Abstract The purpose of the study is to further explore the combined effects of exercise and sulfur dioxide (SO2) exposure on the cardiovascular function as well as the underlying mechanisms. Rats were randomly divided into 4 groups: rest group (RG), exercise group (EG), SO2 pollution group (SG) and SO2 pollution + exercise group (SEG). Changes of aortic pressure and left ventricular pressure, Ang II concentration, ACE concentration and ACE activity in rats’ myocardial tissue were observed. Compared with RG, the systolic blood pressure, pulse pressure, LVSP, +dp/dtmax and -dp/dtmax of EG increased significantly, diastolic blood pressure, resting heart rate and ACE activity decreased significantly; For rats of SG, 4 weeks SO2 exposure increased LVEDP, Ang II concentration, ACE concentration and ACE activity, decreased the +dp/dtmax and -dp/dtmax; For rats of SEG, the systolic blood pressure, pulse pressure, LVSP, +dp/dtmax and -dp/dtmax decreased significantly, HR, LVEDP, Ang II concentration, ACE concentration and ACE activity increased significantly. Results indicate that, the combination of aerobic exercise and SO2 exposure can aggravate the negative effects of SO2 inhalation on cardiovascular function. Renin-angiotensin system plays an important role in mediating the negative effect of SO2 inhalation.

Abstract Severe community-acquired pneumonia (SCAP) is a common critical disease in the intensive care unit (ICU). This study aims to evaluate the clinical significance of miR-181b in SCAP, which has been revealed to be dysregulated in acute respiratory distress syndrome events due to SCAP. There were 50 SCAP patients and 26 healthy volunteers were recruited in this study. The expression of miR-181b was detected by RT-qPCR and the difference between SCAP and healthy controls was evaluated. The diagnosis and prognosis value of miR-181b was assessed by the receiver operating characteristics (ROC), Kaplan-Meier, and Cox regression analysis. miR-181b was significantly downregulated in SCAP compared with healthy controls. The downregulation of miR-181b showed a significant association with the white blood cell count, absolute neutrophils, and the C-reactive protein of patients. The downregulation of miR-181b could distinguish SCAP patients from healthy controls and predicate the poor prognosis of SCAP patients. Downregulated miR-181b serves as a diagnosis and prognosis biomarker for SCAP, which may be useful biological information for the early detection and risk estimation of SCAP.

Abstract Background Neuroblastoma (NB) represents the most common extracranial solid tumor in children. Accumulating evidence shows that microRNAs (miRs) play an important role in the carcinogenesis of NB. Here, we investigated the biological function of miR-1247 in NB in vitro. Methods/results We found miR-1247 was downregulated in NB tissues and cells using quantitative PCR analysis. Gain- and loss-of-function studies demonstrated that miR-1247 significantly suppressed cell proliferation and induced cell cycle G0/G1 phase arrest and cell apoptosis of NB cells in vitro by using MTT, colony formation assay and Flow cytometry analysis. Luciferase assay suggested ZNF346 was the target of miR-1247 and its expression could be down-regulated by miR-1247 overexpression using Western blotting. Furthermore, downregulation of ZNF346 by siRNA performed similar effects with overexpression of miR-1247 in NB cells. Conclusions Our findings suggested miR-1247 directly targeted to repress ZNF346 expression, thus suppressing the progression of NB, which might be a novel therapeutic target against NB.