This study is to prepare the pantoprazole sodium enteric-coated tablet which is compacted by pellets. The enteric-coated pantoprazole sodium pellets were prepared by fluid bed coating technology. The pantoprazole sodium enteric-coated tablets were prepared by direct compression of the enteric-coated pellets and suitable excipients. In vitro dissolution method and scanning electron microscope method were used for the observation of the drug release behavior before and after compression of the pellets. The optimized formulation is: the coating level is 55%, the plasticizer content is 20%, the ratio of Eudragit L30D-55/NE30D is 8 : 2, enteric-coated pellets/excipients (MCC/PPVP/PEG 6000 = 2 : 1 : 1) is 5 : 5, the enteric-coated tablets release in artificial gastric fluid in 2 h is less than 10%, while in artificial intestinal fluid in 1 h is more than 85%. The release behavior of pantoprazole sodium enteric-coated pellets-type tablet is quite well. And it may be used in industrial production.

Objective To evaluate the therapeutic effetive,toxicity and survial rate of non-operation esophageal carcinoma patients treated by tegafur plus cisplatin combined with three-dimensional conformal radiotherapy (3D-CRT).Methods 184 cases of non-operation patients with esophageal carcinoma were divided into two groups.The cases of treatment group were treated by cisplatin and tegafur.The cases of control group were treated by cisplatin and 5-Fu.All patients received 3D-CRT,and the total radiation dose was 50-70 Gy.Each group had 14 cases treated with primary chemotherapy for 1 course,28 cases for 2 courses,and 50 cases without any chemotherapy.Results The recent effect rate was 69.57 ％ (64/92) in treatment group and 67.39 ％ (62/92) in control group,there was no statistical difference (x2 =0.101,P =0.874).Radioactive esophagitis and leukopenia were the main side effect of treatment.The treatment group was significantly lower than that of the control group,the difference had statistical significance.The 1-,2-and 3-year survival rates were 74.9 ％,61.6 ％,52.8 ％,respectively in treatment group and 75.8 ％,56.9 ％,48.0 ％,respectively in control group.The control group survival rates were significantly higher than the treatment group,the difference had statistical significance (x2 =7.325,P =0.007).Conclusions Cisplatin plus tegafur or 5-Fu combined with 3D-CRT is effective way of treatment for non-operation of esophageal carcinoma.The toxicity of cisplatin plus tegafur group is significantly lower than cisplatin plus 5-Fu group,therefor it can improve the quality of life of the patients obviously.

Objectives:To evaluate the adhesive effect of resin and dentin perpared by air abrasion. Methods:Dentin of 48 permanent molars was exposed and treated with ① air sand blasting+whole acid corrosion+Estet. X TM,② air sand blasting+SE BOND,③ air sand blasting+Esthet. X TM,④Turbine+whole acid corrosion+Esthet.X TM respectively with 12 samples in each group. Then resin adhesive was applied.Microtensile testing was used to examine the microtensile bond strength. SEM was used to observe the change of resin jags. Results:The microtensile bonding strength in group ①,②,③ and ④ was 27.96?1.42, 29.84?2.56,14.48?2.45 and 27.73?1.48 respectively (① vs ③,② vs ③ and ③ vs ④ P

Objectives: To investigate the affecting factors on expenditure in Medical insurant inpatients. Methods: 593 medical insurant inpatients, who were from Feb 1, 2001 to Feb 31, 2002 in Nanjing Jinling hospital, were enrolled in this study. The inpatient expenditure was analyzed from the aspect of operation or not, age, and payment mode, used the descriptive analysis and multi factor analysis on affecting factors of the total expense, self bearing expense, and self affording expense. Results: The hospitalized days, operation or not, severity of disease were important affecting factors. The self bearing expense of medical insurant inpatients was associated with hospitalized days, operation or not, and total expense. While the self affording expense of them was associated with expense of drug, hospital bunk, radiation and others. Conclusions: We can control these associated affected factors to lighten the economic weight of patients, and to reduce the ratio of individual payment.

