Objective: To investigate the antidepressant mechanism of supercritical CO2 extract from Compound Chaigui Precription from the perspective of cAMP signaling pathway. Methods: The rats model were established by chronic unpredictable mild stress (CUMS). The rats were administrated with high, medium and low doses of supercritical CO2 extract from Compound Chaigui Precription and venlafaxine as intervention drugs. The protein expression levels of cAMP, PKA, p-CREB and BDNF in tissues and their corresponding mRNA levels were explored for their antidepressant mechanism. Results: Compared with the blank group, the expression levels of cAMP, PKA, p-CREB and BDNF in the hippocampus of the model group were significantly decreased (P < 0.05, P < 0.01). After the intervention of the Compound Chaigui Precription, compared with the model group, there was a significant difference in the callus of each dose group. At the same time, the mRNA levels of TrkB, PKA, p-CREB and BDNF in the hippocampus of the model group were significantly decreased (P < 0.05, P < 0.01). After the intervention, there was a callback in each dose group compared with the model group, with significant differences. Conclusion: Supercritical CO2 extract from Compound Chaigui Precription can exert antidepressant effect by regulating cAMP-PKA-CREB-BDNF signaling pathway.

Objective To observe the expressions of efflux pump gene cluster adeAB in acinetobacter baumannii isolated from the burn patients and the expression changes of its upstream regulatory genes adeR and adeS and determine the influence of those genes on drug resistance of acinetobacter baumannii.Methods Nine drug-resistant strains and nine sensitive strains of acinetobacter baumannii isolated from the burn patients treated between June 2012 and March 2013 were used.After strain identification using 16SrDNA sequencing,acinetobacter baumannii standard strain ATCC19606 was employed as the control.mRNA expressions of efllux pump genes adeA and adeB and their upstream regulatory genes adeR and adeS were detected by real-time quantitative PCR.Results (1) adeA and adeB genes presented higher expressions in drug-resistant strains (3.71 ±0.95,76.16 ± 8.75) than in sensitive strains (0.92 ± 0.94,0.72 ± 0.78) (F =38.71,663.65 respectively,both P ＜ 0.05).(2) adeS and adeR genes showed higher expressions in drug resistant strains (18.02 ± 6.71,3.02 ± 2.69) than in sensitive strains (1.64±1.51,0.76±0.61) (F =51.04,5.57 respectively,bothP＜0.05).Conclusions The over-expression of efflux pump gene cluster adeAB induced by the expression alteration of its upstream regulatory genes adeR and adeS is closely associated with the drug resistance of acinetobacter baumannii in the burn patient.Besides,the regulatory genes may depend on adeS to sense the nosocomial environment condition,activate or inactivate adeR and hence regulate efflux pump expression.

Objective To investigate the influence of abaI expression on acinetobacter baumannii biofilm formation.Methods Acinetobacter baumannii strain S isolated from bums patients was collected for the study,while the standard strain ATCC19606 was served as the control.At 6,24 and 48 hours,the gene expressions of abaI,pgaA,pgaB and pgaC were detected by real-time fluorescent quantitative PT-PCR,secretion of N-acyl-homoserine lactones (AHLs) by biological sensor and biofilm formation by MTT method.Results (1) Gene expressions of abaI,pgaA,pgaB and pgaC at 6 hours were 8.63 ±5.93,1.98 ± 1.93,1.01 ± 1.32 and 2.67 ± 3.46 respectively,which showed a quick increase at 24 hours (22.81 ± 17.60,5.13 ± 4.32,5.66 ± 3.97,11.97 ± 7.75 respectively),followed by a rapid decline in 48 hours (3.43 ± 0.88,1.30 ± 0.24,3.01 ± 3.00,3.02 ± 3.29 respectively).Gene expressions of pgaB and pgaC at 6 hours and that of pgaA and pgaC at 48 hours revealed statistically significant differences from those at 24 hours (P ＜ 0.05).(2) AHLs showed a level of 18.49 ± 11.03 at 6 hours,reached a peak of 52.23 ± 15.95 at 24 hours,then descended to 5.53 ± 0.94 at 48 hours.AHLs level at 24 hours showed statistically significant difference from that at 6 hours and 48 hours (P ＜ 0.05).(3)Biofilm formation at 24 hours and 48 hours was 2.83 ±0.44 and 2.71 ±0.15 respectively,far higher than that at 6 hours (0.49 ± 0.11,P ＜ 0.05).(4) In the correlation analysis among AHLs,biofilm formation and gene abaI,pgaA,pgaB and pgaC expressions,significant positive correlation was found between abaI and pgaA and between AHLs and pgaC expression (P ＜ 0.05).Conclusion Acinetobacter baumannii may regulate gene expressions of pgaA and pgaC responsible for biofilm formation to adjust to the external environment by means of changing abaI gene expression and AHLs secretion.

