Wnt/β-catenin signaling pathway is highly conserved in evolution,which involves in the regulation of a variety of biological processes such as embryonic growth,development,energy metabolism and stem cells maintenance.Aberrant activation of Wnt/β-catenin signaling pathway has a closely relationship with tumorigenesis.Investigating the role of Wnt/β-catenin signaling in glioma cell proliferation,invasion,apoptosis and tumor angiogenesis will provide novel therapeutic targets and intervening measures for glioma treatment.

the effect of maintaining integrity of epithelial cells by increasing occludin protein expression,and the effect is related with the up-regulation of occludin mRNA.

Adult ; Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cyclin D1 ; metabolism ; Female ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Male ; Middle Aged ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mouth Mucosa ; chemistry ; metabolism ; pathology ; Mouth Neoplasms ; metabolism ; pathology ; Prognosis

OBJECTIVE:To a evaluation method for the measurement uncertainty for the content of Bisacodyl enteric-coated tablet. METHODS:HPLC external standard method was conducted for content determination of Bisacodyl enteric-coated tablet, and mathematical model for uncertainty evaluation was established to systematically analyze and evaluate the influential factors in processes of solution preparation and instrument measurement. RESULTS:HPLC external standard method showed the content was 97.8%,confidence probability was 95%,expanded uncertainty was 2.8%,and determination result was (97.8 ± 2.8)%,k=2. CONCLUSIONS:The established method is suitable for the evaluation of measurement uncertainty for the content of Bisacodyl en-teric-coated tablet. Regularly calibrated verification for HPLC equipment and strict control of the weighing process will help to im-prove the accuracy measured by HPLC.

Objective To evaluate the educational effectiveness of feedback debriefing in clinical training.Methods Forty medical students and fifteen teachers were enrolled in the 2015 after-internship clinical training,which was newly designed to obtain the debriefing part.The test scores and single technical practices were collected and analyzed,before and after the training.DASH scoring system was used to evaluate the effect of debriefing in the team simulation.Results were statistically analyzed by SAS 9.2(SAS institute Inc).Quantitative data were described by x ± s,while qualitative data were described by number and/or constituent ratio.Student's t test and Wilcoxon rank sum test were applied as needed.A P-value ＜ 0.05 was considered to be significant.Results The scores of the students before and after the assessment were (41.88 ± 8.54) vs.(65.06 ± 13.83),and the difference was statistically significant(P=0.000).Individual skills before and after the course had a different degree of improvement.The average DASH-scores evaluated by the students,teachers and supervisors were (39.3 ± 2.12) (very good),(35.1 ± 4.18) (good) and (37.2 ± 3.03)(very good),separately.Conclusions Potent debriefing helps to improve the effectiveness of simulationbased clinical training.

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Background N-ethyl-N-nitrosourea (ENU)-induced mouse mutagenesis is a powerful approach for the study of gene function and the generation of human disease models.Objective This study was to create the corneal morphologic change and map the mutant gene of a kind of corneal opacity in ENU mutagenesis in mouse.Methods ENU was intraperitoneally injected in forty C57BL/ 6J (B6) male mice aged 8-10 weeks old.The male mice were mated with the same strain female mice.Their progenies were screened for visible eye mutation,and the mutant mice were mated with the same strain mice to confirm the heredity of mutation phenotypes.Hematoxylin & eosin staining was used to examine the histopathological change of cornea in one mouse with ENU-induced corneal opacity.To map the mutant gene,[(B6×D2)F1 ×B6] N2 mutant mice were bred,and the genome of the N2 mice was scanned by microsatellite markers distributed equally on the mouse chromosome.The microsatellite linked to the mutant gene was determined by the log odds score.This experimental procedure was approved by Ethic Committee about Experimental Animal Care and Use of Yangzhou University.Results The founder mouse,which was the progeny of an ENU-treated B6 male mouse and an untreated B6 female mouse,had a corneal opacity phenotype.After mating the mutant with B6 mice,19 of 59 descendants appeared corneal opacity phenotype.Thickening of corneal stroma,neoangiogenesis,infiltration of inflammatory cells and proliferation of fibroblasts were exhibited in cloudy cornea in ENU-induced mutated mice under the optical microscope.After linkage analysis between microsatellite markers and the mutant gene,the mutant gene was linked to D2Mi307,which was located at 63.42 cM.Three cases of 26 N2 mice underwent recombination with the LOD 3.79.The mutant gene associated with the cornea phenotype was located on chromosome 2.Conclusions This study map the mutant gene associated with the cornea phenotype on chromosome 2.The strain might be used as a mouse model for heritable human corneal opacity.

