ABSTRACT
This work was supported by Science and Technology Program of Health and Family Planning Commission of Jiangxi Province (No.20161106) Abstract Objective: To investigate the prognostic value of subventricular zone (SVZ) invasion in glioma patients. Methods: The clini-cal data of 175 patients with glioma diagnosed based on pathology in Jiangxi Province Cancer hospital between January 2010 and July 2015 were analyzed retrospectively. There were 59 cases of World Health Organization (WHO) gradeⅡ, 59 cases of WHO gradeⅢ, and 57 cases of WHO gradeⅣat the first diagnosis. There were 75 cases of SVZ invasion (SVZ+) and 100 cases of SVZ non-invasion (SVZ-) according to preoperative magnetic resonance imaging. The survival outcomes of both cohorts were compared using the Log-rank test. The correlation between the recurrence pattern and SVZ involvement was analyzed using Chi-square tests. Results: The me-dian follow-up time was 63 months. The 5-year overall survival (OS) and progression-free survival (PFS) rates were 42.2% and 37.5%, respectively. These were 20.9% and 15.3% in the SVZ+group, compared with 57.1% and 44.1% in the SVZ-group, respectively (P<0.001 and P<0.001, respectively). The SVZ+group had fewer cases of total resection, larger lesions (maximum diameter greater than 5.0 cm), and more cases of gradeⅣ(P<0.001, P<0.001, and P=0.018, respectively). There were 89 cases of recurrence. The total recur-rence rate was 62.7% in the SVZ+group, compared with 42.0% in the SVZ-group (P=0.007); the distant recurrence rates were 21.3% and 7.0% (P=0.004), respectively. Conclusions: SVZ invasion is a poor prognostic factor for OS and PFS in gliomas, which is positively correlated with a low total resection rate, large lesions, and gradeⅣlesions, and increases the probability of total recurrence and dis-tant recurrence.
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Aim Toclarifytheeffectofacteosideon proliferation of neural stem cells (NSCs ) from adult mice,as well as the involved signaling pathway.Meth-ods NSCswereisolatedfromthesubventricularzone (SVZ)of adult C57BL/6 mice,then identified by im-munofluorescence staining with Nestin,the marker of NSCs.NSCs were exposed to acteoside (5,10,20,40μmol·L-1 )in absence of mitogen(EGF/bFGF)for 24 h.We employed CCK8 assay to detect NSCs viability and BrdU staining to identify NSCs proliferation.We performed Western blot to quantify the expression level ofp-AktinducedbyacteosideonNSCs.Results With-out mitogen,acteoside increased NSCs proliferation by activating p-Akt,which can be blocked by LY294002, the inhibitor of PI3K/AKT signaling pathway.Conclu-sion ActeosidepromotestheproliferationofNSCsfrom adult mice by activating PI3K/AKT pathway.
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0.05).In SVZ,nNOS expression in ischemic model group was reduced on days 1-14,but increased on day 21;after Ligustrazine administration,nNOS expression was obviously decreased on days 3-14 in all Ligustrazine dose groups,but began to increase on day 21.In CC,nNOS expression in ischemic model group was reduced on days 3-14,and began to increase on day 21;in the different-dose Ligustrazine groups,nNOS expression was significantly decreased on days 3-14,especially in medium-and high-dose groups,but increased on day 21.In striatum and cortex peri-infarction,nNOS expression in ischemic model group was obviously decreased on days 3 and 7,but enhanced on days 14 and 21;in various-dose Ligustrazine groups,nNOS expression was decreased on days 3-21,especially in medium-and high-dose groups,but increased slightly on day 21.In DG and CA1 areas,nNOS expression in ischemic model group was reduced on days 3 and 7,but began to increase on day 14;nNOS expression in all Ligustrazine groups were decreased during 3-21d.There were significant differences between ischemic model group and different-dose Ligustrazine groups at different time points(P