Objective To investigate the effects of 20% lipid emulsion on plasma ropivacaine concentration and myocardial ropivacaine content in rats. Methods Sixty male pathogen-free SD rats weighing 220-270 g were randomly divided into 2 groups (n = 30 each): group A normal saline and group B lipid emulsion.The animals were anesthetized with intraperitoneal 4% pentobarbital 40 mg/kg. The femoral vein was cannulated for drug and fluid administration. ECG (lead Ⅱ) was continuously monitored. 1% ropivacainc 5 mg/kg was injected iv. A bolus of 20% lipid emulsion 5 ml/kg was then injected iv in group B, while in group A equal volume of normal saline was administered instead of 20% lipid emulsion. The animals were sacrificed at 5, 10,20, 40, 60 and 120 min after ropivacaine infusion (5 animals at each time point). Blood samples and myocardial specimens were taken for determination of plasma and myocardial ropivacaine levels by HPLC. Results Plasma ropivacaine concentration at 20 min after ropivacaine administration was significantly higher in group B than in group A. The myocardial ropivacaine concents at 5, 10 min after ropivacaine administration were significantly lower in group B than in group A. Conclusion 20% lipid emulsion infusion can bind ropivacaine and decreasee myocardial ropivacaine content thus reducing the cardiac toxicity of ropivacaine.

Child, Preschool ; Diarrhea, Infantile ; therapy ; Female ; Humans ; Infant ; Moxibustion

Coal Mining ; Humans ; Occupational Diseases ; prevention & control ; Occupational Health ; Tuberculosis ; prevention & control

In recent years,antibiotics have been playing more and more important roles in maintaining human health with the increasing variety and quantity.However,under the influence of different reasons caused by subjective or objective factors,antibiotics irrational use has induced bacterial resistance and adverse reactions,which are becoming more and more serious.The paper put forward the countermeasures of antibiotics irrational use and provided reference for rational use of antibiotics based on the present situation analysis in China and foreign experience in order to control the irrational use.

Objective To investigate the synergistic effects of 9-cis-retinoic acid(9-cis-RA) and 8-cl-cAMP on growth inhibition and apoptosis induction in H460 and H292 cell lines of non-small-cell lung cancer(NSCLC). Methods Experimental groups included 9-cis-RA groups(1,5,10 and 20 ?mol/L),8-cl-cAMP groups(5,10,20 and 50 ?mol/L),9-cis-RA(5 and 10 ?mol/L) combined with 8-cl-cAMP(10 ?mol/L) groups and blank control group.The cell growth inhibition rates were detected by trypan blue staining,and the apoptosis of H460 and H292 cells were observed by Hoechst33258 fluorescence microscope,DNA gel electrophoresis and flow cytometer(FCM). Results 9-cis-RA inhibited the growth of H460 cells in a time-and dose-dependent manner,and induced the apoptosis of H460 cells(P

Objective To investigate the value of soluble epithelial cadherin(sE-cad)in the differential diagnosis of pleural effusion. Methods Patients were divided into malignant pleural effusion group,infective pleural effusion group and transudation group.sE-cad in pleural fluids obtained during the first thoracocentesis was measured by enzyme-linked immunosorbent assay(ELISA).The concentration of sE-cad in all kinds of pleural effusions was compared.The cut-off value of sE-cad for the differential diagnosis of benign and malignant pleural effusion was determined by ROC curve.The diagnostic value of sE-cad was also compared with common tumor markers such as CEA,CA199,CA125 and NSE.Results The concentration of sE-cad was significant higher in the malignant pleural effusion than in the benign pleural effusion[(38.38?4.15)ng/mL vs(14.17?0.80)ng/mL,P

Objective To investigate the changes of interleukin(IL)-2 and interferon(IFN)-γin serum and synovial fluid of patients with joint injure with Kashin-Beck disease(KBD), and study the roles of IL-2 and IFN-γ in KBD joint injure. Methods In accordance with the "Diagnostic Criteria of Kashin-Beck disease"(GB16003-1995),48 cases of KBD patients and 26 healthy people(control group) from KBD endemic area in Long county Shaanxi province were enrolled in the study. KBD patient were 24 males and 24 females, respectively, aged 40 to 65 years (mean age 51 years). Forty-eight serum specimens and 28 synovial fluid specimens of patients(14 males and 14 females,respectively) were collected. Healthy control group were 13 males and 13 females, respectively. Twenty-six serum specimens of healthy controls were collected. Serum and synovial fluid IL-2 and IFN-γ levels were determined by enzyme-linked immunosorbent assay(ELISA). Results In healthy controls and KBD patients, the midian of serum IL-2 were 46.8 ng/L and 55.7 ng/L, respectively, and IFN-γ were 52.3 ng/L and 48.8 ng/L, respectively. The difference was not statistically significant between healthy controls and KBD patients(t = 0.62, 0.70, all P ＞ 0.05).In synovial fluid of KBD patient, the midian of IL-2 and IFN-γwere 48.3 ng/L and 44.1 ng/L, respectively. The difference was not statistically significant between serum and synovial fluid in KBD patients(t = 0.69, 1.72, all P ＞0.05). Conclusion Serum and synovial fluid IL-2 and IFN-γare not significantly increased in KBD patients with articular damage, indicating that IL-2 and IFN-γare not involved in KBD joint injury.