ABSTRACT
BACKGROUND: Prone position ventilation is a widely used lung protection ventilation strategy. The strategy is more convenient to implement in children compared to adults. Due to the precise mechanism of improving oxygenation function, development of pediatric prone ventilation technology has been largely focused on children with acute respiratory distress syndrome. There is a paucity of high-quality studies investigating the effects of prone position ventilation after pediatric cardiac surgery. The purpose of this study is to evaluate the feasibility and effectiveness of prone position ventilation in infants who develop postoperative acute lung injury after surgery for congenital heart disease. METHODS: A single-center, randomized controlled trial of pediatric patients with acute lung injury after surgery for congenital heart disease who will receive prone position ventilation or usual care (control group). A total of 68 children will be enrolled according to the inclusion criteria. The main outcome measures will be lung compliance and oxygenation index. The secondary outcomes will be duration of mechanical ventilation, length of stay in cardiac intensive care unit, reintubation rate, and complication rate. DISCUSSION: This study will investigate the feasibility and effectiveness of prone position ventilation techniques in children who develop postoperative acute lung injury after surgery for congenital heart disease. The results may help inform strategies to improve airway management after surgery for congenital heart disease. TRIAL REGISTRATION: ClinicalTrials.gov NCT04607993 . Initially registered on 29 October 2020.
Subject(s)
Acute Lung Injury , Heart Defects, Congenital , Acute Lung Injury/diagnosis , Acute Lung Injury/etiology , Acute Lung Injury/therapy , Child , Feasibility Studies , Heart Defects, Congenital/surgery , Humans , Infant , Lung/surgery , Prone Position , Prospective Studies , Randomized Controlled Trials as Topic , Respiration, Artificial/adverse effectsABSTRACT
Bladder cancer (BC) is the ninth most common malignancy throughout the world. The molecular mechanisms of this disease remain largely unclear. The glycolytic enzyme enolase 1 (ENO1) has been shown to regulate the development of various cancers. However, the significance of ENO1 in BC is underdetermined. In this study, we found that ENO1 was highly expressed in BC tissues and cells. High expression of ENO1 was associated with the poor survival of BC patients. Using lentivirus-mediated knockdown and over-expression, we revealed that ENO1 was critical for the growth and proliferation of BC cells. ENO1 over-expression also promoted the proliferation of SV-HUC-1 cells. At the molecular level, the cell cycle and apoptosis related genes were regulated by ENO1. ß-catenin expression was positively regulated by ENO1. Furthermore, ectopic expression of ß-catenin reversed the effect of ENO1 knockdown on T24 cell proliferation and growth. Opposite results were observed in ß-catenin knockdown T24 cells. Our findings suggested that ENO1 functioned as an oncogene in BC through regulating cell cycle, apoptosis and ß-catenin. Targeting ENO1/ß-catenin cascade may benefit for BC patients.
