Through the microarray analysis, long noncoding RNA TPT1-AS1 (TPT1-AS1) was identified in the development of glioma. However, the specific effect of TPT1-AS1 on glioma autophagy in the recent years has not fully been investigated. Therefore, the purpose of our present study is to investigate the function of TPT1-AS1 on affecting autophagy of glioma cells through regulation of microRNA-770-5p (miR-770-5p)-mediated stathmin 1 (STMN1). Initially, the expression of TPT1-AS1, miR-770-5p, and STMN1 were determined in glioma cell lines, followed by the prediction and validation of their interaction. After that, the effects of TPT1-AS1, miR-770-5p, and STMN1 on the in vitro glioma cell proliferation and autophagy were assessed using EdU assay and macrophage-derived chemokine (MDC) and on the in vivo tumor development and autophagy were evaluated using a nude mouse xenograft tumor assay and immunofluorescence assay. In comparison with the normal cells, the glioma cells displayed upregulated expression of TPT1-AS1 and STMN1, but a downregulated miR-770-5p expression. miR-770-5p, which directly targeted STMN1, could be downregulated by TPT1-AS1. Subsequently, in glioma cells, TPT1-AS1 can function to competitively bind to miR-770-5p, thus regulatEing STMN1 expression. Moreover, glioma cell proliferation and autophagy could be mediated through the TPT1-AS1/miR-770-5p/STMN1 axis. From our data we conclude an inhibitory function of TPT1-AS1 in glioma cell autophagy by downregulating miR-770-5p and upregulating STMN1, which may be instrumental for the therapeutic targeting and clinical management of glioma.

With secure and dependable antihypertensive effects, telmisartan is an antihypertensive drug. Telmisartan was reported showing distinct neuroprotective effect in cerebral IR injury but the underlying mechanisms are still unclear. The aim of this study was to evaluate the effect of telmisartan prevents cerebral ischemia-reperfusion (I/R) injury-mediated oxidative stress and inflammation in model rat to explore possible molecular mechanism. Male Sprague-Dawley (SD) rats were used to induce cerebral I/R injury using middle cerebral artery occlusion. 30 SD rats were randomly and evenly divided into 3 groups: Sham, I/R, telmisartan treated ischemia-reperfusion group. The results showed that telmisartan improved neurological impairments, inhibited apoptosis, resisted oxidative stress and inflammation in hippocampus of cerebral I/R injury rats. However, pretreatment with telmisartan inhibited the activation of adrenocorticotropic hormone (ACTH), vasopressin, catecholamine and natriuretic peptides activities in cerebral IR injury rat. These findings confirm the involvement of telmisartan prevents cerebral ischemia-reperfusion injury-mediated oxidative stress and inflammation in model rat.

As a phosphatase, SHP-2 has been identified to be involved in regulating several cell functions, including growth, division, adhesion and motility. Therefore, SHP‑2 may affect the response of glioma to radiotherapy, such as via enhancing angiogenesis. The present study aimed to investigate the function of SHP‑2, a protein tyrosine phosphatase, in the radiosensitivity of glioma. U251, U87 and SHG44 glioma cell lines were transfected with small interfering (si)RNA against SHP‑2 and cell proliferation was assessed using a cell counting kit 8 assay, cell apoptosis was assessed by fluorescence‑activated cell sorting and immunoblotting, cell invasion was determined by an invasion assay, and the vasculogenic mimicry capacity was assessed by a tube formation assay. SHP‑2 siRNA transfection reduced the proliferation and increased apoptosis in the glioma cell lines. Downregulation of SHP‑2 suppressed glioma cell invasion and vasculogenic mimicry. These results demonstrated that no significant difference was observed between glioma tissues and normal brain tissues, however, silencing of SHP‑2 inhibited cell proliferation, invasion and vasculogenic mimicry in the glioma cell lines. SHP‑2 may be a novel therapeutic target for glioma.

Objective To investigate the relationship between the expression of connective tissue growth factor(CTGF) and aggressive of human pituitary adenom,that provides the theoretical basis for the biological treatment of pituitary adenoma. Methods Quantitative real time PCR( qRT-PCR) and Western blot were used to detecte the expression of CTGF in 16 cases of non-invasive pituitary adenoma and 52 cases of invasive pituitary adenoma(IPA) . Results CTGF expression was found in all cases of invasive pituitary adenomas and noninvasive pituitary adenomas. The expression of CTGF in invasive pituitary adenoma was higher than that of in noninvasive pituitary adenoma(P=0. 01) . Conclusions The expression of CTGF in invasive pituitary adenoma is significantly higher than that of in the noninvasive pituitary adenoma and related with the size of pituitary adenoma.

