There was no significant advantage of the sTAP block over local infiltration or no intervention for postoperative pain control in pediatric patients undergoing non-laparoscopic major abdominal surgeries.

Background: Delayed extubation after cardiac surgery is associated with high morbidity and mortality, increased intensive care unit length of stay, and healthcare cost. Acute type A aortic dissection (ATAAD) generally results in prolonged mechanical ventilation due to the complexity of surgical management and some postoperative complications. This study aimed to elucidate the perioperative risk factors for delayed extubation in patients undergoing ATAAD surgery. Methods: A retrospective cohort study including 239 patients who were diagnosed with ATAAD and underwent emergency surgery from October 2004 to January 2018 was performed. The potential perioperative risk factors for delayed extubation were collected. This study defined delayed extubation as the time to commence extubation being greater than 48 hours. The clinical data were analyzed with univariate and multivariate analyses to identify risk factors for delayed extubation following ATAAD surgery. Results: The incidence of delayed extubation was 48.5% (n=116). Multiple logistic regression analysis showed perioperative risk factors for delayed extubation included preoperative cardiac tamponade [odds ratio (OR) 3.94, 95% confidence interval (CI) 1. 39-11.17, P=0.010], central arterial cannulation (ascending aorta and proximal aortic arch) for cardiopulmonary bypass (CPB) (OR 4.

Biofilm-based infection is a major healthcare burden. Methicillin-resistant Staphylococcus aureus (MRSA) is one of major organisms responsible for biofilm infection. Although biofilm is induced by a number of environmental signals, the molecule responsible for environmental sensing is not well delineated. Here we examined the role of ion transporters in biofilm formation and found that the sodium-glutamate transporter gltS played an important role in biofilm formation in MRSA. This was shown by gltS transposon mutant as well as its complementation. The lack of exogenous glutamate also enhanced biofilm formation in JE2 strain. The deficiency of exogenous glutamate intake accelerated endogenous glutamate/glutamine production, which led to the activation of the urea cycle. We also showed that urea cycle activation was critical for biofilm formation. In conclusion, we showed that gltS was a critical regulator of biofilm formation by controlling the intake of exogenous glutamate. An intervention to target glutamate intake may be a potential useful approach against biofilm.

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