Neuropilin-1 is a member of the neuropilins family protein, which contains a large extracellular domain (a1a2, b1b2 and c), a single transmembrane domain, and a short cytoplasmic tail. NRP-1 plays a critical role in angiogenesis and stimulates endothelial cell division and migration by binding VEGF(165) with b1b2 domain. In the present study, we report the establishment of a monoclonal antibody (A6-26-11-26 clone) specific for NRP-1 b1b2 through hybridoma method. Western blot analysis indicates that our NRP-1 b1b2 MAb can combine both NRP-1 b1b2 and NRP-1 originated from tumor cells. This monoclonal antibody against NRP-1 b1b2 will be useful in the further development of cancer target strategy.
To solve processing problems caused by bacterial activity in sugar industry, a sensitive method for dextran detection is expected. In this study, monoclonal antibodies (mAbs) against dextran were prepared using dextran T40 conjugated with bovine serum albumin as immunogens. Basing on the mAbs, a competitive enzyme-linked immunosorbent assay (ELISA) method to measure dextran quantitatively was developed. Results demonstrated that this competitive ELISA method had a calibration curve with correlation coefficient of 0.9986, IC 50 value of 204.2 ng/mL and detection value ranging from 26.3 ng/mL to 1174.9 ng/mL. In addition, cross-reaction assay suggested the method had no significant crossreaction with dextran-related substances such as b-glucan, starch, sucrose, sugar and glucose. Besides, spike recovery assay indicated this quantitative method for dextran detection had a perfect accuracy.
PRACTICAL APPLICATIONSWith wide detection range, high specificity and good calibration curve, this developed competitive ELISA method will be reliable to detect dextran quantitatively in sugar industry, and even may be commercially applied into kit development.
Herein, we have reported a new one-step potentiometric immunoassay for the sensitive and specific detection of human plasma cardiac troponin I (cTnI), a biomarker of cardio-cerebrovascular diseases.
Hypertrophic cardiomyopathy (HCM), a genetically and clinically heterogeneous cardiomyopathy, is commonly caused by mutations in the MYBPC3 gene or other various sarcomeric genes. HCM patients carrying sarcomeric gene mutations may experience an asymptomatic period at early stage but still possess an escalating risk of developing adverse cardiac events including sudden cardiac death. It is crucial to determine the phenotypic and pathogenic effects of mutations in sarcomeric genes. In this study, a 65‐year‐old male was admitted with a history of chest pain, dyspnoea, and syncope and with a family history of HCM and sudden cardiac death. On admission, electrocardiogram indicated atrial fibrillation and myocardial infarction. Transthoracic echocardiography revealed left ventricular concentric hypertrophy and systolic dysfunction (48%), which were ascertained by cardiovascular magnetic resonance. With late gadolinium‐enhancement imaging, cardiovascular magnetic resonance found myocardial fibrosis on left ventricular wall. The exercise stress echocardiography test showed non‐obstructive myocardial changes. Whole‐exome sequencing analysis identified a MYBPC3 gene heterozygous nonsense variant (c.1522C>T) in the patient and one of his healthy grandnieces (18‐year‐old). The patient was diagnosed with non‐obstructive HCM, heart failure, atrial fibrillation, and so on. Medications, ICD implantation, and catheter ablation were chosen to maintain heart function. Our study provides the clinical evidence regarding the HCM pathogenicity of MYBPC3 c.1522C>T variant and highlights the significance of family genetic testing in the diagnosis and management of HCM.
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