ABSTRACT
OBJECTIVE: To explore the effect of atrial septal defect (ASD) and venoarterial extracorporeal membrane oxygenation (VA-ECMO) in the treatment of ARDS combined with left ventricular dysfunction (LVD) to find a new effective method for treating severe COVID-19 patients. MATERIALS AND METHODS: Five large animal ARDS models of sheep were established by intravenous injection of Lipopolysaccharide. ASD was made under general anesthesia and VA-ECMO was simulated by extracorporeal circulation machine. The oxygenation of peripheral blood, systemic circulation, and cardiac function were observed under conditions of closed and opened ASD, and the significance of ASD shunt in improving cardiopulmonary function was evaluated. RESULTS: With ASD closed, the atrial shunts disappeared, the peripheral artery pressure of oxygen(PaO2): 141.2±21.4mmHg, the oxygenation index (PaO2/FiO2): 353.0±53.5, the mean blood pressure (MAP): 49.3±13.5 mmHg, the heart was full; with ASD opened, the left-to-right shunt was observed, PaO2: 169.3±18.9mmHg, PaO2/FiO2: 423.3±47.3, MAP: 68.2±16.1 mmHg, the range of cardiac motion significantly increased, heart beat was powerful, and systemic circulation significantly improved. Statistical analysis showed that there were significant differences between opened and closed ASD (P < .01). CONCLUSION: ASD plus VA-ECMO is an effective method for the treatment of ARDS combined with LVD, which is the main cause of death in severe COVID-19 patients. However, further clinical validation is needed.
Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Extracorporeal Membrane Oxygenation , Heart Septal Defects, Atrial/complications , Pneumonia, Viral/complications , Respiratory Distress Syndrome/therapy , Ventricular Dysfunction, Left/complications , Animals , COVID-19 , Diagnosis, Differential , Disease Models, Animal , Pandemics , Respiratory Distress Syndrome/etiology , SARS-CoV-2 , SheepABSTRACT
Abnormal gene expression due to the dysregulation of microRNAs (miRNAs) often occurred in the initiation or progression of cancers. The aim of this present study was to investigate the function role of miR-125b-5p in breast cancer (BC). Expression levels of miR-125b-5p were determined by quantitative Real-time PCR. Biological functions of miR-125b-5p in the progression of BC were investigated with a series of in vitro experiments including cell counting kit-8 assay, colony formation assay, wound-healing assay and transwell invasion assay. The target of miR-125b-5p in BC was validated by luciferase activity reporter assay and western blot assay. We found miR-125b-5p expression was significantly reduced in BC cell lines compared to the normal breast epithelial cell line. Functional assays showed that cell proliferation, colony formation ability, cell migration, and cell invasion can be suppressed by miR-125b-5p overexpression. Besides, KIAA1522 was validated as a direct target of miR-125b-5p in BC. Collectively, our study showed that miR-125b-5p functions as a tumor suppressor and regulates BC progression through targeting KIAA1522.
