Objective To evaluate the effects of dexmedetomidine-propofol-fentanyl combined anesthesia on somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in patients undergoing cervical spine surgery. Methods Thirty-six patients undergoing cervical spine surgery were randomly divided into 2 groups (n = 18 each): propofol-fentanyl combined anesthesia group (group C) and dexmedetomidine-propofol-fentanyl combined anesthesia group (group D). Anesthesia was induced with TCI of propofol and iv injection of fentanyl.After the consciousness disappeared, a laryngeal mask airway was placed and the patients were ventilated. In group D, dexmedetomidine 0.5 μg/kg was injected over 10 min after the consciousness disappeared, followed by an infusion at a rate of 0.5 μg·kg-1 ·h-1 until the end of surgery. In group C, the equal volume of normal saline was administered instead of dexmedetomidine. SEPs (P15-N20) amplitudes and latency were measured and recorded before dexmedetomidine administration and at 10 min of dexmedetomidine infusion. The no-elicitation of MEPs was recorded. Results Compared with group C, there was no significant difference in P15-N20 amplitudes and latency in group D. The no-elicitation rate of MEPs in two groups was 0. Conclusion Dexmedetomidine-propofol-fentanyl combined anesthesia does not affect SEPs and MEPs in patients undergoing cervical spine surgery.

Objective:To explore the effects of sevoflurane (Sev) on proliferation and invasion of breast cancer cells.Methods:Normal human breast epithelial cell line MCF10A and human breast cancer cell line MCF7 were purchased. The expression level of sirtuin 2 (SIRT2) , ATP citrate lyase (ACLY) in breast cancer cells and acetylation level of ACLY were measured. Breast cancer cells were divided into the following groups: Control group, 2% SEV group, 4% SEV group, si-NC group, si-SIRT2 group, 4% SEV+si-NC group, 4% SEV+si-SIRT2 group, SIRT2 group, SIRT2+ACLY-WT group, SIRT2+ACLY-3KQ group, SIRT2+ACLY-3KQ+4% SEV group, si-ACLY group, si-ACLY+ACLY-WT group, si-ACLY+ACLY-3KQ group. MTT and Transwell assay were used to detect cell proliferation and invasion.Results:Compared with MCF-10A cells (1.00±0.15) , SIRT2 was low expressed in Control group cells (0.43±0.03) ( q=11.98, P<0.001) , SEV could induce the expression of SIRT2 ( F=88.71, P<0.001) . In addition, ACLY and ACLY-3K acetylation level were up-regulated in breast cancer cells (all P<0.05) . Knockdown of SIRT2 or overexpression of ACLY and ACLY-3KQ could promote the proliferation and invasion of MCF7 cells (all P<0.05) , while SEV, overexpression of SIRT2 or knockdown of ACLY showed the opposite effects (all P<0.05) . Conclusion:Sev may inhibit the proliferation and invasion of breast cancer cells through SIRT2, which may be related to the regulation of ACLY deacetylation.

Objective:To investigate the effect of ketamine on dryness maintenance of breast cancer (BC) cells by regulating LncRNA PVT1/MYC axis.Methods:BC cell line MCF-7 was treated with different concentration of ketamine (0, 5, 10 or 20 g/ml) or treated with 20g/ml ketamine for different periods (0, 24, 48 or 72h) . Furthermore, the expression of METTL3, PVT1 and MYC in MCF-7 cells was interfered and MCF-7 cells were divided into different groups.Western blot was used to detect the expression levels of stem cell characteristic related molecules (OCT4 and SOX2) . The expression level of PVT1/MYC in each group was detected by qRT-PCR. MeRIP analysis was used to detect THE m6A methylation level of PVT1.Results:Ketamine treatment significantly reduced the number of BC globules and inhibited the protein expression of OCT4 and SOX2 in a dose-and time-dependent manner (all P<0.05) . Ketamine regulated m6A level of METTL3-mediated PVT1. Compared with ketamine+pcDNA3.1 group (207±11) , the number of globules formed in ketamine+PVT1 group (311±15) was significantly increased ( t=12.06, P<0.001) , and the protein expression levels of OCT4 and SOX2 were increased ( t=9.68, P<0.001; t=11.50, P<0.001) . MYC was a downstream regulatory gene of PVT1. Compared with ketamine+PVT1+ Si-NC group, ketamine+PVT1+si-MYC group significantly reduced the number of spheroid formation ( t=0.54, P=0.005) and the expression levels of OCT4 and SOX2 proteins ( t=5.98, P=0.004) ( t=7.33, P=0.002) . Conclusion:Ketamine mediates the expression of PVT1 and its downstream gene MYC by inhibiting THE m6A level of PVT1, thus inhibiting the stem cell-like characteristics of BC cells.

Objective:To evaluate the effect of different doses of compound sodium chloride injection combined with norepinephrine on prevention of hypotension after lumbar anesthesia in the patients undergoing caesarean section.Methods:A total of 150 patients with a singleton fetus, aged 18-45 yr, at ≥37 weeks of gestation, of American Society of Anesthesiologists Physical Status classification Ⅰ or Ⅱ, with height ≥150 cm, weighing ≤100 kg, with body mass index < 40 kg/m 2, scheduled for elective caesarean section under lumbar anesthesia, were divided into 3 groups ( n=50 each) by the random number table method: compound sodium chloride injection 4, 8 and 12 ml·kg -1·h -1 groups (group A, group B, group C). Compound sodium chloride injection 4 ml/kg was intravenously injected for liquid preload before lumbar anesthesia, and 0.5% hyperbaric bupivacaine 12.5 mg was injected to the subarachnoid space for lumbar anesthesia. Norepinephrine was intravenously injected at a dose of 6 μg immediately after intrathecal injection, followed by an infusion of 0.05 μg·kg -1·min -1, and infusion was stopped at 5 min after delivery. Compound sodium chloride injection was intravenously infused simultaneously at a rate of 4, 8 and 12 ml·kg -1·h -1 in A, B and C groups, respectively. The maximum diameter of inferior vena cava (IVCmax) and the minimum diameter of inferior vena cava (IVCmin) were measured by ultrasound, and inferior vena cava collapse index (IVC-CI) was calculated at 1 min before fluid preload (T 1), immediately after fluid preload (T 2), at 5 min after anesthesia (T 3), at 5 min after fetal delivery (T 4) and immediately before leaving the operating room (T 5). The incidence of intraoperative adverse events (hypotension, severe hypotension, bradycardia, hypertension, nausea, and vomiting) and neonatal outcomes (umbilical artery blood gas index and Apgar score at 1 and 5 min after birth) were recorded. Results:Compared with group A, IVCmin was significantly increased and IVC-CI was decreased at T 5 in group B, and IVCmin and IVCmax were significantly increased and IVC-CI was decreased at T 5 in group C ( P<0.05). There was no significant difference in IVCmax, IVCmin and IVC-CI at each time point between group B and group C ( P>0.05). There was no significant difference in the incidence of hypotension, severe hypotension, bradycardia, hypertension, nausea and vomiting among the three groups ( P>0.05). There was no significant difference in the results of blood gas analysis of the umbilical artery and Apgar score at each time point after birth among the three groups ( P>0.05). Conclusions:Compound sodium chloride injection 4, 8 and 12 ml·kg -1·h -1 combined with norepinephrine can effectively prevent the occurrence of hypotension after lumbar anesthesia in the patients undergoing caesarean section without increasing maternal and infant adverse events, and the effect of 8 and 12 ml·kg -1·h -1 for volume supplementation is better than that of 4 ml·kg -1·h -1.