Half of the mice were injected with GMCSF, the other with a placebo saline solution.
一半的小白鼠注射GMCSF，而另一半则注射安慰剂生理盐水。
Conclusions GMCSF-absence inhibits neovascularization during wound repair and leads to the delay of wound healing.
结论GMCSF基因缺失影响创面的新生血管化能力，进而影响创面的愈合。
Conclusion GMCSF can up-regulate the expression of VEGF in human skin fibroblasts, and ERK pathway plays an important role in this process.
结论GMCSF可促进人皮肤成纤维细胞VEGF表达，ERK通路在此过程中发挥重要作用。
Methods Mononuclear cells isolated from mice spleen were induced into DC by GMCSF and IL4, and then detected with their morphology, phenotype and function.
方法联合应用粒细胞—巨噬细胞集落刺激因子（GMCSF）、白细胞介素4（IL4）诱导培养小鼠脾脏单个核细胞分化为DC，并从形态学、表型及功能方面对其加以检测。
Objective: To compare the cytotoxicity of HL60/ADM cells and HL60 cells treated with 131I-GMCSF and to investigate the mechanism of the apoptosis of HL-60/ADM cells induced by 131I-GMCSF.
目的观察131I-GMCSF诱导HL60/ADM细胞凋亡，探讨其诱导HL60/ADM细胞凋亡的机制，比较131I-GMCSF对HL60/ADM细胞和HL60细胞的细胞毒作用，为其临床治疗难治性或复发性急性髓细胞性白血病提供实验依据。
Objective: To compare the cytotoxicity of HL60/ADM cells and HL60 cells treated with 131I-GMCSF and to investigate the mechanism of the apoptosis of HL-60/ADM cells induced by 131I-GMCSF.
目的观察131I-GMCSF诱导HL60/ADM细胞凋亡，探讨其诱导HL60/ADM细胞凋亡的机制，比较131I-GMCSF对HL60/ADM细胞和HL60细胞的细胞毒作用，为其临床治疗难治性或复发性急性髓细胞性白血病提供实验依据。
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