Objective To investigate the effect of different doses of sufentanil combined with dexmedetomidine ( DEX) on hemodynamic and Narcotrend index ( NI) during pediatric anesthesia induction. Methods A total of 45 children with lower abdominal surgery were randomly divided into three groups evenly: sufentanil 0. 1 μg·kg-1+ DEX (S1 group),sufentanil 0. 2 μg·kg-1+DEX (S2 group),and sufentanil 0. 3μg·kg-1+DEX (S3 group). Patients in each group began with intubation at the peak point of administration. Blood pressure,heart rate,perfusion index (PI) and NI were detected at the baseline (t0), delivering DEX 0.5 μg·kg-1·h-1 and sufentanil intravenously for 5 min (t1),delivering sufentanil for 3 min (t2),time of intubation ( t3 ) ,1 min ( t4 ) ,and 5 min ( t5 ) after intubation. The application rate of atropine and propofol was recorded. Patient recovery time and adverse reactions were observed. Results Compared with basicline value at t0 time point, hemodynamic parameters and NI were decreased at t1 and t2 ,while PI was increased in both groups. At t3 ,t4 ,and t5 ,all of the indicators in S1 group were significantly different from those at t0 ,and also significantly different from those in S2 and S3 group. Six patients were treated with propofol in S1 group and four presented with agitation after operation,more than S2 and S3 groups. Three patients were treatment with atropine in S3 group. Conclusion Sufentanil (0. 2 μg·kg-1 ) combined with dexmedetomidine can be used to induce intubation for pediatric anesthesia with stable hemodynamic profile and low incidence of adverse effects.

Objective: To investigate the effects of down-regulation of PTTG1 expression on the proliferation, invasiveness and apoptosis of androgen-independent human prostate cancer LNCaP-AI cells and their sensitivity to androgen antagonists. METHODS: Human prostate cancer LNCaP-AI cells were transfected with siRNA targeting the PTTG1 gene using the Lipofectamine 2000 transfection reagent. The proliferation, invasiveness and apoptosis of the cells were detected by MTT, Transwell assay and flow cytometry, respectively. The protein expressions of PTTG1, p-Akt, and p-ERK were determined by Western blot and the mRNA expression of PTTG1 measured by agarose gel electrophoresis. RESULTS: The siRNA expression vector markedly down-regulated the expression of PTTG1, which effectively suppressed the proliferation of the LNCaP-AI cells, with the inhibition rates of (19.47 ± 2.12), (24.01 ± 2.13) and (48.02 ± 2.22)% at 24, 48 and 72 hours, respectively, after transfection, with statistically significant differences among the three groups (P <0.05). The number of the cells passing through the polycarbonate film was remarkably decreased at 24, 48 and 72 hours (74.67 ± 9.85, 56.44 ± 8.66 and 37.33 ± 6.14) as compared with the baseline (111.11 ± 13.47) (P <0.01), while the apoptosis rate of the cells was significantly increased at 24, 48 and 72 hours (18.32 ± 0.94), (19.94 ± 1.30) and (21.73 ± 1.88)% in comparison with the baseline (［2.17 ± 0.49］%)， (P <0.05). PTTG1 siRNA combined with androgen antagonist flumatide exhibited even more significant effects in inhibiting the proliferation and promoting the apoptosis of the LNCaP-AI cells than either used alone, and in a flumatide dose-dependent manner. The inhibition and apoptosis rates of the LNCaP-AI cells treated with 50 nmol/L flumatide were (27.13 ± 3.52) and (3.94 ± 0.48)%, and those treated with siRNA + 50 nmol/L flumatide were (67.51 ± 5.13) and (19.93 ± 1.72)%, respectively, both with statistically significant differences between the two groups (P <0.05). The inhibition and apoptosis rates of the cells treated with 100 nmol/L flumatide were (43.72 ± 3.90) and (5.33 ± 0.66)%, and those treated with siRNA + 100 nmol/L flumatide were (73.19 ± 4.78) and (23.43 ± 1.76)%, respectively, both with statistically significant differences between the two groups (P <0.05). CONCLUSIONS The siRNA expression vector can down-regulate the expression of PTTG1, which can inhibit the proliferation and invasiveness of LNCaP-AI cells, promote their apoptosis, and increase their sensibility to androgen antagonists. Suppressing the expression of PTTG1 may enhance the effect of androgen-deprivation therapy on advanced prostate cancer.
Androgen Antagonists ; pharmacology ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Humans ; Male ; Neoplasm Invasiveness ; Prostatic Neoplasms ; drug therapy ; metabolism ; pathology ; RNA, Small Interfering ; metabolism ; Securin ; genetics ; metabolism ; Time Factors ; Transfection

ObjectiveTo explore the expression of pituitary tumor transforming gene 1 (PTTG1) during the transformation of prostate cancer from androgen-dependent (ADPC) to androgen-independent (AIPC).

METHODSWe established an AIPC cell model LNCaP-AI by culturing the androgen-dependent LNCaP cell line in the hormone-deprived medium for over 3 months. The cell model was verified and the PTTG1 expression in the LNCaP cells was detected by Western blot and RT-PCR during hormone deprivation.

RESULTSThe AIPC cell model LNCaP-AI was successfully established. The PTTG1 expression was gradually increased in the LNCaP cells with the prolonged time of hormone deprivation and the expressions of matrix metalloproteinases MMP-2 and -9 were elevated at the same time.

CONCLUSIONSThe expression of PTTG1 is increased gradually in AIPC, which may be a target of gene therapy for advanced prostate cancer.

Blotting, Western ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Neoplasms, Hormone-Dependent ; Prostatic Neoplasms ; enzymology ; genetics ; Securin ; genetics