Objective:Observed activity of adjuvant arthritis ( AA) rats Hedgehog signaling pathway and explore the effect of Cyclopamine on rat arthritis and kidney injury.Methods:40 rats were randomly divided into control group,Cyclopamine group,AA+Cyclopamine group and AA model group.We used Freund′s complete adjuvant rat model with Cyclopamine intraperitoneal injection.By measuring paw swelling, systemic inflammation and arthritis semi-quantitative assessment methods of rats to evaluate the model.HE staining was used to detect the renal pathological changes of rats.Western blot was used to detect kidney Gli1 protein expression levels of the rats.Immunohistochemical staining was used to detect the rat kidney TNF-α,IFN-γ,IL-6 expression.Results:After using Cyclo-pamine,the AA rat paw swelling reduced and arthritis refers relieved significantly.Compared with the control group,Cr,BUN and organ coefficient increased significantly in AA model group, and the difference was statistically significant.Meanwhile renal TEM detection appeared obvious pathological changes in rats of AA model group.After using cyclopamine,the content of Cr,BUN and organ coefficient change reduced significantly, so did the pathological.Western blot detected kidney tissue Gli1 protein in each group.Compared to control group,there was no significant difference in Cyclopamine group.AA model group and AA+Cyclopamine group Gli1 protein expression was significantly higher compared with Cyclopamine Gli1 protein group,the difference was statistically significant.AA model group and AA Cyclopamine group Gli1 protein expression was significantly higher,the difference was statistically significant.Compared to the AA model group,AA+Cyclopamine group Gli1 protein levels have decreased significantly,the difference was statistically signifi-cant.Immunohistochemical assay detection found that kidney tissue proinflammatory cytokines TNF-α,IFN-γ,IL-6 expression and semi-quantitative score changed.Compared with the control group, TNF-α, IFN-γexpression of AA model group were significantly increased.After using Cyclopamine,the expression of TNF-α,IFN-γin kidney of AA model reduced significantly.IL-6 expression in AA model group was significantly higher than the control group.Conclusion:Cyclopamine AA can relieve arthritis and kidney injury in rats with arthritis AA,the Hh pathway was on activity state in the process,may altered expression of inflammatory factors.

ObjectiveTo investigate the mechanisms and the effects of magnesium Valproate on the expressions of the kinin B1 and B2 receptors in the hippocampus of the juvenile rats submitted to pilocarpine model of epilepsy.Methods 35 healthy Wistar juvenile rats were randomly divided into six groups,that is the model groups:Ⅰ group,Ⅱ group,Ⅲ group,and intraperitoneal injection of saline water control groups:Ⅰ a group,Ⅱ a group,Ⅲ a group,after succession of 15 rats to kindle to establish the model of epilepsy by pilocarpine.To collect hippocampus tissue after the rats were to put to death,and to compared the expression levels of kinin B1 and B2 receptor mRNA by RT-PCR and western blot in the hippocampus of rats.ResultsBy treated with magnesium valproate,kinin B1 receptor mRNA (0.38 ± 0.051 ) and protein expressions(0.58 ± 0.057 ) decreased and kinin B2 receptor mRNA (0.48 ±0.056 ) and protein expressions(0.48 ± 0.044 ) increased in Ⅰ group,compared with that (0.76 ±0.068,0.89 ± 0.034;0.28 ± 0.034,0.32 ± 0.039 ) of Ⅰ a group(P ＜ 0.05 ).Compared with control group,there were more significant upregulation of kinin B1 receptor mRNA and protein expressions (P＜0.05) in the Ⅰ and the Ⅱ groups and there were no alteration in Ⅲ group.The expressional levels of B2 receptor mRNA and protein were upregulated in the Ⅰ,Ⅱ and Ⅲ groups.ConclusionThe kinin B1 and B2 receptor may play a role in the onset and maintenance of epilepsy.The magnesium valproate increased the expressional levels of kinin B2 receptor,and decreased the expressional levels of kinin B1 receptor.

