Comparison of transmucosal midazolam with inhalation sedation for dental extractions in children. A randomized, cross-over, clinical trial

Background:  The transmucosal route for conscious sedation in children has been reported widely in the field of medicine, but less so in dental patients. The aim of this study was to evaluate the efficacy and safety profile of midazolam (0.2 mg/kg) administered by the buccal transmucosal route, in comparison with nitrous oxide/oxygen inhalation sedation, for orthodontic extractions in 10–16-year-old dental patients. Methods:  Each patient attended for two visits and was randomly allocated to receive buccal midazolam (0.2 mg/kg) or nitrous oxide/oxygen titrated to 30%/70% at the first visit, the alternative being used at the second visit. The patients’ vital signs, sedation levels and behavioural scores were recorded throughout. Post-operatively, side-effects, recall of the visit and satisfaction levels were recorded via questionnaire. Results:  Thirty-six patients, with a mean age of 12.9 years, completed both arms of the trial. The maximum level of sedation was achieved with buccal midazolam in a mean time of 14.42 min, compared with 7.05 min with inhalation sedation. The vital signs with both types of sedation remained within acceptable limits and the reported side-effects were of no clinical significance. Buccal midazolam was found to be acceptable by 65.7%. Only 28.6% of cases preferred this technique, the main disadvantage being the taste of the solution. Conclusion:  Buccal midazolam sedation (0.2 mg/kg) seems to be equally as safe and effective as nitrous oxide/oxygen for the extraction of premolar teeth in anxious children. However, further research is required to refine the midazolam vehicle to improve acceptability

Involvement of CYR61 and CTGF in the Fascin-Mediated Proliferation and Invasiveness of Esophageal Squamous Cell Carcinomas Cells

Fascincarcinoma (ESCC) and involved in the proliferation and invasiveness of ESCC cells. In this study, we retrospectively examined the expression of fascin in ESCC samples by immunohistochemistry and revealed that overexpression of fascin was related to poor patient survival. RNAi-mediated knockdown of fascin in ESCC cells significantly inhibited cell proliferation and invasiveness, whereas forced expression of fascin in immortalized esophageal epithelial cells accelerated cell proliferation and invasiveness. To explore the underlying mechanism, cDNA microarray was performed to identify the differential gene expression profiles between a fascin-depleted cell line by RNAi and the corresponding control ESCC cells. Results showed that 296 genes were differentially expressed on fascin depletion. In this study, we focused on two down-regulated genes: CYR61 and CTGF. We found that restored expression of either CYR61 or CTGF led to a recovery of the suppression of cellular proliferation and invasiveness induced by down-regulation of fascin expression; the protein level of CYR61 and CTGF were up-regulated in ESCCs and their expression pattern correlated with fascin overexpression. Finally, analysis of signal transduction revealed that fascin affected the expressions of CYR61 and CTGF through transforming growth factor (TGF)-β pathway. Taken together, we propose that fascin regulates the proliferation and invasiveness of ESCC cells by modulating the expression of CTGF and CYR61 via TGF-β pathway