Objective To study the correlation of supratentorial gliomas and ependymoma between the features of pathology and the characteristic of CT,MRI and provide relevant data for diagnosis and treatment.Methods We analysised 60 patients with gliomas and 40 with ependymoma,contrasted their characteristic of CT,MRI with the features of pathology.Results The feature of irregular appearance,lobulation,tumor wall,tumor tubercle,necrotic cystiform zone,hemorrhage and tumor blood vessels were showed in CT and MRI,which was accord with the alteration of ultrastructure and the expression of tumous label.Conclusion Studying the morphology of supratentorial gliomas and ependymoma may be helpful to raise the veracity of pathologic grading,provide evidence to select treatment,operation and anti-vasoformation of the tumor etc.

To promote understanding and improve diagnostic level of Rathke′s cysts with CT and MRI,crosscheck analysis was performed between CT,MRI and operative pathology was done in 6 cases.Results: It was misdiagnosed as cranio pharyngioma,hypophysoma and cholesteatoma in CT and MRI before operation.Oval and irregular cystic low density was showed in CT in 4,oval iso density and higher density in 1,respectively,and line like reinforcement of the cystal wall in 2 after intensification.Oval and oval like low signals were showed in 3 and isosignals in 1 on T 1 weighted images of MRI and high signals with clear edge on T 2 weighted images.It suggested that the diagnostic value of MRI was superior to that of CT in Rathke′s cysts.

Objective To investigate the correlation of rCBV with vascular endothelial growth factor (VEGF) protein expression and microvessel density (MVD) in gliomas Methods MR examinations were performed preoperatively in 46 patients with suspected supratentorial gliomas All the 46 cases were proved by operation and pathology Immunohistochemical stain methods were used to demonstrate the situation of VEGF protein expression and quantitatively measure the MVD in gliomas The procedures of MR examinations included plain MR scan, PWI and routine contrast enhanced MR scan The pulse sequence of PWI was single shot GRE EPI T  2WI The CBV maps were calculated from the original data of perfusion images and the maximum rCBV of gliomas was acquired from CBV maps through measurement on the region of interest (ROI) According to the situation of VEGF protein expression, all the 46 cases were divided into two groupsincluding positive VEGF protein expression group and negative VEGF protein expression group Mann Whitney U test was used for comparing the difference between the two groups Spearman′s rho correlation analysis was used for observing the correlation between maximum rCBV and MVD in gliomas Results Of the 46 cases; 12 cases were astrocytomas, 3 were oligodendrogliomas, 1 was mixed glioma, 14 were anaplastic astrocytomas, and 16 were glioblastomas multiforme The maximum rCBV value in VEGF(-) group ( n =14) and VEGF(+) group ( n =32) ranged from 0 33～6 63 and 1 03～10 68, with median of 3 08 and 5 95, respectively The difference in maximum rCBV between the two groups was statistically significant ( Mann Whitney U test | z| =2 638, P

Objective：To investigate the effect of long-chain non-coding RNATTTY10 (lncRNATTTY10) on the migration and invasion of cervical cancer cells, and to explore its regulatory effect on miR-490-3p and HMGB1 (high mobility group box 1) signaling pathways. Methods: Fourteen paris of cervical cancer tissues and corresponding paracancerous tissues resected at the Department of Obstetrics and Gynecology,Affiliated Wuhan Central Hospital of Tongji Medical College fromAugust 2013 to December 2014 were collected for this study. The expression of TTTY10 in cervical cancer tissue and different cervical cancer cell lines were detected by qPCR. Plasmids encoding TTTY10-siRNA or empty plasmids were transfected into cervical cancer CasKicells, and the transfection efficiency was detected by qPCR. Transwell migration assay and Transwell invasion assay were used to detect the migration and invasion abilities of cervical cancer cells after TTTY10 silencing. qPCR was used to detect the expression of miR-490-3p and HMGB1 mRNA after TTTY10 silencing. Dual luciferase reporter assay validated the interaction between miR-490-3p and HMGB1. Western blotting was used to detect the expression of HMGB1 signaling pathway related proteins after TTTY10 silencing. Results: The expression of TTTY10 in cervical cancer tissues was significantly higher than that in paracancerous tissues (P<0.01), the expression of TTTY10 in cervical cancer cell lines was significantly higher than that in cervical epithelial cells (P<0.01). TTTY10-siRNAplasmids could efficiently transfectCasKicells to knockdown TTTY10 expression (P<0.01). Silencing of TTTY10 inhibited the migration and invasion of cervical cancer CasKi cells (P<0.05), promoted the expression of miR-490-3p (P<0.01) and inhibited the expression of HMGB1 mRNAin cervical cancer (P<0.05 or P<0.01). miR-490-3p could specifically bind to the 3'-UTR of HMGB1 mRNA(P<0.01). HMGB1 signaling pathway related proteins were down-regulated after TTTY10 silencing. Conclusion: TTTY10 can target regulate the expression of miR-490-3p and affect the migration and invasion ability of cervical cancer CasKi cells through the HMGB1 signaling pathway; TTTY10 can be used as a diagnostic marker and potential treatment target of cervical cancer.

Objective: To investigate the expression of microRNA-380-5p (miR-380-5p) in cervical cancer tissues and cell lines, and to explore the mechanism of miR-380-5p inhibiting the proliferation and migration of cervical cancer cells. Methods: 16 pairs of cervical cancerous tissues and corresponding para-cancerous tissues were collected from the Department of Obstetrics and Gynecology, the Affiliated Wuhan Central Hospital of Tongji Medical College from December 2016 to July 2017; in addition, cervical cancer cell lines (HCC94, C33A, Hela, SiHa) and human cervical epithelial immortalized H8 cells were also collected for this study. The expression of miR-380-5p in above mentioned tissues and cell lines was detected by Real-time quantitative polymerase chain reaction (qPCR). miR380-5p mimic (experimental group) and miR-NC (negative control group) were transiently transfected into C33A cells by lipofection, and qPCR was used to detect the expression of miR-380-5p in the transfected cells. Cell proliferation and migration were evaluated by cell counting kit (CCK-8) and Transwell assay. Bioinformatics software TargetScan predicted the downstream genes of miR-380-5p, and dual luciferase reporter assay was used to verify the binding of miR-380-5p to the downstream gene RHOA (Ras homolog gene family member A). qPCR and Western blotting were used to detect the expression of miR-380-5p downstream gene-RHOA. Results: The expression level of miR-380-5p in cervical cancer tissues and cell lines was significantly lower than that in para-cancerous tissues and normal cervical epithelial H8 cells (P<0.01); and the expression in C33A cells was the lowest (P<0.01). Compared with the negative control group, the miR-380-5p mimic transfection singnificantly inhibited the proliferation (P<0.05) and migration ability of C33A cells (P<0.01), and down-regulated protein expressions of RHOA, ROCK1, ROCK2, CDK2 and N-cadherin (all P<0.01). Bioinformatics software predicted that RHOA may be a downstream gene of miR-380-5p, and dual luciferase reporter assay proved the specific binding of miR-380-5p to the 3'UTR of RHOA (P<0.01). miR-380-5p could significantly down-regulate RHOA gene expression (P< 0.01). Conclusion: miR-380-5p is low-expressed in cervical cancer cell lines. Over-expression of miR-380-5p may inhibit the proliferation and migration of cervical cancer C33Acells by down-regulating the expression of RHOAgene and its downstream proteins.