共查询到16条相似文献,搜索用时 62 毫秒
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通过脉冲腐蚀法对硅片进行多孔硅的制备,利用玻片通过对共价法、离子吸附法和APTES修饰的戊二醛交联法3种固定适配子方法的对比,以确定较好的固定青霉素适配子的方法。将适配子固定在多孔硅上后,利用交流阻抗法对加入青霉素前后传感器阻抗值进行测定、对比,构建等效电路并进行阻抗拟合。对多孔硅传感器的Nyqu ist谱图进行分析以确定多孔硅表面成功固定了青霉素适配子,从而证明构建纳米生物传感器成功。传感器的线性检测范围为0.05~0.2 mg/L,检测限为0.05 mg/L。 相似文献
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构建1种用于快速检测四环素的新型电化学纳米多孔硅(PS)生物传感器。通过脉冲腐蚀法制得多孔硅基片,将适配子固定于其上,这种四环素适配子能够特异性识别四环素分子,并引起阻抗值的变化。利用电化学交流阻抗法比较固定适配子前后硅片表面阻抗值的变化,以及在体系中加入不同浓度四环素后阻抗谱的变化。选择1个合适的等效电路对测得的阻抗数据进行拟合,获得了四环素浓度与阻抗值的变化规律。传感器的线性检测范围为2.079~62.37 nmol/L,检测限为2.079 7 nmol/L。 相似文献
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同步纯化人心肌肌钙蛋白T、I 总被引:4,自引:0,他引:4
同步纯化人心肌肌钙蛋白T、I李志梁付朝平钱学贤陆青王素华黎梅兰(第一军医大学珠江医院心内科,广州510282)关键词心肌肌钙蛋白T;心肌肌钙蛋白I;同步纯化收稿日期:1996-04-17;接受日期:1996-08-27。心肌肌钙蛋白包括3种不同的蛋白... 相似文献
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心肌肌钙蛋白I(cTnI)是一种仅存在于心肌细胞中,骨骼肌内含量是极低的蛋白.当心肌损伤发生时,cTnI能够快速释放进入血液,4-6h即可检测出浓度的上升,12-24h浓度达到峰值,并可以以较高浓度的形式在血液内维持6-8天,故诊断窗口期较长.用于急性心肌梗死(AMI)的诊断时,其特异性和灵敏度均高于其它血清标记物,已经替代了CK-MB成为诊断AMI的"金标准",具有重要的临床研究价值.本文就cTnI蛋白在急性心肌梗死诊断中的应用及其临床检测方法作以简要综述. 相似文献
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核酸适配体生物传感器是利用固定在电极表面的适配子与被测溶液中心肌肌钙蛋白Ⅰ(cTnⅠ)发生特异性结合,从而达到检测的目的.我们对玻碳电极进行阳极氧化、氨基化修饰,通过碳二亚胺盐酸盐(carbodiimide hydrochloride,EDC)、N-羟基琥珀酰亚胺(N-hydroxysuccinimide,NHS)活化作用将适配子结合在电极表面.cTnⅠ最佳检测范围是0.05~5 nmol/L,最低检测限为0.05 nmol/L,检测时间为5 min. 相似文献
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纳米多孔硅阻抗生物传感器的研究 总被引:1,自引:0,他引:1
构建了1种基于多孔硅材料,无需标记的纳米生物传感器,用于对牛血清白蛋白分子进行检测。通过对多孔硅进行表面处理,形成氧化膜,将抗体固定到多孔硅氧化层表面。在磷酸盐缓冲液中,通过电化学检测系统检测加入抗原后,传感器的阻抗值的变化。磷酸缓冲液(PBS)/抗体-氧化层/硅,构成电解液/绝缘层/半导体(electro-lyte-insulator-semiconductor,EIS)结构。传感器的线性检测范围为0.01~0.27mg/mL,检测限为0.01mg/mL。 相似文献
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本文旨在观察尾部悬吊模拟失重大鼠心肌钙蛋白酶(calpain)与钙蛋白酶抑素(calpastatin)表达的变化,以探讨心肌肌钙蛋白抑制亚基(cardiac troponin I,cTnI)降解的可能机制。采用尾部悬吊模拟失重大鼠模型,Western blotting技术观测心肌calpain-1、calpain-2与calpastatin的表达;PD150606抑制calpain活性,分析cTnI降解程度的变化。结果显示:与同步对照组相比,悬吊2周与4周组大鼠心肌calpastatin表达呈显著性降低(P0.05),calpain-1表达未改变,calpain-2表达略有降低;但是,心肌calpain-1/calpastatin及calpain-2/calpastatin的比值在悬吊2周与4周组明显增高(P0.05,P0.01)。悬吊4周组cTnI降解显著高于对照组(P0.01);然而,用calpain非特异性抑制剂PD150606处理后,对照组及悬吊组cTnI的降解均被显著抑制(P0.01)。这些结果提示模拟失重大鼠心肌calpain活性增高可能增加cTnI的降解。 相似文献
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In this work, a highly sensitive biosensor for detecting cadmium ions (Cd2+) was developed based on a Cd2+-specific DNA aptamer and a hybridization chain reaction (HCR). The Cd2+ aptamer (named S0) was used to recognize Cd2+ and trigger the HCR. Without Cd2+, S0 initiated the HCR to form long nicked dsDNA structures to quench the fluorescence. Then, Cd2+ could bind with S0 to block HCR to recover fluorescence. This biosensor had high sensitivity with a detection limit of 0.36 nM and a linear range from 0 to 10 nM. Moreover, it showed a satisfactory selectivity and recovery rates. 相似文献