Objective: To investigate stathminin expression in human gliomas and normal brain specimans derived microvessels endothelial cells(GDMEC).Methods: Microvascular endothelial cells from human gliomas(GBMEC,n=68) and normal brain(NBMEC,n=20) were purified by incubating with magnetic beads coated with anti-CD105 antibody.There were 24 cases of low grade gliomas(WHOⅠ-Ⅱgrade) and 44 high grade gliomas(WHO Ⅲ-Ⅳgrade).Expression rates and cellular distribution of stathmin in GDMEC and NBMEC were also investigated by immunohistochemistry.Semiquantitative RT-PCR and Western blot were used for comparing the exp-ression of stathmin in GDMEC and NBMEC.Results: Immunohistochemical analysis demonstrated that the rates of stathmin expression in NBMEC,low grade GDMEC,and high grade GDMEC were 20%,66%,and 95%,respectively(P0.05).The expression of stathmin in GDMEC was higher than that in NBMEC.The difference betweenⅠ-Ⅱgrade,Ⅲ-Ⅳgrade and normal human brain tissues were significant(P0.01) respectively.The difference betweenⅠ-Ⅱgrade and Ⅲ-Ⅳ grade was significant(P0.01).Conclusions: With the rise of pathological grades of glioma,the expression of stathmin increased,and it may represent a novel tumor-related target for the therapy of malignant gliomas.

Objective To study the skills of facial nerve and cochlear nerve reservation in acoustic neurinoma surgery. Method 76 patients with acoustic neurinoma were operated via suboccipital retrosigmoid transmeatal approach. Intraoperative electromyographic monitoring,drug treatment( Nimodipine) and microsurgical techniques were used. The facial nerve and cochlear nerve function were evaluated before and after surgery, as well as 1 year after the surgical procedure. Results Total tumor resection was achieved in 71 patients (93% ). Facial nerve was kept anatomicly intact completely in 74(97% ) patients, while the rate of cochlear nerve was 21% (16 patients). One week after surgery,an HB score of Ⅰ was documented in 25 patients,HB Ⅱ in 32.HB Ⅲ in 11 ,HB Ⅳ in 4,HB Ⅴ in 2 and HB Ⅵ in 2 patients. After 1 year,an HB score of Ⅰ was documented in 37 patients,HB Ⅱ in 24,HB Ⅲ in 9,HB Ⅳ in 3 ,HB Ⅴ in 1 and HB Ⅵ in 2 patients. One year after surgery, the hearing function was kept in 16 patients (21% ). Conclusions Effective nerve function monitoring,excellent microsurgical skills and drug treatment are very important for keeping facial nerve and cochlear nerve function in acoustic neurinoma surgery.

Objective To investigate the expression of Stathmin/oncoprotein 18 (Op18) in human brain gliomas and its significance.Methods Fifty-six cases of human brain gliomas were examined by immunohistochemical staining and Western blot method (including 10 cases of normal cerebral tissues).Results The immunohistochemical analysis demonstrated that the positive rate of Stathmin in normal human brain tissues, grade Ⅰ~Ⅱ gliomas and grade Ⅲ~Ⅳ gliomas were 20%, 65% and 100% respectively. There was significant difference between normal human brain tissues and grade Ⅰ~Ⅱ glioma, grade Ⅲ~Ⅳ gliomas (P0.05) respectively; the difference between Ⅰ~Ⅱ grade glioma and Ⅲ~Ⅳ grade glioma was significant (P0.05). The expression level of stathmin in the gliomas was higher than that of normal brain tissues by Western blot method. There were significant difference between normal brain tissues and grade Ⅰ~Ⅱ glioma, grade Ⅲ~Ⅳ glioma (P0.01) respectively; the differences between grade Ⅰ~Ⅱ glioma and grade Ⅲ~Ⅳ glioma were significant (P0.01). Conclusion Stathmin overexpresses in human brain gliomas which may be a new biotherapy target in the treatment of brain gliomas.