OBJECTIVE:To optimize the formulation of nisoldipine buccal adhesive tablets. METHODS: The formulation was optimized by orthogonal design with the dosage ratio of carbopol to chitosan in drug-containing layer and protection layer, the content of lactose and the tabletting hardness as factors. The bioadhesiveness and in vitro drug release rate of the tablets was measured as well. RESULTS: The optimal formulation was as follows: the ratio of carbopol to chitosan in drug-containing layer and protection layer were 22.5∶22.5 and 33.3∶16.7 mg, respectively; the dosage of lactose was 10 mg, and tabletting hardness was 5 kg. The averge bioadhesiveness of 3 bacthes of optimized preparations was 79.5 g?cm-2, and the average in vitro drug release rate of the tablets in 12 h was more than 95%. CONCLUSIONS: The optimized nisoldipine buccal adhesive tablets enjoy ideal bioadhesiveness and slow-release character.

OBJECTIVE: To discuss therapy regimes and pharmaceutical care for the inpatient with intracranial infection after craniotomy. METHODS: Clinical cases were taken as example and therapy regimes was analyzed in order to put out full range and individualized pharmaceutical care for patients with intracranial infection after craniotomy. RESULTS: Reasonable medication was provided by implementing pharmaceutical care. CONCLUSION: It is necessary to deliver pharmacetical care to the inpatient with intracranial infection after craniotomy.

OBJECTIVE:To determinate the dissolution of Compound Flavone capsules by HPLC.METHODS:Nova-Pak C18(250mm? 4.0mm,5? m) column was used with column at room temperature.The mobile phase consisted of methanol-0.4% H3PO4(50:50) at a flow rate of 1.0mL? min-1.The detective wavelength was 360nm.The dissolution of the Compound Flavone capsules was determined by basket stirring technique with 0.1mol? L-1 hydrochloric acid as dissolvent at a speed of 100r? min-1.RESULTS:The cumulative dissolution rate of Compound Flavone capsules was above 80% at 30 minutes.The linear range of Quercetin was 0.065 84～ 0.658 4?g(r=0.999 9).The average recovery was 99.35%,RSD=0.92%(n=6).CONCLUSION:The method is simple,accurate and reproducible,and suitable for the guality control of Compound Flavone capsules.

Acute respiratory distress syndrome (ARDS) is a serious state threaten human health with a high mortality about 30%-40%. At present, there is no effective treatment for ARDS. Microvesicles derived from mesenchymal stem cells (MSC-MVs) have a heterogeneous subcellular structure secreted by MSCs. It plays an important role in the repair of tissue and organ damage.Recent studies have shown that MSC-MVs, played an important role in repairing lung injury, may replace MSC for cell therapy. Therefore MSC-MVs may bring new hope for ARDS treatment.

OBJECTIVE: To provide the latest medicinal information for medical workers. METHODS: The drug instructions were managed using computer technology, and the inquiry service for drug information was provided in the hospital network. RESULTS & CONCLUSION: The established network bridged the communication between doctors and pharmacists, and enabled them to better understand medicinal information and prescribe medicines, and therefore serve the patients better.

The study aims to develop a rapid, sensitive and specified method of liquid chromatography with heated electrospray ionization tandem mass spectrometry (LC-HESI/MS/MS) for simultaneous determination of amlodipine, benazepril and benazeprilat in human plasma using amlodipine-d4 and ubenimex as internal standards (ISs). Selected reaction monitoring (SRM) with heated electrospray ionization (HESI) was used in the positive mode for mass spectrometric detection. Analytes and ISs were extracted from plasma by simple protein precipitation. The reconstituted samples were chromatographed on a C18 (100 mm x 4.6 mm, 5 microm) column with mixture of methanol-acetonitrile-5 mmol.L- ammonium acetate-formic acid (30 : 30 : 40 : 0.1) as mobile phase at a flow rate of 0.6 mL.min-1. The standard curves were demonstrated to be linear in the range of 0.02 to 6.00 ng.mL-1 for amlodipine, 0.2 to 1,500 ng.mL-1 for benazepril and benazeprilat with r2>0.99 for each analyte. The lower limit of quantitation was identifiable and reproducible at 0.02, 0.2 and 0.2 ng mL-1 for amlodipine, benazepril and benazeprilat, respectively. The intra-day and inter-day precision and accuracy results were within the acceptable limit across all concentrations. The plasma samples were stable after four freeze-thaw cycles and being stored for 93 days at -20 degrees C. The method was applied to a pharmacokinetic study of a fixed-dose combination of amlodipine and benazepril on Chinese healthy volunteers.

