Emergency medical services最新文献

Background: Distal radial artery cannulation at the "anatomical snuffbox" carries several theoretical advantages over conventional radial arterial cannulation at the wrist. However, these two techniques have not been evaluated in perioperative settings.

Methods: In this randomized controlled trial, n = 200 patients requiring arterial cannulation for perioperative monitoring were recruited. Patients were randomized to either ultrasound guided distal radial artery cannulation group (group D) or ultrasound guided conventional radial artery cannulation group (group W). Primary outcome of this study was first attempt cannulation success rate.

Results: First attempt cannulation success rate was significantly lower in distal radial artery cannulation (57% in group D and 77% in group W; p = 0.003). Use of alternative cannulation site was significantly higher in group D when compared to group W (p = 0.015) and number of attempts for successful cannulation was significantly higher in group D when compared to group W (p = 0.015). None of the patients in any group developed thrombosis and related complications and intraoperative catheter dislodgement. Time to puncture the artery (p < 0.0001), total cannulation time (p < 0.0001), and actual catheter insertion time (p < 0.0001) were significantly higher in group D in comparison to group W.

Conclusion: Distal radial artery cannulation was associated with lower first attempt cannulation success rate and requires longer time to perform. As distal radial artery is a new technique, further studies are required in different clinical settings.

Background: The contribution of autophagy to cancer therapy resistance remains complex, mainly owing to the discrepancy of autophagy mechanisms in different therapy. However, the potential mechanisms of autophagy-mediated resistance to icotinib have yet to be elucidated.

Methods: The effect of autophagy in icotinib resistance was examined using a series of in vitro and in vivo assays. The results above were further verified in biopsy specimens of lung cancer patients before and after icotinib or gefitinib treatment.

Results: Icotinib increased ATG3, ATG5, and ATG7 expression, but without affecting Beclin-1, VPS34 and ATBG14 levels in icotinib-resistant lung cancer cells. Autophagy blockade by 3-MA or silencing Beclin-1 had no effects on resistance to icotinib. CQ effectively restored lung cancer cell sensitivity to icotinib in vitro and in vivo. Notably, aberrantly activated STAT3 and highly expressed FOXM1 were required for autophagy induced by icotinib, without the involvement of AMPK/mTOR pathway in this process. Alterations of STAT3 activity using genetic and/or pharmacological methods effectively affected FOXM1 and ATG7 levels increased by icotinib, with altering autophagy and icotinib-mediated apoptosis in resistant cells. Furthermore, silencing FOXM1 impaired up-regulated ATG7 induced by STAT3-CA and icotinib. STAT3/FOXM1 signalling blockade also reversed resistance to icotinib in vivo. Finally, we found a negative correlation between STAT3/FOXM1/ATG7 signalling activity and epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) treatment efficacy in patients undergoing EGFR-TKIs treatment.

Conclusions: Our findings support that STAT3/FOXM1/ATG7 signalling-induced autophagy is a novel mechanism of resistance to icotinib, and provide insights into potential clinical values of ATG7-dependent autophagy in icotinib treatment.