The triggering receptor expressed by myeloid cells-1 (TREM-1) plays an important role in infectious and autoimmune diseases but how it contributes to ventilation-induced lung injury (VILI) and inflammation is unclear. Here, we examine the possibility that TREM-1 activates signaling dependent on Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (Myd88) and nuclear factor (NF)-κB, which leads in turn to VILI. In a mouse model of VILI, which we validated based on lung edema and histopathology as well as cytokine levels, we examine mRNA and protein levels of TREM-1, TLR4, MyD88, NF-κB and its inhibitory protein I-κB in animals subjected to ventilation at normal or high tidal volume.
View Article and Find Full Text PDFBackground Dexmedetomidine (DEX), an α-adrenergic receptor agonist, produces ideal sedation and early postoperative recovery for premedication in paediatric surgery, reducing preoperative anxiety and facilitating smooth induction of anaesthesia. We performed a meta-analysis to compare the effects of DEX and midazolam (MDZ) in paediatric anaesthesia with sevoflurane. Methods PubMed, Ovid, Web of Science, and Public Health Management Corporation were searched through December 2016 for randomized controlled trials (RCTs) that compared DEX and MDZ in children undergoing sevoflurane anaesthesia.
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