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Objective:To evaluate the cost-effectiveness of duloxetine, escitalopram oxalate and mirtazapine in the treatment of depression. Methods:Totally 120 cases of patients were randomly divided into three group. Group A was given duloxetine 40mg twice a day, group B was with escitalopram oxalate at the initial dose of 10mg per day, and up to 20mg per day in 2 weeks, and group C was treated with mirtazapine 30mg per day. The treatment course was eight weeks. At the 1st, 2nd, 3rd, 4th and 8th weekends after the treatment, Hamilton depression scale ( HAMD) was used to evaluate the total effective rate, and treatment emergent symptom scale ( TESS) was applied to assess the adverse drug reactions. Results:The total effective rate of group A, B and C was 87. 5%,90% and 92. 5% with the cost of 23 822. 22 yuan,33 866. 02 yuan and 19 586. 62 yuan, respectively. The cost-effectiveness ratio respectively was 27 225, 37 629 and 21 175. The incidence of adverse reactions respectively was 30%, 30% and 17. 5%. Conclusion:The cost-effectiveness of mirtazapine is the lowest in the treatment of depression, which can be considered as the best treatment regimen.
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Objective To investigate the effect of all-trans retinoic acid (at-RA) on fetal alveolar epithelial type Ⅱ cells (fAEC Ⅱ s) proliferation and the expression of pulmonary surfactant C (SPC) as well as aquaporin 5 (AQP5).Methods fAEC Ⅱ s were isolated and purified from fetal lung of pregnant SD rats (19 days).After being cultured for 1 day,and the fAEC Ⅱ s were interfered by at-RA for 1,2 and 3 days.Cell proliferation,viability as well as growth state,expressions of SPC mRNA as well as AQP5 mRNA and expressions of protein SPC as well as AQP5 were respectively detected by using 4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT),inverted microscope,real-time fluorescence quantitative PCR (RT-PCR) and Western blot.Results (1) When fAEC Ⅱ s were treated with at-RA for 1 day,and the cell proliferation and viability did not change (P ＞ 0.05),while the proliferation and viability were significantly improved in 2 days (P ＜ 0.05),and the difference was the most obvious (P ＜ 0.05) at 3 days.(2)Compared with the control group,the cell growth state was better,and the cell adherence was tighter and the refraction was higher in at-RA group.(3) Compared with the control group,at-RA up-regulated the expressions of AQP5 mRNA and AQP5 protein(t =-19.58,-10.44,-16.01,-46.25,-12.79,-27.96,all P ＜ 0.05),and the percentages of control group were 281.07％,766.67％,1 163.33％ and 792.65％,1 310.52％,1 561.56％ in 1,2 and 3 days respectively.(4) Compared with control group,the expressions of SP-C mRNA and SPC protein were up regulated when cells were exposed to at-RA for 1 and 3 d,but while they were down-regulated at 2 days(protein:the percentages of control group were 615.480％,369.450％ and 11.269％,respectively ; mRNA:728.33 ％,400.83 ％,66.57％,respectively)(t=-26.34,-25.26,13.80,-25.25,-31.71,9.12,all P＜0.05).Conclusions at-RA can promote the proliferation and differentiation of fAEC Ⅱs,enhance the fAEC Ⅱ s viability,and improve the expression of SPC and AQP5.
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Objective To study the effects of the Notch ligands Dlk1 and recombinant human nucleu factorκB (Jagged1) on the proliferation and transdifferentiation of the type Ⅱ alveolar epithelial cells when the Notch signaling pathway activated.Methods The primary type Ⅱ alveolar epithelial cells (AEC Ⅱ) cultured with recombinant protein Dlk1 and recombinant human nucleu factor-κB (rhNF-κB) (activator of Jagged1),respectively,and then cultured with DMEM (containing 120 mL/L FBS) as controls.Proliferation and differentiation conditions of the AEC Ⅱ were observed at 48 h,72 h,96 h time point by the light microscope and electron microscopes separately.Cell number was counted with hemacytometer; the proliferation rate was measured by methyl thiazolyl tetrazolium (MTT) ; Immunofluorescence double standard method was used to detect the AEC Ⅱ specific surfactant protein C (SP-C) and AEC Ⅰ specific protein aquaporin5 (AQPS) ;the expression of SP-C,AQPS,Dlk1,Jagged1,Notch1 and Hes1 mRNA were detected by real time-PCR.Results The cell population and proliferation:compared with control group,AEC Ⅱ proliferation was promoted in the Dlk1 group [cell numbers (× 109/L) 9.05 ± 0.45 vs 7.95 ± 0.65,11.68 ± 0.43 vs 8.68 ± 0.52,11.55 ± 0.17 vs 8.73 ± 0.48,all P ＜ 0.05 ; MTT results (value A) 0.699 ± 0.050 vs 0.462 ± 0.080,0.912 ± 0.080 vs 0.535 ±0.040,0.726 ±0.050 vs 0.540 ±0.020,all P ＜0.05] and decelerated AEC Ⅱ transdifferentiation into AEC Ⅰ ; while AEC Ⅱ proliferation was inhibited in rhNF-κB group [cell numbers (× 109/L) 4.95 ± 0.33 vs 7.95 ± 0.65,4.73 ±0.71 vs 8.68 ± 0.52,4.04 ± 0.11 vs 8.73 ± 0.48,all P ＜ 0.05; MTT results (value A) 0.398 ± 0.030 vs 0.462 ± 0.080,0.402 ± 0.070 vs 0.535 ± 0.040,0.380 ± 0.110 vs 0.540 ± 0.020,all P ＜ 0.05] and accelerated AEC Ⅱ transdifferentiation into AEC Ⅰ.One-Way ANOVA showed that the difference among the 3 groups had statistical significance (cell numbers:F =486.73,P =0.02; cell proliferation:F =37.16,P =0.02).The mRNA expression:compared with control group,the expression of SP-C mRNA of Dlk1 group was significantly higher (P ＜ 0.05) while the expression of AQP5 mRNA was remarkably lower and delayed (P ＜ 0.05),the expression of Jagged1 mRNA was weak or little,Dlk1 and Notch1 mRNA were up-regulated (P ＜ 0.05),and the Hes1 mRNA was reduced (P ＜ 0.05) ; the expression of SP-C mRNA of rhNF-κB group was significantly reduced (P ＜ 0.05),while the AQP5 mRNA expressed ahead of time and increased (P ＜ 0.05),Jagged1,Hes1 and Notch1 mRNA were higher (P ＜ 0.05),and the Dlk1 mRNA was weak.One-Way ANOVA showed that the difference in the expressions of SP-C,AQP5,D1k1,Jagged1,Hes1 and Notch1 mRNA among the 3 groups had staistical significance (F =96.80,P =0.01 ; F =82.55,P =0.01 ; F =269.80,P=0.00;F =312.34,P =0.00;F =169.17,P =0.01;F =19.85,P =0.02).Conclusions There are varied effects on proliferation and differentiation of the AEC Ⅱ when the Notch signaling is activated by different ligands:Dlk1 promoted proliferation and inhibited differentiation,while Jagged1 inhibited proliferation and promoted transdifferentiation.