Objective:To establish a method for the determination of zolpidemtartrate in human plasma by SPE-HPLC. Methods:The samples were extracted by solid phase with a Hypersil BDS C18 column and determined by an internal standard method. The mobile phase was methanol:acetonitrile:water (45 ∶45 ∶110), the flow rate was 1. 0 ml·min-1, the column temperature was 35℃, and the detection wavelength was 254nm. Results:The linear relationship of zolpidemtartrate was within the range of 0. 511 5-4. 092 0 μg· ml-1 . The relative recovery was greater than 90%. The intra-and inter-day RSDs were all less than 10%. Conclusion:The method is quite simple, quick and accurate with little interference, which is suitable for the clinical determination of zolpidemtartrate.

Objective: To establish an HPLC method for the simultaneous determination of chloromycetin and metronidazole in chlortalidone and metronidazole spirits. Method:The HPLC method was performed on an NOV-pak C18 (150 mm × 4. 6 mm, 5 μm) column and the mobile phase consisted of methanol and water (75∶25). The flow rate was 1. 0 ml·ml-1, the detection wavelength was 297nm, the temperature of column was 30℃ and the sample size was 20 μl. Result: The calibration curve of metronidazole was linear within the range of 5-80μg·ml-1(r=0. 999 7), and the average recovery was 100. 83% with RSD of 1. 82%(n=6). The cal-ibration curve of chlortalidone was linear within the range of 50-800μg·ml-1(r=0.999 7), and the average recovery was 100.2%with RSD of 0. 55%(n=6). Conclusion: The method is simple, rapid, accurate and reproducible, and can be used in the quality control of chlortalidone and metronidazole spirits.

Objective To study the effect of uremic serum on the calcification and osteogenic transition of cultured human umhilical artery smooth muscle cells(HUASMC).Methods Sera from 40 healthy controls(control group),40 nondialysis uremic patients(nondialysis group)and 45 uremic patients on dialysis(dialysis group)were detected fi)r biochemical indexes concerned and used to treat the cultured HUASMC.Alizarin red S stain was applied to examined calcium deposition in the cell layer.Calcium concentration was determined calorimetrically by the Ocresolphtha]ein complexone method,and corrected by total cell proteins.The mRNA expression of bone specific alkaline phosphatase(BAP),osteopontin(OPN)and bone morphogenelic protein 2(BMP2)was estimated by realtime PCR.OPN and BMP2 protein expression was assessed by Western blotting and fluorometry method was used to check the BAP concentration. Results Serum biochemical detection revealed thai both uremic groups had higher levels of phosphate,triglyseride,iPTH,C-reactive protein(CRP)and IL-6,and lower level of fetuin-A than healthy control(P＜0.05).Furthermore,dialysis serum had higher levels of triglyseride,CRP and IL-6 than nondialysis serum(P＜0.05).Compared with control group,both uremic scra induced more cell layer calcium deposition and higher mRNA and protein expression levels of BMP2,BAP and OPN(P＜0.05).Higher mRNA and protein expression levels of above factors were found in dialysis group as compared to nondialysis group(P＜0.05). Conclusions Uremic serum can induce HUASMC calcification and osteogenic transition in vitro,which may be one of the mechanisms involved in vascular calcification of ESRD patients.Microinflammatory state may promote the osteogenic transition and vascular calcification in dialysis patients.

OBJECTIVE:To discuss the mode and feasibility of informatization and automation construction in the inpatient pharmacy. METHODS:The practice of informatization and automation construction of inpatient pharmacy in our hospital was intro-duced,as well as the change of drug dispensing model. The influence of them on drug dispensing process was analyzed. RESULTS&CONCLUSIONS:2 automatic single dose tablets dispense packing machines,2 rapid dispensing machines and 2 automatic injec-tion chests are introduced in automatic inpatient pharmacy of our hospital. The informatization construction contain the establish-ment of inpatient pharmacy database,drug dispensing and recheck,the application of code,etc. Due to the implementation of auto-matic drug dispensing information system,drug dispensing mode have changed,i.g. drug dispensing by area instead of wards;in-jection and large volume transfusion are dispensed by wards;oral preparation and discharge medication are dispensed by prescrip-tion;dispensed drugs are distributed to wards with professional logistics. The implementation of informatization and automation of inpatient pharmacy in our hospital improve pharmaceutical administration and pharmaceutical care,and add automatic expiry date management and code tracking to guarantee the accuracy,timeliness and high efficiency of drug dispensing.