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Phosphorylation-dependent conformational transition of the cardiac specific N-extension of troponin I in cardiac troponin 总被引:1,自引:0,他引:1
Howarth JW Meller J Solaro RJ Trewhella J Rosevear PR 《Journal of molecular biology》2007,373(3):706-722
We present here the solution structure for the bisphosphorylated form of the cardiac N-extension of troponin I (cTnI(1-32)), a region for which there are no previous high-resolution data. Using this structure, the X-ray crystal structure of the cardiac troponin core, and uniform density models of the troponin components derived from neutron contrast variation data, we built atomic models for troponin that show the conformational transition in cardiac troponin induced by bisphosphorylation. In the absence of phosphorylation, our NMR data and sequence analyses indicate a less structured cardiac N-extension with a propensity for a helical region surrounding the phosphorylation motif, followed by a helical C-terminal region (residues 25-30). In this conformation, TnI(1-32) interacts with the N-lobe of cardiac troponin C (cTnC) and thus is positioned to modulate myofilament Ca2+-sensitivity. Bisphosphorylation at Ser23/24 extends the C-terminal helix (residues 21-30) which results in weakening interactions with the N-lobe of cTnC and a re-positioning of the acidic amino terminus of cTnI(1-32) for favorable interactions with basic regions, likely the inhibitory region of cTnI. An extended poly(L-proline)II helix between residues 11 and 19 serves as the rigid linker that aids in re-positioning the amino terminus of cTnI(1-32) upon bisphosphorylation at Ser23/24. We propose that it is these electrostatic interactions between the acidic amino terminus of cTnI(1-32) and the basic inhibitory region of troponin I that induces a bending of cTnI at the end that interacts with cTnC. This model provides a molecular mechanism for the observed changes in cross-bridge kinetics upon TnI phosphorylation. 相似文献
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《Biomarkers》2013,18(8):668-672
AbstractObjective: Information is limited on the prognostic implications of cardiac troponin I (cTnI) changes during the first days of non-ST elevation acute coronary syndrome (NSTE-ACS).Methods: High-sensitivity cTnI levels were measured at study inclusion and after 48?h in 1615 conservatively managed NSTE-ACS patients from the Global Use of Strategies To Open Occluded Coronary Arteries (GUSTO) IV trial.Results: Patients with moderately increased cTnI levels and without a relevant decrease over time had a significantly raised mortality at 30 days and 1 year. No relevant associations between cTnI changes and recurrent myocardial infarction were seen.Conclusion: The cTnI change is predictive for subsequent mortality in selected conservatively managed NSTE-ACS patients. 相似文献