ObjectiveTo observe the effect of betulinic acid(BetA) on the growth of human cytokine induced killer(CIK) cells and the killing activity of CIK cells on the gastric cancer cells in vitro before and after induced by betulinic acid,explore its mechanism.MethodsPeripheral blood mononuclear cell (PBMC) were separated form the healthy and were induced with various of cytokine to become CIK cells in vitro.CIK cells were collected on the tenth day and were induced with betulinic acid in different concentrations,followed by 48 h,the colorimetric methyl thiazolyl tetrazolium(MTT) method assay the proliferation rate of human CIK cells.Flow cytometry (FCM) was used to detect the expression changes of perforin,granzyme B and CD107a of human CIK cells before and after betulinic acid-induced.Lactate dehydrogenase (LDH) release assay was used to measure the influence on cytotoxic activity of CIK cells induced by betulinic acid against gastric cancer cell line SGC-7901 in vitro.Western blot assay was used to measure the extracellular signal-regulated kinase1/2 (ERK1/2),and adapter proteins SH2-domain containing leukocyte protein of 76KD(SLP-76) and linker for activative of T cells(LAT) expression changes of human CIK cells before and after drug-induced.ResultsBetulinic acid can promote CIK cells growth when the concentration were in 0.08-10 μg/ml,the expression of perforin,granzyme B and CD107a of CIK cells were significantly higher than control group(P＜0.05) when the concentration of betulinic acid were in 0.3 μg/ml.In the meanwhile,the cytotoxic activity of CIK cells in vitro against gastric cancer cell line SGC-7901 were also remarkably higher than the control group (P＜0.05).The expression of SLP-76,LAT and ERK1/2 were significantly increased to a certain extent than the control group( P＜0.05 ),when CIK cells were treated with betulinic acid.ConclusionThese results suggest that betulinic acid can promote CIK cells growth in some concentrations and increase the cytotoxic activity of CIK cells against gastric cancer cell line SGC-7901,its mechanism may related with two factors,on the one hand,enhancing the activity of SLP-76,LAT and ERK1/2,on the other hand,increasing the expression of perforin,granzyme B and CD107a on the surface of CIK cells.

Objective To investigate the mechanisms of tigecycline nonsusceptibility in carbapen-ems-resistant Acinetobacter baumannii ( CRAB) strains in order to provide a theoretical basis for a reasonable use of antibiotics and the control of nosocomial infection .Methods Susceptibility testing of 120 non-dupli-cate CRAB strains to tigecycline was performed by using the broth microdilution method .Minimal inhibitory concentrations ( MIC) of tigecycline against the A.baumannii strains were determined by using the broth mi-crodilution method before and after exposing the strains to Carbonylcyanide-m-chlorophenylhydrazone (CCCP), which was the efflux pump inhibitor .Polymerase chain reaction (PCR) was used to amply the ef-flux pumps genes including adeB, adeJ, adeG, abeM, adeE, adeRS, tetX and tetX1.The real-time PCR was performed to measure the expression of efflux pumps genes including adeB, adeJ, adeG, abeM and adeE.Results A total of 120 CRAB strains were collected including 13 (10.8%) tigecycline non-suscep-tible A.baumannii (TNAB) strains and 107 (89.2%) tigecycline susceptible A.baumannii (TSAB) strains.The MIC values of tigecline to the 120 CRAB strains were in a range of 0.25 μg/ml to 8 μg/ml. The adeR and adeJ genes were detected in 90.0%and 92.5%of the 120 CRAB strains, respectively.The positive rates of adeB, adeS, adeG and abeM genes among the 120 CRAB strains were all 94.2%.None of the three genes including adeE, tetX and tetX1 were detected .The mean expression levels of adeB and adeJ in TNAB strains were respectively increased by 18.69 folds and 5.46 folds as compared with those in sensi-tive strains.No significant increase in the expression of adeG and abeM genes was observed in TNAB strains . A 4-fold decrease in the MIC was observed in 8 out of 13 TNAB isolates treated with 10 μg/ml of CCCP .The CCCP could partially reverse the resistance pattern of tigecycline .Conclusion The efflux pump sys-tems of adeABC and adeIJK rather than the abeFGH and abeM systems might play an important role in reduc-ing the tigecycline susceptibility in carbapenems-resistant A.baumannii strains.

