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Objective To determine the median effective plasma concentration (Cp50) of remifentanil inhibiting cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Methods Twenty-two female patients scheduled for elective laparoscopic gynaecological surgery under general anesthesia, aged20-60 years, with a BMI 18-30 kg/m2, falling into ASA physical statusⅠ orⅡ, were enrolled in this study.Anesthesia was induced with propofol and remifentanil target-controlled infusion and iv injection of rocuronium 0.6 mg/kg.The target plasma concentration (Cp) of remifentanil and propofol were set at 5 ng/ml and 4μg/ml respectively.3 minutes after endotracheal intubation, the Cp of remifentanil was adjusted.The target Cp was set at 6 ng/ml in the first patient.CO2 pneumoperitoneum was performed after the target effect-site concentration and Cp were balanced.Each time Cp increased/decreased by 20%in the next patient depending on whether or not the cardiovascular response to CO2 pneumoperitoneum occurred.The positive cardiovascular response was defined as HR and/or MAP increasing by 20% within 3 minutes after CO2 pneumoperitoneum.The Cp50 and 95% confidence interval (CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery were calculated.Results The Cp50 (95% CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 (4.14-5.08) ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Conclusion The Cp50 of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.
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AIM: To investigate the mechanism of the AP-1 signal transduction pathway inhibited by JIP in nasopharyngeal carcinoma cells. METHODS: AP-1 activity was triggered by Dox-induced LMP1 expression in Tet-on-LMP1-HNE 2 cells (L7). The retention of phospho-JNK in the cytoplasm caused by JIP was examined with immunofluroscence assay. RESULTS: 24 h after transfection of L7 cells with the JIP expression plasmid, the translocation of activated JNK was inhibited, which resulted in the retention of phospho-JNK in the cytoplasm and down-regulation of the AP-1 activity. CONCLUSION: JIP down-regulates the activity of AP-1 through the inhibition of the translocation of JNK.