Background: Kawasaki disease (KD) is a common, yet unknown etiology disease in Asian countries, which causes acquired heart disease in childhood. It is characterized by an inflammatory acute febrile vasculitis of medium-sized arteries, particularly the coronary arteries. High-mobility group box-1 protein (HMGB1) is a non-histone chromosomalbinding protein present in the nucleus of eukaryotic cells, which contains 215 amino acid residues. Although the cellular signal transduction mechanisms of HMGB1 are currently unclear, the important role of the receptor for advanced glycation end-products (RAGE), the main receptor for HMGB1 has been reported in detail. The purpose of our study was to verify the mechanism and clinical significance of HMGB1-RAGE in coronary artery injury of Kawasaki disease. Methods: 52 blood samples of patients in KD were collected, and the coronary artery Z score was calculated according to the echocardiographic results. The Z score ≥ 2.0 was classified as coronary artery lesions (CAL); otherwise, it was no-coronary artery lesions (NCAL). In addition, the fever group and control group were set. Among them, the fever group were children with fever due to respiratory tract infection at the same time period as KD (heat peak ≥ 38.5 ℃). The normal group were children at a routine physical examination in the outpatient clinic of Nantong University and the physical examination center of the child care insurance, and there were no infectious diseases and heart diseases. The serum levels of HMGB1, RAGE, and NF-κB in each group were detected by ELISA. The animal model of KD was established using the New Zealand young rabbits. We used RT-qPCR/H&E staining/immunohistochemistry/ELISA and western blot to detect the level of HMGB1/RAGE and NF-κB. Results: In this study, we found that the HMGB1/RAGE/NF-κB axis was elevated in the serum of children with KD. In addition, an animal model of KD was subsequently prepared to examine the pathological changes of the coronary arteries. We found that the serum levels of HMGB1/RAGE/NF-κB in rabbits with KD were significantly higher than those of the control group. Moreover, the lumen diameter of the coronary artery was slightly enlarged, and the wall of the tube became thinner and deformed. In addition, the HMGB1/RAGE/NF-κB levels in the coronary artery were higher in the rabbits with KD in the acute phase. Conclusions: On the whole, the findings of this study demonstrate that the expression of HMGB1/RAGE/NF-κB is altered at different stages of KD, suggesting that the HMGB1/RAGE/NF-κB signaling pathway plays an important role in vascular injury in KD. The results of this study may have important implications for the early warning of coronary artery lesions in KD.
Abstract. Magnetic Resonance Imaging (MRI) has been one of the most revolutionary medical imaging modalities in the past three decades. It has been recognized as a potential technique in the clinical diagnosis of diseases as well as tumor differentiation. Although MRI has now become the preferred choice in many clinical examinations, there are some drawbacks, which still limit its applications. One of the crucial issues of MRI is the geometric distortion caused by magnetic field inhomogeneity and susceptibility effects. The farther the lesion from the center of a magnetic field (off-center field), the more severe the distortion becomes, especially in low-field MRI. Hence, it might hinder the diagnosis and characterization of lesions in the presence of field inhomogeneity. In this study, an innovative multi-orientated water-phantom was used to evaluate the geometric distortion. The correlations between the level of image distortion and the relative off-center positions, as well as the variation of signal intensities, were both investigated. The image distortion ratios of axial, coronal and sagittal images were calculated.
Background:The greatest complication of Kawasaki disease (KD) is coronary artery injury, and the requirement for early diagnosis and treatment is paramount. Thus, markers of vascular endothelial injury are of important clinical significance. Methods:According to our diagnostic criteria, blood samples were collected from 43 patients with KD, who were then divided into coronary artery lesions (CALs) and non-CALs (NCALs) groups according to their Z-score. As the control group, an additional 26 blood samples were collected from healthy children. Flow cytometry (FCM) and enzyme-linked immunosorbent assays (ELISA) were used to detect the expression levels of plasma endothelial microparticles (EMPs) and von Willebrand factor (vWF). Results:The expression levels of plasma CD31+/CD42b-EMPs, CD105+/CD54+EMPs, and vWF were higher in children with KD than those in the control group, and the differences were statistically significant (P<0.05).Also, the expression levels of CD31+/CD42b-EMPs, CD105+/CD54+EMPs and vWF in those in the CALs group at the acute and subacute stages were significantly higher than those in the NCALs group (P<0.05). Furthermore, receiver operating characteristic (ROC) curve analysis revealed that the area under the curve (AUC) of CD31+/CD42b-EMPs combined with vWF was 0.896, which indicates a higher diagnostic value in predicting CALs in children with KD. Conclusions:In our study, expression levels of EMPs and vWFare expected to used for early diagnosis, and which are associated with coronary artery injury in KD.
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