Objective To explore the role of interleukin-23 (IL-23)/interleukin-17 (IL-17) signaling pathway in viral myocarditis (VMC) and evaluate the intervention effect of Aastragaloside. Methods Seventy-five male BALB/c mice were randomly divided into 4 groups, control group (n=15), model group (n=20), low-dose intervention group (n=20) and high-dose intervention group (n=20). Mice in control group were inoculated with 0.1 ml virus cultivation solution intraperitoneally while mice in the other 3 groups were treated with 0.1ml virus cultivation solution containing 1×102 TCID50 coxsackievirus B3 (CVB3) to establish VMC model. On the day of inoculation, mice in low- and high-dose intervention groups were intra-gastrically administered with 0.1 ml of 1% and 9%Astragaloside solution respectively, whereas those in control and model groups were treated with 0.1 ml carboxymethycellulose solution. Astragaloside or carboxymethycellulose was given once a day and continued 15 days. The number of mice death and the performance of mice were recorded in experimental period. All mice were sacrificed on day 15. The heart and blood sample were obtained. Histological cross sections of heart were stained with hematoxylin-eosin and scored for myocardial histopathologic changes under optical microscope. Th17 cells were analyzed by flow cytometry. The mRNA and protein expression levels of myocardial IL-23 and IL-17 were detected by real-time quantitative PCR and Western blotting, respectively. Results The mortality was statistically significant differ-ences among the four groups (P= 0.013), which was the lowest in the control group. The myocardial histopathologic scores, the percen-tage of Th17 cells, as well as expression levels of myocardial IL-23 and IL-17 mRNA and protein were significantly lower in high-dose intervention group than those in model group and low-dose intervention group, but higher than those in control group (P < 0.05). The myocardial histopathologic scores, the percentage of Th17 cells, as well as ex-pression levels of myocardial IL-23 and IL-17 mRNA and protein were significantly higher in model group and low-dose in-tervention group (P < 0.05). There were no significant difference in the above mentioned indicators between low-dose inter-vention group and model group (P > 0.05). Conclusions Astragaloside may dose-dependently protect against VMC by in-hibiting IL-23/IL-17 signaling pathway.

Objective To explore the expression of interleukin-17 (IL-17) in the murine myocardium with viral myocarditis (VMC) ,and the influence of astragaloside intervention on its expression .Methods 60 male 4-week-old Balb/c mice were randomly divided into four groups ,namely normal control group ,model control group ,low-dose and high-dose intervention groups ,15 mice in each group .Mice in the latter three groups were inoculated with 0 .1 mL coxsackie B3 virus intraperitoneally .Then ,mice in low-dose and high-dose intervention groups were treated with 0 .01 g/L and 0 .09 g/L astragaloside solution ,respectively .All mice were killed on 15 days .The mortality and heart weight/body weighty (HW/BW ) were calculated .Histological cross sections of heart were stained with hematoxylin-eosin and histopathologic scores of inflammatory cells infiltration and myocardial necrosis were eval-uated under optical microscope .The expression levels of myocardial IL-17 mRNA and protein were detected through real-time quan-titative PCR and Western blot .The contents of IL-6 and tumor necrosis factor-α(TNF-α) in the myocardium were examined by ELISA .Results The mortality and histopathologic scores of inflammatory cells infiltration and myocardial necrosis in high-dose in-tervention group were significantly lower than those in model controlgroup (P<0 .05) .Compared with normal control group ,the HW/BW ,the expression levels of myocardial IL-17 mRNA and protein as well as the contents of IL-6 and TNF-αin the myocardi-um were markedly increased in model control group(P<0 .01) ,whereas these parameters were significantly decreased in high-dose intervention group as compared to model group (P<0 .05) .Conclusion IL-17 may be involved in the pathogenesis of VMC .The therapeutic effect of astragaloside on VMC may be associated with inhibiting IL-17-mediated inflammatory response .

The development of primary or acquired taxane resistance inevitably becomes to be the main problem.Ixabepilone is effective in metastatic breast cancer (MBC) patients including those heavily pretreated or resistant to taxanes.Eribulin has been used for the treatment of MBC patients who have received at least two prior chemotherapy regimens.New microtubule-targeting agents are promising to be effective options for patients progressing after standard taxane-containing chemotherapy.