The paper described the professional approach of Shanghai Hospital Development Center(SHDC)in developing a professional team of public hospital directors by such means as operation and management-autonomy,fixed tenures system,performance appraisal,part-time job control and income distribution. Recommendations raised include an organic unity of management functions of investors and power of management of the directors to motivate them in their management;building a comprehensive investor management system and strict cadre management mechanism to enhance supervision of the directors.

BACKGROUND:In the initial stage of multiple sclerosis,central immune cells activate and release a large number of inflammatory factors,causing white matter demyelination and even involving gray matter neurons.The equilibrium of differentiation between different subsets of CD4+ T cells plays an important role in the progression of experimental autoimmune encephalomyelitis.The previous results of the research group showed that the active ingredient astragalus glycoprotein in astragalus can regulate the immune response in experimental autoimmune encephalomyelitis mice,and whether it has a regulatory effect on the differentiation of T cell subsets has not been determined. OBJECTIVE:To explore the therapeutic effects and immune regulatory mechanisms of astragaloside IV on experimental autoimmune encephalomyelitis mice. METHODS:Female C57BL/6 mice were divided into the normal control group,experimental autoimmune encephalomyelitis disease model group,and astragaloside IV treatment group(n=8 per group).Myelin oligodendrocyte glycoprotein peptides 35-55 were used for experimental autoimmune encephalomyelitis model induction in the last two groups.On day 10 to 28 after immunization,the astragaloside IV treatment group was treated with 40 mg/kg per day astragaloside IV intragastrically.Body weight and clinical scores of mice in each group were recorded from the immunization day to the 28th day.On the 28th day after immunization,the mouse spinal cord was taken and made into frozen sections for hematoxylin-eosin staining and Lux fast blue staining to observe pathological changes in the spinal cord.Percentage of splenic T cell subsets was detected using flow cytometry.Western blot assay was used to determine the protein expression of interferon-γ,interleukin-17 and interleukin-6 in the spinal cord.Levels of interferon-γ,interleukin-17,interleukin-6 and interleukin-4 in supernatants of cultured splenocytes were determined by ELISA. RESULTS AND CONCLUSION:(1)Compared with the experimental autoimmune encephalomyelitis disease model group,astragaloside IV could reduce the degree of weight loss in experimental autoimmune encephalomyelitis mice(P<0.05),ameliorate clinical symptoms(P<0.05),inhibit the infiltration of inflammatory cells and alleviate myelin loss(P<0.01,P<0.05).(2)Compared with the experimental autoimmune encephalomyelitis disease model group,astragaloside IV could inhibit the proportion of CD4+T cell subsets expressing interferon-γ(P<0.001)and interleukin-17(P<0.001),but increase percentages of CD4+ interleukin-10+(P<0.001)and CD4+ transforming growth factor-β+(P<0.01)T cell subsets.(3)Astragaloside IV could inhibit the expression of interferon-γ(P<0.05,P<0.01),interleukin-17(P<0.05,P<0.05),and interleukin-6(P<0.05,P<0.05)in the spinal cord and spleen,and up-regulate the expression of interleukin-4(P<0.01)in spleen.(4)These findings confirm that astragaloside IV alleviates clinical symptoms in experimental autoimmune encephalomyelitis mice,which may be related to regulating the splenic T cell subsets,therefore,inhibiting the infiltration of inflammatory cells into the center and reducing the demyelination.