AIM: To examine the change of serum tumor necrosis factor-? (TNF-?), nitric oxide (NO) in patient with congestive heart failure (CHF) and the effect of angiotensin Ⅱ (AngⅡ), valsartan on TNF-? and NO production in culture peripheral blood mononuclear cells (PBMC), to assess the relationship between the renin-angiotensin system and cytokines. METHODS: Venous blood of both healthy volunteers (n=12) and patients with CHF (n=16) were collected. Serum TNF-? and NO were examined. Peripheral blood mononuclear cells (PBMC) were obtained from both the control and the patients groups and cultured with AngⅡ at concentrations of 0, 0.01, 0.1, 1 ?mol/L, respectively. AngⅡ at concentration of 0.1 ?mol/L combined with 0.1 ?mol/L of valsartan was also used. After 24 h incubation, the contents of TNF-? and NO in the culture supernatants were measured. RESULTS: Serum TNF-? and NO production in CHF group were significantly higher than that in control group (P0.05) were observed. AngⅡ stimulated TNF-? and NO release from PBMC of patients with CHF and normal person, which was inhibited by valsartan. CONCLUSIONS: AngⅡ obviously increases TNF-? and NO production from PBMC, which indicates there is relationship between the renin-angiotensin system and TNF-?, NO. The fact that valsartan inhibits TNF-? production may be one of the mechanisms in treating CHF.

Objective To evaluate the cost-effectiveness of Morphine-midazolam, propofol and midazolam used for sedation in patients with mechanical ventilation. Methods Ninety-three patients with mechanically ventila-Morphine-midazolam group:priming dose 0.05 mg/kg and 0.05 mg/kg of morphine and midazolam,then continuous The index of ideal level of sedation was on the Ramsay scale. The sedation time, the time from discontinuation to ex-tubation, sedation costs, blood pressure were measured. Results The time in midazolam group (6.0±2.4) h was longer than that of propofol (4.6±1.7) h (P<0.01), but there was no significant relationship between morphine-midazolam group (5.6±2.7) h and midazolam group (4.6±1.7) h (P>0.05). The sedation costs in morphine-mi-dazolam group (101.7±20.4) yuan were lower than those of midazolam group (127.7±21.3) yuan (P<0.05) and propofol group(199.7±65.9) yuan (P<0.01). The ratio of hypotension in propofol group (35.4%, 11/31) hap-pened more frequent than that of midazolam group (3.2%, 1/31) (P<0.01) and morphine-midazolam group (9.7%, 3/31) (P<0.05). Conclusions Morphine-midazolam is a safe, effective and economic drug compared with midazolam and propofol used for sedation in patients with mechanical ventilation.

OBJECTIVE:To study the protective effects of autophagy inhibitor 3-Methyladenine (3-MA) against lipopolysac-charide(LPS)-induced acute lung injury in mice and its mechanism. METHODS:Mice were randomly divided into normal control group,model group (LPS 15 mg/kg),drug control group (3-MA 20 mg/kg),low-dose and high-dose groups (LPS 15 mg/kg+3-MA 20,40 mg/kg),with 10 mice in each group. Except for normal control group and drug control group,other groups were giv-en LPS intraperitoneally to induce acute lung injury model,and drug control group and low-dose and high-dose groups were given equivalent dose of 3-MA intraperitoneally 1 h before modeling. 6 h after modeling,lung wet/drug mass ratio (W/D) was deter-mined respectively,and pathology change of lung tissue was observed by HE staining. TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein expression were detected by Western blot. RESULTS:Compared with normal control group,W/D, TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein expression increased in model group (P<0.01). Compared with model group,W/D,the expression of TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein decreased in low-dose group (P<0.05),white just only LC3BⅡ/Ⅰ protein decreased high-dose group(P<0.01). CONCLUSIONS:In LPS-induced acute lung injury model in mice,the excessive autophagy could activate the NF-κB pathway and involve the inflammatory responses and induce lung cells apoptosis. The moderate autophagy inhibition by 3-MA can ameliorate inflammatory response and protect lung tissue.

The PCR product of PvpA gene was cloned into prokaryotic expression vector pET41a(+) and the recombinant expression vector was then transformed into E.coli DH5a after identified by restriction enzyme digestion and PCR.The positive recombinant plasmid was transformed into E.coli BL21 (D3) and induced to express PvpA protein.The obtained protein was analyzed by SDS-PAGE and Western blotting,purified by Ni-NTA affinity chromatography.The results showed that the purified PvpA fusion protein was obtained successfully.The expressed protein reacted to the high anti-PvpA immune serum from rabbit specially by western blotting.This study would be helpful to established a new diagnostic method for the detection of M.gallisepticum.