Objective:To study the anti-tumor effects by vaccination of mice with murine melanoma B16 cells expressing calreticulin (CRT) and Human papillomavirus 16 E2 fusion protein.Methods:Mice were inoculated with B16 cells expressing CRT,E2,or CRT-E2 by intraperitoneal injection. The inoculation was repeated after one week. The activity of CTLs and NK cells,the proliferation of T cells and the amount of IFN-? secreted by spleen lymphocytes were analysed.Results:The activity of CTLs and NK cells,and the amount of IFN-? secreted by spleen lmyphocytes from mice vaccinated with CRT-E2 fusion protein were significantly higher than those of the other groups(P

Objective To investigate whether miR-200a suppresses cell proliferation by targeting AP-2γexpression, and reveal molecular mechanism that miR-200a functions as a tumor-suppressor in neuroblastoma cells. Methods Dual-luciferase reporter gene assay was employed to examine the effect of miR-200a on AP-2γpromotor luciferase activity. Neu-roblastoma cells were transfected with miR-200a mimics, and the expressions of AP-2γmRNA and protein were detected by RT-PCR and Western blot assay. The effects of AP-2γdown-regulation on cell proliferation were observed after AP-2γshRNA was transfected into neuroblastoma cells. Neuroblastoma cell proliferation was detected by MTS assay after being co-transfected with miR-200a mimics and AP-2γplasmid. Results Results showed that miR-200a could inhibit proliferation of neuroblastoma cells at cell viability (66.33 ± 5.13) compared with that of control group (100 ± 0), and also miR-200a can bind to the 3'untranslated region of AP-2γpromotor and inhibit its luciferase activity with an inhibit ratio at (0.624±0.051). AP-2γmRNA and protein expressions were significantly down-regulated when miR-200a was over-expressed in neuroblas-toma cells. Furthermore, results showed that shRNA-mediated down-regulation of AP-2γthat suppressed the cell prolifera-tion of neuroblastoma at (62.5±2.4) by comparing with the control group (100±0). Moreover, restoring AP-2γexpression re-versed the effect of miR-200a with a cell viability suppression at (92.4±1.4). Conclusion miR-200a suppresses cell prolif-eration by targeting AP-2γexpression in neuroblastoma cells.

Background and purpose:MicroRNAs are 19 to 25-nucleotide noncoding RNA molecules. The aim of this article was to investigate the expression and clinical signiifcance of microRNA-141 in childhood B-cell acute lymphoblastic leukemia (ALL). Methods:Bone marrow samples were collected from 35 children with B-cell ALL and 15 children with non hematologic disease. Total RNA was acquired from bone marrow. Real-time PCR was performed to detect the expression level of miR-141. Results:The relative expression level of miR-141 in B-cell ALL group was remarkably lower than those in the control (P<0.05). The expression of miR-141 in newly diagnosed samples was lower than those in Day 30 and Week 12 samples respectively (P<0.05). Besides, the expression of miR-141 in Day 30 samples was lower than those in week 12 samples (P<0.05). The expression of miR-141 in children over 10 years old was signiifcantly lower than those in children under 10 years old (P<0.05). The expression of miR-141 in low-risk group was higher than those in mid-risk and high-risk group respectively (P<0.05), and there was signiifcant difference between mid-risk and high-risk groups (P<0.05). Conclusion:MiR-141 is likely to have tumor suppressor effect and to be a potential prognostic biomarker in childhood B cell ALL.

Objective To explore the expression and clinical signiifcance of microRNA-200a in childhood B-cell acute lymphoblastic leukemia (ALL). Methods Bone marrow samples were collected from 45 children with B-cell ALL and 18 chil-dren without hematology disease as control. Total RNA was acquired from bone marrow. qRT-PCR was performed to detect the expression level of miR-200a. Results The relative expression level of miR-200a in B-cell ALL group was signiifcantly lower than that in control group (P<0.05);the expression of miR-200a in children over 10 years old was signiifcantly lower than those in children under 10 years old (P<0.05);the expression of miR-200a in newly diagnosed samples was lower than those in those samples taken on Day 33 and at Week 12, respectively (P<0.05, P<0.01). In addition, the expression of miR-200a in low-risk group was higher than those in mid-risk and high-risk group, respectively (P<0.05). Conclusions Low level of miR-200a had a close correlation with the development and prognosis of childhood B cell ALL, which could be used as a potential target of thera-py and a biomarker of childhood B cell ALL in the future.

