Objective:To study the regularity and characteristics of adverse drug reaction ( ADR) in our hospital. Methods: A retrospective analysis was conducted on 306 ADR reports collected in our hospital in 2013. The reports were statistically analyzed in re-spect of sex, age, route of drug administration, drug categories, organs/systems involved in ADR and clinical manifestations, classifi-cation of ADR, causality assessment, constituent ratio of the reporters etc. Results:In the 306 ADR reports, the incidence of ADR be-tween the age of 51 and 60 was the highest (20. 26%); the ratio of the ADR induced by intravenously drip administration was the highest in respect of the route of administrations (65. 58%);the radio of ADR induced by antibacterial agents was the highest in re-spect of drug types (20. 78%);digestive system was the maln lesion in ADR cases (23. 91%). The ADR cases were mostly reported by doctors (97. 71%). Conclusion:Our hospital should enhance the ADR monitoring and reporting, promote the clinical rational drug use, reduce or avoid the risk of ADR and protect medication safety of patients.

Objective To investigate the expression of osteopontin and matrix metalloproteinase-9 (MMP9),and the relationship of osteopontin and MMP9 in malignant melanoma.Methods Expression of osteopontin and MMP9 was measured by immunohistochemical SP method in 23 patients with primary cuta- neous malignant melanoma,17 patients with metastatic melanoma and 20 patients with pigmented nevus. Results Osteopontin and MMP9 were expressed respectively in 87.5% and 75.0% of 40 malignant melanoma specimens,15.0% and 10.0% of 20 pigmented nevus specimens.The expression of both osteo- pontin and MMP9 was significantly higher (both P＜0.05) in malignant melanoma than in pigmented ne- vus.There was no correlation between the expression of osteopontin and MMP9,with age,sex,lymph node metastasis or location of lesions (P＞0.05).Twenty-nine cases were positive for both osteopontin and MMP9,4 negative for either osteopontin or MMP9.Conclusion Both osteopontin and MMP9 were over- expressed in malignant melanoma,but neither was related to lymph node metastasis.

Objective: To evaluate the clinical value of multislice CT (MSCT) in the diagnosis and preoperative TNM staging of gastric carcinoma. Methods: Fifty patients with advanced gastric carcinoma were examined by MSCT, gastrointestinal series (GI), fiberoptic gastroscopy (FG) and transabdominal ultrasonography (US). The results of the 4 methods were compared with postoperative pathological results. Forty patients, who were diagnosed as having advanced gastric carcinoma by both MSCT and US, had their TNM staging evaluated and the results were compared with postoperative pathological TNM evaluation. Results: The detection rates of MSCT, FG, GI and US for advanced gastric carcinoma were 98%, 100%, 88% and 80%, respectively. The detection rate of MSCT was not significantly different with that of FG, but was obviously higher than that of GI (P=0.027) and US (P=0.004). The accuracy of MSCT in preoperative TNM staging was significantly higher than that of US(92.5% vs 72.5%). Conclusion: MSCT, with two-phase thin slice incremental scanning image, multiplaner reformats (MPR) and three-dimension (3D) image, is more advantaged in detecting the gross type, size, location, invasion and metastasis of advanced gastric carcinoma, thus greatly improving the detection rate and preoperative TNM staging of advanced gastric carcinoma.

Objective To construct PPAR?and PPAR?response element (PPRE)-controlled luciferase expression vectors,and to determine whether the traditional Chinese medicine emodin activates PPAR?and improves the glucose uptake by HepG2 hepatocytes.Methods (1) PPAR?and PPRE luciferase expression vectors were constructed and were applied to screen more than 20 ingredients of the traditional Chinese medicine. (2) HepG2 cells were incubated with emodin which can activate PPAR?and PPRE luciferase activity,and the PPAR?mRNA expression level was evaluated by RT-PCR/Southern blot.(3) PPAR?and glucose transporter 2 (Glut2) proteins were determined by Western blot analysis in HepG2 cells treated with emodin.(4) The glucose uptake rate was measured using 2-deoxy-[~3H]-D-glucose in HepG2 cells after treatment with emodin.Results (1) Emodin stimulated luciferase activity controlled by PPRE in dose-dependent manner at concentrations of 0.04 to 180?mol/L in COS-7 cells.The highest value was about 4 folds of control in the cells treated with 90?mol/L emodin (P

Objective To investigate the expression of peroxisome proliferators-activated receptor ? (PPAR?) in trophoblast and relation between PPAR? ligands and trophoblast invasion.Methods We examined the expression of PPAR? by immunohistochemistry,immunocytochemistry and real time quantitative PCR.We next examined,using the cytotrophoblast culture model,the biological role of PPAR? ligands in vitro.Results PPAR? was mainly localized in the nuclei of villous cytotrophoblast and extravillous cytotrophoblast of cell islands and cell columns.In villous tissue and cultured trophoblast from early first trimester,the level of expression of PPAR? mRNA and protein was 36.0?5.1,13.4?3.1 and 1.35?0.08,1.13?0.11;from late first trimester it was 23.3?5.5,6.1?1.3 and 1.17?0.03,0.86 ?0.05,and the expression of PPAR? was obviously decreased (P

