ObjectiveTo investigate the effect of dexmedetomidine in the prevention of etomidate-induced myoclonus.MethodsWe searched for randomized controlled trials (RCTs) regarding the use of dexmedetomidine in preventing etomidate-induced myoclonus in the databases PubMed, EMBASE, the Cochrane Library, and CNKI. We extracted data and assessed the quality of the literature and adopted RevMan 5.2 to conduct meta-analysis on each effective index and employed funnel plot to test publication bias.ResultsThe results showed that the incidence of etomidate-induced myoclonus in the dexmedetomidine treated groups was significantly lower than that of the control groups (risk ratio [RR]=0.27, 95% confidence interval [CI] [0.15, 0.47], P<0.00001). With regard to the severity of etomidate-induced myoclonus, incidences of etomidate-induced myoclonus in the dexmedetomidine treated groups resulting in mild myoclonus (RR=0.37, 95% CI [0.19, 0.75], P=0.006), moderate myoclonus (RR=0.21, 95% CI [0.12, 0.37], P<0.00001), or severe myoclonus (RR=0.18, 95% CI [0.08, 0.38], P<0.00001) were significantly lower than those of the control groups. No statistically significant difference was found (RR=0.70, 95% CI [0.47, 1.04], P=0.08) between etomidate-induced myoclonus in the dexmedetomidine treated groups and that of the midazolam treated groups.ConclusionDexmedetomidine can effectively prevent the incidence of etomidate-induced myoclonus and reduce the severity of etomidate-induced myoclonus. In addition, there were no significant differences between the effects of dexmedetomidine and midazolam in preventing etomidate-induced myoclonus.

Background: Research on the clinical outcomes of surgical patients anaesthetized with sevoflurane and the association of sevoflurane with post-operative cognitive dysfunction (POCD) is scarce. We evaluated whether sevofluranebased anesthesia increased the incidence of POCD and worsened prognosis compared to propofol-based anesthesia in elderly cancer patients. Material/Methods: This single-center, prospective, double-blind randomized controlled trial included 234 patients aged 65 to 86 years undergoing tumor resection who received sevoflurane-based (Group S) or propofol-based (Group P) anesthesia during surgery. A series of neuropsychological tests was performed to evaluate cognitive function before surgery and at 7 days and 3 months post-operation, and the results were compared to those of healthy controls. Results: At 7 days post-operation there were no significant differences in the incidence of POCD between patients who received sevoflurane-based or propofol-based anesthesia during surgery: Group S was at 29.1% (32 out of 110 patients) versus Group P at 27.3% (30 out of 110), P=0.764. At 3 months, Group S was at 11.3% (12 out of 106 patients) versus Group P at 9.2% (10 out of 109), P=0.604. During the first 2 days post-operation, the QoR-40 global score was significantly lower in Group S compared to Group P [POD 1: P=0.004; POD 2: P=0.001]. There were no significant differences in in-hospital post-operative complications, post-operative length of hospital stay, all-cause mortality at 30 days, and 3 months post-operation, or post-operative quality of life at 3 months between patients in Group S and Group P. Conclusions: Sevoflurane-based anesthesia did not increase the incidence of POCD compared to propofol-based anesthesia at 7 days or 3 months post-operation or impact short-term post-operative prognosis.

How Wnt signalling including canonical and non-canonical pathways are initiated at the cell surface is not completely understood. Here we report that Wnt receptor Frizzled (Frz) and the co-receptors LRP5 and LRP6 (LRP5/6) directly interact with each other and this interaction is regulated by the LRP6 ectodomain. Importantly, through direct binding to Frz, LRP5/6 are able to prevent Frz-regulated non-canonical pathway activation and further non-canonical pathway-mediated tumour metastasis. Knockdown of endogenous LRP5/6 promotes otherwise-nonaggressive tumour cells to migrate in vitro, whereas a soluble recombinant protein of LRP6 ectodomain suppresses migration and metastasis of otherwise-aggressive tumour cells in vitro and in vivo. Furthermore, the expression level of membrane LRP5/6 correlates inversely with metastasis in mouse and human breast cancer. Our study suggests a previously unrecognized mode of receptor interaction, revealing the mechanism of LRP5/6 in inhibition of non-canonical pathway, and a possible clinical use of the LRP6 ectodomain to impede metastasis.

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