Objective To investigate whether astragaloside ( AST) Ⅳ could inhibit lipopolysac-charide (LPS)-induced activation of astrocytes and the possible mechanism. Methods Effects of different concentrations of AST Ⅳ on astrocyte viability were determined by MTT to select the optimum concentration for the following experiments. Primary astrocytes were induced by LPS to construct the inflammatory model. Astrocytes were divided into three groups: PBS, LPS and LPS+ASTⅣ(LPS+ASTⅣ) groups. The release of nitric oxide (NO) was detected by Griess method. Expression of glial fibrillary acidic protein ( GFAP), an astrocyte marker, and TLR4 were analyzed by immunohistochemistry and Western blot. Cytokines of IL-6, TNF-α, IL-4 and IL-10 in the supernatants of cell culture for 24 h collected after stimulation were meas-ured by ELISA. Results ASTⅣsignificantly inhibited the LPS-induced activation of astrocytes and NO re-lease (P<0. 01), suppressed the expression of TLR4 (P<0. 05) and reduced the secretion of IL-6 (P<0. 01) and TNF-α (P<0. 01), but increased the secretion of IL-4 and IL-10 (P<0. 05 and P<0. 01). Con-clusion AST Ⅳ could significantly inhibit the LPS-induced activation of astrocytes and suppress inflamma-tory responses, and the possible mechanism might be related to reduced secretion of inflammatory factors af-ter blocking the expression of TLR4.

BACKGROUND:Astrocytes play an important role in the pathology of central nervous system diseases.The phenotypic and functional changes in astrocytes suggest that it may be an effective therapeutic target for central nervous system diseases.Our previous studies have confirmed that astragaloside can inhibit the lipopolysaccharide-induced astrocyte inflammatory response.Whether astragaloside can regulate the phenotype and function of astrocytes through Notch-1 and its downstream signaling pathway remains unclear. OBJECTIVE:To explore the effect of astragaloside on astrocyte activation and inflammatory response induced by inflammation and its possible mechanism. METHODS:Cerebral cortex astrocytes derived from neonatal C57BL/6 mouse were cultured in vitro.CCK-8 assay was used to determine the optimum concentration of astragaloside and Notch active inhibitor DAPT.The astrocytes were divided into five groups:PBS group,lipopolysaccharide group,lipopolysaccharide + astragaloside group,lipopolysaccharide + DAPT group and lipopolysaccharide + DAPT + astragaloside group.The secretion level of inflammatory factors was detected by ELISA,and the level of nitric oxide was detected by Griess method.The astrocytes and splenic mononuclear cells were co-cultured in Transwell chamber to observe the migration of CD4T cells.The expression of astrocyte activation marker GFAP,A1 marker C3 and A2 marker S100A10 as well as Notch 1 and Jag-1 was detected by immunofluorescence staining.The expressions of CFB,C3,S100A10,PTX3,Notch-1,Jag-1,and Hes were detected by western blot assay. RESULTS AND CONCLUSION:(1)According to the results of CCK8 assay,the final concentration of astragaloside was selected as 25 μmol/L and the final concentration of DAPT was 50 μmol/L for follow-up experiments.(2)Compared with PBS group,interleukin-6,interleukin-12 and nitric oxide secretion levels in the lipopolysaccharide group were significantly increased(P<0.05,P<0.05,P<0.01).Compared with the lipopolysaccharide group,interleukin-6(all P<0.05),interleukin-12(P>0.05,P<0.05,P<0.05)and nitric oxide(P<0.05,P<0.01,P<0.01)secretion significantly reduced in the lipopolysaccharide + astragaloside group,lipopolysaccharide +DAPT group,lipopolysaccharide + DAPT + astragaloside group.(3)Compared with the PBS group,the expression of GFAP that is the marker of activated astrocytes and the migration of CD4 T cells were significantly increased in the lipopolysaccharide group(P<0.01).Compared with the lipopolysaccharide group,astrocyte activation was significantly inhibited and CD4 T cell migration was significantly reduced in the lipopolysaccharide + astragaloside,lipopolysaccharide +DAPT,lipopolysaccharide + DAPT + astragaloside group(P<0.05,P<0.05,P<0.01).(4)Compared with the PBS group,the expressions of A1 markers C3 and CFB in the lipopolysaccharide group were increased(P<0.01,P<0.05),and the expressions of A2 markers S100A10 and PTX3 were decreased(P<0.01,P<0.05).Compared with the lipopolysaccharide group,C3(all P<0.01)and CFB(both P<0.05)were significantly reduced and S100A10(all P<0.01)and PTX3(P<0.05,P<0.05 and P>0.05)were increased in the lipopolysaccharide + astragaloside,lipopolysaccharide +DAPT,lipopolysaccharide + DAPT + astragaloside group.(5)Compared with the PBS group,the expressions of Jag-1,Notch-1 and Hes in the lipopolysaccharide group were significantly increased(all P<0.01).Compared with the lipopolysaccharide group,the expressions of Jag-1(all P<0.01),Notch-1(all P<0.01)and Hes(P<0.05,P<0.01 and P<0.01)were significantly reduced in the lipopolysaccharide + astragaloside,lipopolysaccharide +DAPT,lipopolysaccharide + DAPT + astragaloside group.(6)The results indicate that astragaloside can promote the transformation of astrocytes from A1 to A2 by regulating Notch-1 signaling pathway,reduce the secretion of inflammatory factors and the migration of CD4 T cells,and thus inhibit astrocyte activation and inflammatory response.