Objective To investigate the role of recombinant Vibrio vulnificus cytolysin (rVvhA) in inducing THP-1 cells damage and study the pathway of associated calcium influx .Methods Inverted mi-croscope, CCK-8 cell proliferation kit, Fluo3/AM staining and caspase activity detection were performed to analyze the damage of THP-1 cells induced by rVvhA and the pathway of calcium influx .Results rVvhA had cytotoxic effects on THP-1 cells in a dose-dependent manner .The concentrations of extracellular K +and LDH were respectively up-regulated after 1 h and 6 h of 12 μg/ml rVvhA intervention .Verapamil , Mibe-fradil and SKF-96365 could not prevent the influx of free Ca 2+induced by rVvhA .The activities of caspase-3 and caspase-9 were singanificantly enhanced by rVvhA in a time-dependant manner .Conclusion rVvhA can induce THP-1 cells damage through triggering extracellular calcium influx via porous channel on cell membrane.Moreover, rVvhA might induce THP-1 cell apoptosis through activating caspase-9/3-dependent pathway .

Objective To explore the effects of reoperation on treatment of recurrent pelvic endometriosis(RPEM).Methods The clinical data of 47 cases of RPEM reoperation in our hospital from April 2005 to October 2010 was investigated,and the efficacy was analyzed compared with the first operation data.Results The cases of painful nodules was significantly different between reoperation group and the first operation group(28 vs 14,x2 =8.436,P =0.004 ).There was significant difference on laparoscopic surgery cases between reoperation group and the first operation group (25 vs 40,x2 =7.259,P =0.007 ).The operation time in reoperation group was significantly longer than that in the first operation group( [ 106.4 ±41.0] min vs [ 78.4 ± 26.4 ] min,t=3.995,P ＜ 0.01 ),and the amout of intraoperative hemorrhage in reoperation group was more than that in the first operation group ( [ 143.2 ± 118.3 ] ml vs [ 70.6 ± 68.1 ] ml,t =3.660,P ＜ 0.01 ).However,there was no significant difference on symptoms,cyst location and clinical stage between these two groups(P ＞0.05).Conclusion Due to the pelvic adhesion would be dense and extensive in RPEM,it should be carefully dissected during reoperation.At the same time,the operator should pay attention to the anatomical location and try to restore the normal anatomy of the pelvic organs and physiological state,and try to reduce postoperative adhesions.Complete removal of the lesions is the key to improve the treatment effect and prevent recurrence and reoperation.

AIM: To detect the expression of the Calreticulin and HPV E2 Fusion Protein in B16, and study the effects on proliferation and apoptosis of B16 cell lines in vivo. METHODS: To construct eukaryotic fluoresce expression vector pEGFP-CRT-E2, pEGFP-CRT and pEGFP-E2. Then the recombinant plasmids were transfected into B16 cells by Lipofectamine 2000. The expression of proteins was detected by Western blot. The location of different GFP fusion proteins in B16 was tested by inverted fluoresce microscope. Flow cytometry was applied to detect the effects of fusion proteins on the growing of B16 and then the apoptosis effects of B16 induced by different proteins were observed. RESULTS: The correctly constructed recombinant plasmid pEGFP-CRT-E2 and the expression of CRT-E2 gene could be detected in B16 cells. Apoptosis of B16 cells could be detected after the transient transfection. Meanwhile, the apoptosis rate of B16 cells transfected by pEGFP-CRT-E2 was much higher than that of control cells. And cell cycle G1/G0 arrest was also found (P < 0.01). CONCLUSION: The eukaryotic expression plasmid pEGFP-CRT-E2 is successfully constructed and it could correctly express the fusion protein in B16 cells. And the B16 cells transfected by plasmid pEGFP-CRT-E2 could induce apoptosis.