Objective To investigate the effect of glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide on hypoxia/reoxygenation (H/R)-induced cardiomyocytes death under high glucose condition and the potential mechanisms.Methods H9C2 cardiomyocytes were divided into 4 groups:normal glucose (N,5 mmol/L),high glucose (G,20 mmol/L),high glucose in combination with liraglutide (L,100 nmol/L),high glucose in combination with liraglutide and wortmannin (W,25 nmol/L).The apoptosis of H9C2 was detected by TUNEL assay.Nitric oxide synthetase(eNOS),nitric oxide (NO) and reactive oxygen(ROS) in supernatants were measured by enzymatic analysis,p-PI3K,PI3K,p-Akt,Akt,Bcl-2,caspase-3 were examined by western blotting.Results Compared with cells in N group,the apoptosis of H9C2 cells induced by H/R was markedly increased [(15.79 ± 3.92) ％ vs (9.74 ± 1.14) ％,P =0.028] in G group.The same was true for ROS [(489.63 ±21.01) U/ml vs (338.50 ±43.60) U/ml,P ＜0.001] and caspase-3 levels (1.87 ±0.03 vs 1.15 ±0.04,P ＜0.001),but not for Bcl-2 protein expression (1.79 ± 0.06 vs 1.89 ±0.03,P =0.047).Pretreatment of cells with liraglutide (100 nmol/L) prevented the cell death induced by high glucose and H/R together with decrease of ROS and caspase-3 levels and increase of Bcl-1 expression.Moreover,treatment of cells with liraglutide also significantly increased phosphorylation of PI3K and Akt (p-PI3K/PI3K:0.87 ± 0.07 vs 0.59 ± 0.09,P =0.002;p-Akt/Akt:0.34 ± 0.01 vs 0.08 ± 0.01,P＜0.001),eNOS[(41.29 ±0.56) μmpl/L vs (37.20 ±0.52)μxmpl/L,P ＜0.001]and NO [(31.24 ±0.40) μmpl/L vs (26.66 ±0.53) μmpl/L,P ＜0.001] levels.Furthermore,addition of PI3K/Akt inhibitor wortmanin markedly inhibited the expression of p-PI3K/PI3K,p-Akt/Akt,reversed the changes of eNOS,NO,caspase-3 and Bcl-2 by liraglutide,and abolished the protective effect of liraglutide on cell apoptosis.Conclusions GLP-1 receptor agonist liraglutide treatment could alleviate cardiomyoeytes apoptosis induced by high glucose and H/R through the activation of PI3K-Akt-eNOS-NO signaling pathway and inhibition of oxidative stress.

Objective To investigate the correlation between heat-shock protein 70-2 (HSP70-2) gene+1267A/G polymorphism and coronary heart disease (CHD) in Han Chinese population. Methods Using the method of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) , the polymorphism and genotype and allele distribution of HSP70-2 gene + 1267A/G in 185 CHD patients and 149 controls were analyzed. Results The HSP70-2 gene + 1267A/G polymorphism was found in this study population.The distribution of HSP70-2 genotypes was in Hardy-Weinberg equilibrium. The frequency of G allele in CHD group was significantly higher than that in control (61.89% vs51.68%, P ＜ 0. 01). After multiple logistic regression analysis, HSP70-2 gene (GG + AG) genotype was an independent risk factor of coronary heart disease. Conclusion HSP70-2 gene + 1267A/G polymorphism was associated with CHD risk of Han Chinese population, the G allele might serve as a genetic risk factor of coronary heart disease.