Preventing and mitigating major risk exposure is an important task for modern countries to maintain sustained and healthy economic development and overall social stability. In this manuscript, the authors introduced Israel′s current medical and health care risk prevention system, including the regional health emergency response coordination mechanism, hospital′s external emergency rescue capacity building and hospital′s internal security system. Israel′s risk prevention system has been tested by wars and terrorist attacks, as well as many infectious diseases outbreaks. Thus the authors expected that its successful experiences can be introduced as a reference for improving China′s medical and health care risk prevention system.

BACKGROUND:Current studies have confirmed that Ganoderma lucidum polysaccharides can promote nerve regeneration in neurodegeneration-related diseases.The occurrence of neurodegenerative diseases is closely related to mitochondrial dysfunction,but the role of Ganoderma lucidum polysaccharides on the regulation of apoptosis and mitochondrial function in neurodegenerative diseases is not yet clarified. OBJECTIVE:To explore the regulatory effects and mechanisms of Ganoderma lucidum polysaccharides on apoptosis and mitochondrial dysfunction in H2O2-induced SH-SY5Y cells. METHODS:SH-SY5Y cells were divided into three groups:control group,H2O2 group,and Ganoderma lucidum polysaccharides group.Cells in the control group were normally cultured.Cells in the H2O2 group were treated with 300 μmol/L H2O2 for 24 hours.In the Ganoderma lucidum polysaccharides group,the intervention with 300 μg/L Ganoderma lucidum polysaccharides was conducted first for 1-2 hours,followed by the addition of 300 μmol/L H2O2 for 24 hours.The mitochondrial membrane potential was detected by JC-1 kit.Apoptosis was detected by TUNEL staining kit.The activities of malondialdehyde and superoxide dismutase were detected by malondialdehyde test kit and superoxide dismutase test kit,respectively.The apoptosis and expression of mitochondrial dynamics-related proteins were detected by immunofluorescence staining and western blot assay. RESULTS AND CONCLUSION:(1)Compared with the control group,the mitochondrial membrane potential and superoxide dismutase activity were significantly reduced,as well as apoptotic rate and malondialdehyde levels were significantly increased in the H2O2 group(P<0.05).After treatment with Ganoderma lucidum polysaccharides,the membrane potential and superoxide dismutase activities were significantly increased,and apoptotic rate and malondialdehyde levels were significantly reduced compared with the H2O2 group(P<0.05).(2)The expression levels of pro-apoptotic proteins Bax and Caspase-3 were significantly increased,but the expression of anti-apoptotic protein Bcl-2 was significantly decreased in the H2O2 group compared with the control group(P<0.05).Compared with the H2O2 group,the levels of Bax and Caspase-3 were significantly decreased,but the expression of anti-apoptotic protein Bcl-2 was significantly increased in the Ganoderma lucidum polysaccharides group(P<0.05).(3)Compared with the control group,the expression of mitochondrial splitting proteins Fis1 and p-Drp1 was significantly increased,but the expression of mitochondrial fusion proteins OPA1,Mfn1,and Mfn2 was decreased in the H2O2 group(P<0.05).Compared with the H2O2 group,Fis1 and p-Drp1 expression was significantly reduced,but the expression levels of OPA1,Mfn1,and Mfn2 were significantly increased in the Ganoderma lucidum polysaccharides group(P<0.05).(4)The above results confirm that Ganoderma lucidum polysaccharides can attenuate H2O2-induced oxidative stress damage and apoptosis in SH-SY5Y cells by ameliorating mitochondrial dysfunction.