Novel role for integrin ß4 in asthmatic children infected with Mycoplasma pneumoniae.

Objectives: The regulatory role of integrin ß4 (ITGB4) in asthmatic children infected with Mycoplasma pneumoniae (MP) was analyzed, and its potential molecular mechanisms and function were studied.Methods: We collected epidemiological data from 70,455 asthmatic children. The immunofluorescence assay was used to test 9 index IgMs against respiratory tract pathogens for 736 serum samples. Then, 98 children with severe asthma were treated via fiberoptic bronchoscope examination. During the surgery, the patients' lavage fluid was collected. Additionally, differences in transforming growth factor-beta (TGF-ß) expression between the MP-infected and noninfected groups were examined. Experiments were performed using white blood cell counting methods and flow cytometry for 98 asthmatic children.Results: We tested 736 specimens, and the percentages of MP, RSV, and ADV infections were 50.27%, 11.68%, and 10.05%, respectively. The percentage of eosinophils was increased significantly in the AS-I-MP group, and their TGF-ß expression levels were increased, which was related to tissue fibrosis. Furthermore, MP infection exacerbated the decreasing trend of ITGB4 expression in patients' blood compared with the noninfected group.Conclusions: There might be a chain reaction from MP infection to an increase in ITGB4, a decrease in TGF-ß, a large accumulation of eosinophils and the development of asthma in children.

Surgical treatment of anomalous right upper lobe pulmonary vein obstruction caused by compression between pulmonary artery and trachea: a case report.

The normal anatomical course of right upper lobe pulmonary vein involves drainage anteriorly to the pulmonary artery, ultimately reaching the left atrium. However, anomalies can occur with the most common variation involving the convergence of the right upper lobe pulmonary vein with the superior vena cava. In a rare pulmonary vascular malformation, the anomalous right upper lobe pulmonary vein takes a path between the right pulmonary artery and right main bronchus [1]. During a clinical consultation, a patient presented in our hospital with this specific anomalous right upper lobe pulmonary vein, along with an atrial septal defect and a patent ductus arteriosus. As a consequence of this aberrant positioning, the right upper lobe pulmonary vein was compressed between the pulmonary artery and trachea, leading to pulmonary vein obstruction. Thus, a successful pulmonary vein replantation was performed to correct the congenital malformation.

Comprehensive microRNA profiling reveals potential augmentation of the IL1 pathway in rheumatic heart valve disease.

BACKGROUND: Valvular heart disease is a leading cause of cardiovascular mortality, especially in China. More than a half of valvular heart diseases are caused by acute rheumatic fever. microRNA is involved in many physiological and pathological processes. However, the miRNA profile of the rheumatic valvular heart disease is unknown. This research is to discuss microRNAs and their target gene pathways involved in rheumatic heart valve disease. METHODS: Serum miRNA from one healthy individual and four rheumatic heart disease patients were sequenced. Specific differentially expressed miRNAs were quantified by Q-PCR in 40 patients, with 20 low-to-moderate rheumatic mitral valve stenosis patients and 20 severe mitral valve stenosis patients. The target relationship between certain miRNA and predicted target genes were analysis by Luciferase reporter assay. The IL-1ß and IL1R1 expression levels were analyzed by immunohistochemistry and western blot in the mitral valve from surgery of mitral valve replacement. RESULTS: The results showed that 13 and 91 miRNAs were commonly upregulated or downregulated in all four patients. Nine miRNAs, 1 upregulated and 8 downregulated, that had a similar fold change in all 4 patients were selected for quantitative PCR verification. The results showed similar results from miRNA sequencing. Within these 9 tested miRNAs, hsa-miR-205-3p and hsa-miR-3909 showed a low degree of dispersion between the members of each group. Hsa miR-205-3p and hsa-miR-3909 were predicted to target the 3'UTR of IL-1ß and IL1R1 respectively. This was verified by luciferase reporter assays. Immunohistochemistry and Western blot results showed that the mitral valve from rheumatic valve heart disease showed higher levels of IL- 1ß and IL1R1 expression compared with congenital heart valve disease. This suggested a difference between rheumatic heart valve disease and other types of heart valve diseases, with more inflammatory responses in the former. CONCLUSION: In the present study, by next generation sequencing of miRNAs, it was revealed that interleukin 1ß and interleukin 1 receptor 1 was involved in rheumatic heart diseases. And this is useful for diagnosis and understanding of mechanism of rheumatic heart disease.

A Detailed Study to Discover the Trade between Left Atrial Blood Flow, Expression of Calcium-Activated Potassium Channels and Valvular Atrial Fibrillation.

Background: The present study aimed to explore the correlation between calcium-activated potassium channels, left atrial flow field mechanics, valvular atrial fibrillation (VAF), and thrombosis. The process of transforming mechanical signals into biological signals has been revealed, which offers new insights into the study of VAF. Methods: Computational fluid dynamics simulations use numeric analysis and algorithms to compute flow parameters, including turbulent shear stress (TSS) and wall pressure in the left atrium (LA). Real-time PCR and western blotting were used to detect the mRNA and protein expression of IKCa2.3/3.1, ATK1, and P300 in the left atrial tissue of 90 patients. Results: In the valvular disease group, the TSS and wall ressure in the LA increased, the wall pressure increased in turn in all disease groups, mainly near the mitral valve and the posterior portion of the LA, the increase in TSS was the most significant in each group near the mitral valve, and the middle and lower part of the back of the LA and the mRNA expression and protein expression levels of IKCa2.3/3.1, AKT1, and P300 increased (p < 0.05) (n = 15). The present study was preliminarily conducted to elucidate whether there might be a certain correlation between IKCa2.3 and LA hemodynamic changes. Conclusions: The TSS and wall pressure changes in the LA are correlated with the upregulation of mRNA and protein expression of IKCa2.3/3.1, AKT1, and P300.

Low concentration of rutin treatment might alleviate the cardiotoxicity effect of pirarubicin on cardiomyocytes via activation of PI3K/AKT/mTOR signaling pathway.

Cancer is the leading cause of deaths around the world, especially in low- and middle- income countries. Pirarubicin (THP) is an effective drug for treatment of cancer, however, there still exists cardiotoxic effects of THP. Rutin is a kind of antioxidative compound extracted from plants, and might be a protective compound for cardiomyocytes. Phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway is critical for cellular survival, proliferation and metabolism, and thus we speculated rutin might perform a protective role in cardiomyocytes via PI3K/AKT/mTOR signaling pathway. And in this experiment, we first established a cardiotoxicity model of THP in mice model and cell models, and then found that rutin treatment could increase the proliferation of cells at low concentration. Then we explored the possible mechanism of the protective effect of rutin using Western blotting, quantitative polymerase chain reaction (qPCR) and ELISA methods, and found that the activation of PI3K/AKT/mTOR/nuclear factor-κB (NF-κB) signaling pathway was increased, and expression of downstream molecules involved in antioxidative stress were also increased. We further noticed that concentration of angiogenesis promoting factors were also increased in medium of cultured cells. Thus, we speculated that rutin could increase the activation of PI3K/AKT/mTOR signaling pathway, further decrease the oxidative stress level via increasing the expression of antioxidative stress enzymes with the increasing concentration of angiogenesis promoting factors, resulting in the protective role in cardiomyocytes and cardiac function.