Objective To investigate the protective effects of MicroRNA-214 on myocardial injury induced by myocardial ischemia and reperfusion,as well as the regulation mechanism of PI3K and its downstream protein kinase B(AKT)and FoxO1(PI3K / AKT / FoxO1).Methods Wistar rats were randomly divided into 4 groups:sham operation group(Sham group),myocardial ischemia reperfusion injury(IRI)group(IRI group),microRNA-214+sham operation group(MS group),microRNA-214+IRI group(MI group),(n=10,each).The cardiac function was detected at 6 h after ischemia-reperfusion operation.And blood lactate dehydrogenase(LDH),creatine kinase(CK),creatine phosphate kinase isoforms MB(CK-MB),cardiac troponin T(cTnT),serum B natriuretic peptide(pro-BNP)in plasma were detected by enzyme-linked immunosorbent assay(ELISA).Interleukin 10(IL-10),Interleukin 6(IL-6)and tumor necrosis factor α(TNF-α)were assayed.Pathological changes of myocardial tissue were detected by HE and Masson.The expression of microRNA-214 was detected by RT-PCR.The expression of Bax,Caspase-3,BCl2,PI3K,Akt,FoxO1 was detected by Western Blot.Results Compared with Sham group,IRI group showed a significantly increases in myocardial injury parameters of LDH,CK,IL-6 and TNF concentration in plasma,and a significantly reduced concentration of IL-10(P<0.05).And compared with Sham group,MI group showed a significantly increased expression of microRNA-214(P<0.05)and showed a significantly increased myocardial parameters of Bax,Caspase-3,PI3K,Akt protein,and a decreased level of BCl2,FoxO1(P<0.05).Compared with IRI group,microRNA-21 group showed a reduced myocardial ischemia-reperfusion-induced myocardial injury in rats and a reduced plasma concentration of LDH,CK,IL-6 and TNF-alpha,a inhibited expression of caspase-3,Bax,myocardial PI3K and Akt,and a promoted expression of BCl2 and FoxO1 protein(P<0.05).Conclusions MicroRNA-214 reduces the myocardial injury induced by myocardial ischemia-reperfusion through PI3K/Akt signaling pathway.

Objective To investigate the influences of UVA on the secretion and expression of chemokine CXCL11/I-TAC by HaCaT cells induced by interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α). Methods HaCaT cells were cultured in the presence of IFN-7 and TNF-a and irradiated with UVA of 2, 4 and 8 J/cm~2, respectively; those cells receiving neither treatment with IFN-γ or TNF-α nor UVA irradiation served as the negative control, and those receiving only cytokine treatment but no irradiation as the positive control. After another 24-hour culture, enzyme-linked immunosorbent assay (ELISA) was performed to detect the protein levels of CXCL11/I-TAC in the supernatant of HaCaT celb, real time PCR to measure the mRNA expression of CXCL11/I-TAC in these HaCaT cells. Results As far as the negative control HaCaT cells were concerned, there was a minor secretion of CXCL11/I-TAC protein and expression of CXCL11/I-TAC mRNA. After treatment with IFN-7 and TNF-a of 10 μg/L, the protein and mRNA expressions of CXCL11/ I-TAC were synergistically upregulated, whereas the induced secretion and expression of CXCL11/I-TAC by HaCaT cells were dose-dependently inhibited by UVA irradiation. Conclusions UVA irradiation inhibits the secretion and expression of CXCL11/I-TAC by HaCaT cells, which in turn suppresses the chemotaxis of Th1/ Tel cells in some degree.

Objective:To investigate the expression of Th1 chemokine CXCL9,CXCL10,CXCL11,Th2 chemokine CCL22 and their receptors in the lesions of bullous pemphigoid (BP).Methods:Immunohistochemical assay was performed to detect the expression of CXCL9,CXCL10,CXCL11,CCL22 and their receptors CXCR3 and CCR4 in BP lesions and normal control skin.Results:CXCL9,CXCL10,CXCL11,CCL22,CXCR3 and CCR4 were overexpressed in BP lesions than those in normal control skin (P＜0.01).The positive rates of CXCL9,CXCL10,CXCL11 and CXCR3 in BP lesions were 50%(15/30),46.7%(14/30),46.7%(14/30) and 53.3%(16/30),respectively.The positive rates of CCL22 and CCR4 were 66.7% (20/30) and 56.7% (17/30).Conclusion:The overexpression of Th1 chemokine CXCL9,CXCL10,CXCL11,Th2 chemokine CCL22 and their receptors may play important roles in the pathogenesis of BP.