Objectives To evaluate the expression profile of myoD microRNA-29 (miR-29) family in L6 myoblast differentiated to myotube or L6 myotube treated by glucose and insulin, and to further probe the molecular mechanism of myoD regulating the expression of miR-29 clusters.
Methods The expression of myoD and miR-29 family was detected by using real-time PCR and Western blot analysis. The potential promoter and transcription factors binding sites of miR-29 clusters were predicted by Promoter scan and transcriptional factor search. The promoter sequence of miR-29b1-a and miR-29b2-c cluster was cloned into a luciferase reporter plasmid and the regulatory effect of myoD was analyzed by using dual luciferase reporter assay. Electrophoretic mobility shift assay was further conducted to indicate the binding of myoD on specific sequence. Moreover, overexpression of myoD was achieved by a recombinant adenovirus system (Ad-myoD). L6 cells were infected with Ad-myoD and real-time PCR was conducted to analyze the expression of miR-29b and miR-29c.
Results The expression levels of myoD, miR-29a, miR-29b, and miR-29c were increased in L6 myoblast differentiated to myotube. The expression of myoD, miR-29b, and miR-29c was up-regulated in L6 myotube treated with glucose and insulin, but miR-29a depicted no significant change. Dual luciferase reporter gene assay showed that myoD functioned as a positive regulator of miR-29b2-c expression and myoD could bind to the specific sequence located at the promoter region of miR-29b2-c cluster. Enforced expression of myoD led to a marked increase of miR-29b and miR-29c levels in L6 cells.
Conclusion MyoD might act as a crucial regulator of myogenesis and glucose metabolism in muscle through regulating the expression of miR-29b2-c.

OBJECTIVETo address the hypothesis that hydrogen sulfide (H(2)S) is a functionally significant stimulator in the development of glioblastoma (GBM) and explore the mechanism of stimulation.

METHODSForty adult Sprague-Dawley (SD) rats were given intracerebral injection of rat C6 glioma cell suspension, and an intraperitoneal injection of sodium hydrosulfide (NaHS), an exogenous H(2)S donor. The 40 rats were randomly divided into 4 groups of 10 rats in each: the control group, NaHS group, C6 glioma group (intracerebral implantation of C6 glioma cells) and C6-NaHS group (intracerebral implantation of C6 glioma cells and intraperitoneal injection of NaHS). Food and water were freely available during all phases of the experiment. Physical symptoms were observed and the tumor size was measured. Histological changes were examined by pathology. Immunohistochemical staining was used to analyze the expression of HIF-1α and integrated optical density (IOD) was used to determine the tumor microvessel density (MVD). The H(2)S content in the brain was measured.

RESULTSThe physical symptoms of tumor-bearing rats became more serious after NaHS injection. The H(2)S level in the C6 glioma group was higher than that in the control group [(35.25 ± 1.03) nmol/g vs. (29.12 ± 0.94) nmol/g, P < 0.05], and the highest H(2)S level was found in the C6-NaHS group. The pathological examination showed that the implanted tumors were predominantly spheroid with a distinct border and no capsule could be detected. Neovascular proliferation was also observed. Foci of tumor necrosis, intratumoral hemorrhage, pseudopalisades and tumor cavity were clearly observed. The glioma cells had scant eosinophilic cytoplasm and enlarged hyperchromatic nuclei. All these phenomena were more markedly in the C6-NaHS group compared with that in other three groups. The mean tumor volume was significantly different between the C6 and C6-NaHS rats [(32.0 ± 6.9) mm(3) vs. (67.8 ± 11.9) mm(3), P < 0.001]. Immunohistochemical analysis exhibited that the hypoxia-inducible factor-1alpha (HIF-1α) and CD34 expression were significantly increased after the intraperitoneal injection of NaHS in the C6-NaHS rats (comparing the IOD between C6-NaHS group and C6 group, HIF-1α: 133 962.9 ± 451.4 vs. 38 569.8 ± 408.6, P < 0.001; CD34: 73 368.6 ± 404.8 vs. 14 570.6 ± 748.7, P < 0.001). Moreover, compared with the C6 group, there were higher MVD in the C6-NaHS group [(41.2 ± 7.9)/mm(2) vs. (97.0 ± 10.8)/mm(2), P < 0.001].

CONCLUSIONSH(2)S serves as a stimulator in the development of rat glioblastoma and exogenous H(2)S strongly promotes the tumor growth. The stimulating mechanisms include the increase of HIF-1α expression and neovascular formation. H(2)S may be a significant regulator in the development of tumor.

