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BACKGROUND: Our previous study was the first to find that bone marrow stromal cells could secrete neutrophil chemokine-3. Moreover, the expression of cytokine-induced neutrophil chemoattractant 3 (CINC-3) could be up-regulated by 1. 5 times during the differentiation of neural stem cells into neurons regulated by bone marrow stromal cells. These results suggest that CINC-3 may promote the proliferation and differentiation of neural stem cells. OBJECTIVE: To observe the effect of CINC-3 on survival and proliferation of hippocampal neural stem cells in neonatal rats. METHODS: Hippocampal neural stem cells from neonatal Sprague-Dawley rats were isolated and cultured in vitro, and passage 3 neural stem cells were divided into control and CINC-3 groups. The survival rate of the cells was measured by MTS method, cell survival and proliferation were observed using cell growth curve and live/dead cell staining, and the expression of Nestin in neural stem cells was detected by real-time PCR and immunofluorescence staining for observation of neural stem cell proliferation. RESULTS AND CONCLUSION: (1) When the concentration of CINC-3 increased from 1 to 20 μg/L, the survival rate of neural stem cells increased gradually. When the concentration of CINC-3 was 10 μg/L, the survival rate of neural stem cells was the highest and the cell viability was the best (P < 0. 05). When the concentration of CINC-3 further increased to 20 μg/L, there was no significant difference in the survival rate of neural stem cells. (2) The positive rate of Nestin in the CINC-3 group was significantly higher than that in the control group (P < 0. 05). (3) The expression of Nestin mRNA in the CINC-3 group was significantly higher than that in the control group (P < 0. 05). These findings indicate CINC-3 can promote the survival and proliferation of hippocampal neural stem cells.
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Objective@#To analyze the prognostic value of CD7 expression in newly diagnosed acute myeloid leukemia (AML) patients, and to further explore the correlation between CD7 expression and CEBPA mutation, and to clarify the prognostic value of CD7+ in AML patients with wild-type (WT) or mutant-type (MT) CEBPA.@*Methods@#The clinical data of 298 newly diagnosed non-M3 AML patients between January 2010 and December 2016 were analyzed retrospectively. The clinical characteristics and prognosis of CD7+ and CD7- patients were respectively compared in all patients, and in patients with WT and MT CEBPA. The relationship between CD7 expression and CEBPA mutation was determined by chi-square, and the effects of CEBPA mutation on survival and prognosis in CD7+ group by Kaplan-Meier method.@*Results@#In CD7+ group, the frequencies of CEBPA mutation were 10.1% (single site) and 33.9% (double site) , significantly higher than those of the CD7- group (5.3% and 4.2%) (P=0.000) . Subgroup prognostic analysis showed a lower CR rate (P=0.001) and a higher RR (P=0.023) in CD7+ group comparing to those of CD7- group in AML patients with wild type CEBPA. There were no statistical difference between CD7+ group and CD7- group in overall survival (OS) and disease free survival (P>0.05) , while in the CEBPA mutant group the CD7+ group has higher OS (P=0.019) and DFS (P=0.010) . Based on the CD7 expression and CEBPA mutation, 298 cases were divided into 3 subgroups, named as CD7+-CEBPA MT group, CD7- and CD7+-CEBPA WT group. The 3-year OS of the 3 groups were 80.2%, 48.0% and 30.6%, respectively (P<0.001) , and the 3-year DFS were 74.1%, 37.4% and 22.2%, respectively (P<0.001) .@*Conclusion@#The CEBPA mutation rate was higher in CD7+ AML patients then that of CD7- patients. CD7 expression has opposite prognostic significance in AML patients carrying the wild-type or mutant-type CEBPA. Based on CD7 expression and CEBPA mutation, a new risk stratification model can be established, which is helpful to guide the clinical individualized treatment for AML patients.
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BACKGROUND:Isoflurane cannot only induce a wide range of large neuronal apoptosis, but also inhibit hippocampal neurogenesis in neonatal rats, thereby resulting in hippocampus-dependent learning and memory defects. OBJECTIVE:To investigate the isoflurane effect on proliferation and differentiation of the hippocampal neural stem cels. METHODS:Twenty-six Sprague-Dawley rats were randomly divided into air group and isoflurane group (n=13 per group). Rats in the isoflurane group were subjected to 2.5% isoflurane inhalation for 3 minutes folowed by 1.5% isoflurane inhalation for 4 hours. Rats in the air group only breathed in air. After the intervention, blood glucose and arterial blood gas changes were detected in the two groups. Additionaly, rats in the two groups were given intraperitoneal injection of 5-bromodeoxyuridine before and after intervention. At 24 hours after the last injection of 5-bromodeoxyuridine, brain tissues were taken to make frozen sections for immunofluorescence staining. RESULTS AND CONCLUSION:There were no significant difference in pH, PaO2, PaCO2, HCO3, BE and SaO2 levels between the two groups (P> 0.05). Compared with the air group, the number of BrdU+ cels was significantly less in the isoflurane group (P < 0.05), while the number of NeuroD+/BrdU+ cels was significantly higher in the isoflurane group (P < 0.05). The incidence of adverse reactions was 23% in the isoflurane group, which was significantly higher than that in the air group (7.7%;P < 0.05). These findings indicate that isoflurane can inhibit the proliferation of neural stem cels in the hippocampal dentate gyrus, and promote their differentiation into neurons.
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Objective To observe the migration and inhibition mechanism of MicroRNA218-Robo1 pathway for breast cancer.Methods A total of 40 BALB/c-nu/nu female mice were randomly divided into four groups.Each group was transfected over-expression MicroRNA218 MDA-MB-231 breast cancer cells, co-over-expression MicroRNA218 and Robo1 MDA-MB-231 breast cancer cells, knock-down Robo1 MDA-MB-231 breast cancer cells and the control MDA-MB-231 breast cancer cells.The tumor volume was examined every two weeks.Results Tumor volume of MicroRNA218 group was obviously less than control group, tumor volume of Robo1 knock out group was obviously less than common MicroRNA218 high expression and Robo1 group, the difference was statistically significant;MicroRNA218 and Robol knockout group than the control group, the increase in breast cancer cells apoptosis, cell proliferation and angiogenesis is restrained.Conclusions MicroRNA218 inhibited the migration of breast cancer by down-regulating the expression of Robo1.