease is a fairly reliable tool for screening Japanese patients who need anti‐copper treatment. Caution is needed for patients with possible idiopathic copper toxicosis because the maximal score is 4 points.  相似文献   
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目的:通过检测阿尔茨海默病(Alzheimer disease,AD)模型大鼠海马铜蓝蛋白(glycan-phosphatidyli-nositol ceruloplasmin,GPI-Cp)的变化,探讨AD时脑铁增高的机制。方法:取雄性(290±10)g SD大鼠,经海马内注射(amyloid beta-peptide 1-40,Aβ1-40)建立AD模型,于1、2、3和4周取各组大鼠脑组织,分离海马,用RT-PCR检测GPI-Cp mRNA表达情况,免疫组织化学染色检测GPI-Cp蛋白表达情况。结果:海马的星形胶质细胞、血管内皮细胞、室管膜细胞均有GPI-Cp的mRNA和蛋白表达;而海马的锥体细胞仅轻度表达,颗粒细胞不表达。注射Aβ1-40后,模型组海马GPI-Cp mRNA和蛋白表达均随着时间延长逐渐降低,具有统计学意义(P<0.01)。结论:海马内注射Aβ1-40可引起大鼠海马GPI-Cp表达减少,GPI-Cp表达减少可能是AD时脑铁增高的原因。  相似文献   
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We conducted a microarray study to identify genes that are differentially regulated in the spinal cords of mice with the inflammatory disease experimental autoimmune encephalomyelitis (EAE) relative to healthy mice. In total 181 genes with at least a two‐fold increase in expression were identified, and most of these genes were associated with immune function. Unexpectedly, ceruloplasmin (Cp), a ferroxidase that converts toxic ferrous iron to its nontoxic ferric form and also promotes the efflux of iron from astrocytes in the CNS, was shown to be highly upregulated (13.2‐fold increase) in EAE spinal cord. Expression of Cp protein is known to be increased in several neurological conditions, but the role of Cp regulation in CNS autoimmune disease is not known. To investigate this, we induced EAE in Cp gene knockout, heterozygous, and wild‐type mice. Cp knockout mice were found to have slower disease evolution than wild‐type mice (EAE days 13–17; P = 0.05). Interestingly, Cp knockout mice also exhibited a significant increase in the number of astrocytes with reactive morphology in early EAE compared with wild‐type mice at the same stage of disease. CNS iron levels were not increased with EAE in these mice. Based on these observations, we propose that an increase in Cp expression could contribute to tissue damage in early EAE. In addition, endogenous CP either directly or indirectly inhibits astrocyte reactivity during early disease, which could also worsen early disease evolution. © 2014 Wiley Periodicals, Inc.  相似文献   
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目的:改进血清铜蓝蛋白(CP)的检测方法。方法:不连续淀粉-琼脂糖凝胶电泳分离血清CP,利用其氧化酶活性使 苯胺氧化,形成的有色产物沉积物凝胶板上CPR 相应位置,可直接观察CP量的变化。结果:通过比较各种联苯胺的显色时间及显色效果。从而筛选出一种更为有效的血清CP测定方法。结论:氧化酶活性盐酸联苯胺显示法是最有效的血清CP检测方法。  相似文献   
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Human ceruloplasmin, a copper binding α2-glycoprotein, was purified by a single-step procedure using acharan sulfate affinity chromatography. Acharan sulfate was immobilized to amine-functionalized agarose matrix through carboxylic acids. Ceruloplasmin in human plasma was obtained from 0.4 M NaCl salt elution and characterized by SDS-PAGE (132 and 125 kDa), isoelectric focusing (pI 4.6), Western blotting, and MALDI-TOF-MS peptide mass fingerprinting. Ceruloplasmin was purified 106 fold with a specific oxidase activity of 0.53 U/mg protein.  相似文献   
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