Animals ; Antigens, CD34 ; metabolism ; Brain ; metabolism ; pathology ; Brain Neoplasms ; metabolism ; pathology ; Glioblastoma ; metabolism ; pathology ; Hydrogen Sulfide ; metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Injections, Intraperitoneal ; Male ; Neoplasm Transplantation ; Neovascularization, Pathologic ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sulfides ; administration & dosage ; pharmacology ; Tumor Burden

To investigate the implementation effect of health education path in neo-natal disease screening , then promoting popularization and development of neonatal disease screening . [ Methods] The health education path was worked out for neonatal disease screening .A total of 986 cases of single birth mothers and their newborns were as the observation group , in which the path of health educa-tion was implemented for them .And 1 052 cases of single birth mothers and their newborns were as the con-trol group, in which the traditional method of health education was done .Comparison was made between the two groups in neonatal disease screening rate , positive recall rate , degree of parturient about understanding and mastering the knowledge of neonatal disease screening , parturient satisfaction and parental satisfaction . [ Results] The neonatal disease screening rate , positive recall rate , degree of parturient about under-standing and mastering the knowledge of neonatal disease screening , parturient satisfaction and parental satisfaction were all better in the observation group than those in the control group ( P <0.05 ). [ Conclusion] The health education path for neonatal disease screening can effectively promote its devel-opment and popularization .

OBJECTIVE To investigate the neuroprotective effect and the mechanism of Yueju alcohol extract (YJ-E) on chromaffin cells(PC12)injury in rats induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ion(MPP+).METHODS PC12 cells were given 1 mmol MPP+ to establish Parkinson's disease(PD) model in vitro.The protective effects of YJ-E on PC12 cells were measured by MTT assay and Hoechst staining.The expression of pituitary adenylate cyclase activating poly-peptide(PACAP)and the phosphorylation of extracellular regulated kinase(ERK)and cAMP response element binding pro-tein(CREB)were determined by Western blotting.RESULTS YJ-E(1.0,2.0,4.0 mg/mL)improved the survival of MPP+-injured PC12 cells significantly(P<0.01),and displayed no significant effect on normal PC12 cells(P>0.05).Meanwhile, YJ-E up-regulated the expression of PACAP and the phosphorylation of ERK and CREB significantly(P<0.01)of MPP+-in-jured PC12 cells.CONCLUSION YJ-E shows promising neuroprotective effects on PC12 cells in MPP+-induced Parkinson's disease model,and the mechanism may be associated with the up-regulation of the expression of PACAP and the phosphoryla-tion of downstream ERK and CREB.

OBJECTIVESTo evaluate the expression profile of myoD microRNA-29 (miR-29) family in L6 myoblast differentiated to myotube of L6 myotube treated by glucose and insulin, and to further probe the molecular mechanism of myoD regulating the expression of miR-29 clusters.

METHODSThe expression of myoD and miR-29 family was detected by using real-time PCR and Western blot analysis. The potential promoter and transcription factors binding sites of miR-29 clusters were predicted by Promoter scan and transcriptional factor search. The promoter sequence of miR-29b1-a and miR-29b2-c cluster was cloned into a luciferase reporter plasmid and the regulatory effect of myoD was analyzed by using dual luciferase reporter assay. Electrophoretic mobility shift assay was further conducted to indicate the binding of myoD on specific sequence. Moreover, overexpression of myoD was achieved by a recombinant adenovirus system (Ad-myoD). L6 cells were infected with Ad-myoD and real-time PCR was conducted to analyze the expression of miR-29b and miR-29c.

RESULTSThe expression levels of myoD, miR-29a, miR-29b, and miR-29c were increased in L6 myoblast differentiated to myotube. The expression of myoD, miR-29b, and miR-29c was up-regulated in L6 myotube treated with glucose and insulin, but miR-29a depicted no significant change. Dual luciferase reporter gene assay showed that myoD functioned as a positive regulator of miR-29b2-c expression and myoD could bind to the specific sequence located at the promoter region of miR-29b2-c cluster. Enforced expression of myoD led to a marked increase of miR-29b and miR-29c levels in L6 cells.

CONCLUSIONMyoD might act as a crucial regulator of myogenesis and glucose metabolism in muscle through regulating the expression of miR-29b2-c.

Animals ; Cell Differentiation ; drug effects ; physiology ; Cell Line ; Gene Expression Regulation ; drug effects ; physiology ; Glucose ; pharmacology ; Hypoglycemic Agents ; pharmacology ; Insulin ; pharmacology ; Mice ; MicroRNAs ; biosynthesis ; genetics ; Multigene Family ; physiology ; Muscle Fibers, Skeletal ; cytology ; metabolism ; MyoD Protein ; genetics ; metabolism ; Myoblasts ; cytology ; metabolism ; Sweetening Agents ; pharmacology