The present study is to measure the expression of microRNA (miRNA or miR)-133b in circulating blood of children with viral myocarditis before and after drug treatment, and to investigate its relationship with the severity of myocardial lesions. A total of 36 children patients with viral myocarditis who received treatments at our hospital between June 2014 and June 2016 were enrolled in the present study, including 21 boys and 15 girls (age range, 9 months - 16 years).Quantitative real-time polymerase chain reaction was used to determine the expression of miR-133b in peripheral blood of patients and cardiomyocytes infected with CVB3. CCK-8 assay was used to test the proliferation of cardiomyocytes. ELISA was used to determine the levels of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) in peripheral blood and cardiomyocyte culture supernatants. Western blotting and ELISA were performed to measure the levels of tumor necrosis factor-α and interleukin-6 in cardiomyocytes infected by CVB3 and cell culture supernatants. Bioinformatics was used to predict the target gene of miR-133b. Silencing of Rab27B gene was achieved by transfection with its small-interfering RNA. Dual luciferase reporter assay was carried out to test whether miR-133b directly targets Rab27B. Reduced expression of miR-133b in peripheral blood was possibly correlated with myocardial injuries in viral myocarditis miR-133b. Expression of miR-133b was significantly reduced in cardiomyocytes infected with CVB3 virus. Overexpression of miR-133b inhibited cardiomyocyte injuries caused by CVB3 virus infection, and the enhanced production and release of cytokines TNF-α and IL-6 by cardiomyocytes infected with CVB3 virus. Rab27B promoted injuries of cardiomyocytes induced by CVB3 infection and facilitated the synthesis and release of cytokines TNF-α and IL-6 by cardiomyocytes. miR-133b was able to bind to the 3'-untranslated region seeding region of Rab27B mRNA. The present study demonstrates that expression of miR-133b in peripheral blood from children with viral myocarditis is reduced, and negatively correlated with myocardial injuries. miR-133b inhibits the proliferation of cardiomyocytes and the release of cytokines TNF-α and IL-6, and alleviates CVB3 infection-induced myocardial injuries by targeting Rab27B.

Background and objectives: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most clinically common type of sleep-related breathing disorders. In this study, the effect of OSAHS on ST segment elevation myocardial infarction (STEMI) was investigated. Methods: Seventy-fi ve patients with STEMI were included in this study. The patients were divided into two groups: STEMI accompanied by OSAHS (O + ) group (33 patients) and STEMI without OSAHS (O -) group (42 patients). The differences of the clinical characteristics between the two groups were compared. The relationship between oxyhemoglobin desaturation index (ODI) and Gensini Score, and the relationships between OSAHS and clinical parameters were analyzed by a regression analysis. Results: AMI mainly occurred from 10 pm to 6 am in the O + group (45.5 %) and from 6 am to 2 pm in the O -group (52.3 %). The peak of serous creatine kinase (CK), high-sensitivity C-reactive protein (hs-CRP), N-terminal Pro-brain natriuretic peptide (NT-proBNP), and left ventricle end-diastolic volume index (LVEDVI) were significantly increased in the O + group compared to the O -group, while the left ventricular ejection fraction (LVEF) were signifi cantly decreased. The regression analysis showed that ODI was positively correlated with Gensini Score, while serous CK, hs-CRP, NT-proBNP, and OSAHS were independently associated with left ventricular insuffi ciency (LVI), and the incidence of LVI in O + group was 5.8 times as O -group. Conclusions: In STEMI patients with OSAHS, myocardial infarction mainly occurred from 10 pm to 6 am, and the incidence of LVI was signifi cantly higher than STEMI patients without OSAHS (Tab. 5, Fig. 2 Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most common type of sleep-related breathing disorders, which was caused by throat obstruction (1, 2). The syndrome associates somnolence and one or two of the following symptoms: severe snoring, nocturnal respiratory arrest, repeated nocturnal awakening, non-recuperative sleep, diurnal fatigue, and altered concentration (3 4). OSAHS may act to cause and promote the progression of hypertension, coronary artery disease (CAD), acute myocardial infarction (AMI) and cerebral vascular disease (1, 5). It is reported that its incidences in adult women is 2 %, and in adult men is 4 % (6). While in China, its incidence is about 3.62 % in people beyond 30 years, which means that there are more than 47 million of patients in China by now (7).Numerous studies showed that OSAHS is closely associated with the development and progression of CAD. The changes of hemodynamics, enhancement of the sympathetic activity, and oxidative stress that are caused by OSAHS can accelerate the process of artherosclerosis (8, 9). Peker et al (10) reported that the incidence of OSAHS is higher in the patients with CAD than in normal people, and OSAHS can raise the mortality of angiocardiopathy, while patients treated by continuous positive airway pressure (CPAP) can reverse this state. The results of Peker et al (10) al...