1 Introduction In the last decades,the furazan fused ring compounds have been paid much more attention owing to their characteristics,such as high density,high specific volume and high nitrogen content.A novel energet...1 Introduction In the last decades,the furazan fused ring compounds have been paid much more attention owing to their characteristics,such as high density,high specific volume and high nitrogen content.A novel energetic compound based on furazan fused ring,6-nitroimino-4,8-dinitro-5,6,7,8-tetrahydro-4H-imidazo furazano pyrazine(NIFDNP),was firstly designed and its properties of physico-chemical and detonation were calculated by Gaussian 09 program[4] and VLW method[5].Using glyoxal展开更多
目的:S100钙结合蛋白A9(S100A9)激活核因子κB(NF-κB)促进小胶质细胞toll样受体7(TLR7)的表达和炎症因子释放的作用及其机制研究。方法:CCK-8实验检测BV2小胶质细胞的增殖率;转录组测序并结合GO分析、KEGG富集分析和STRING数据库对差...目的:S100钙结合蛋白A9(S100A9)激活核因子κB(NF-κB)促进小胶质细胞toll样受体7(TLR7)的表达和炎症因子释放的作用及其机制研究。方法:CCK-8实验检测BV2小胶质细胞的增殖率;转录组测序并结合GO分析、KEGG富集分析和STRING数据库对差异基因(DEGs)进行比对并从差异表达基因中筛选出目标基因;Real time RT-PCR验证TLR7的表达;免疫荧光染色检测CD68、CD206的表达;Western Blot检测CD68、CD206、TLR7、p65、p-p65的表达;ELISA检测白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达。结果:中等浓度的S100A9对小胶质细胞无增殖抑制效应;实验组CD68蛋白的表达水平较对照组明显增加,而CD206蛋白的表达水平明显下降,提示S100A9促进BV2小胶质细胞向促炎型激活;Toll样受体4(TLR4)的抑制剂TAK-242明显抑制S100A9刺激BV2小胶质细胞后TNF-α和IL-6的表达水平;TLR4/NF-κB通路激活促进TLR7蛋白表达。结论:中等浓度的S100A9可以促进小胶质细胞向促炎型极化,通过激活TLR4/NF-κB通路促进TLR7表达和包括TNF-α和IL-6在内的多种炎症因子的释放,S100A9具有明显的促炎作用。展开更多
目的:探讨弥漫大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)患者治疗前血清β2微球蛋白(β2-microglobnlin,β2-MG)和内皮细胞生长因子(vascular endothelial growth factor,VEGF)蛋白表达与Bcl-6和Ki-67表达的临床相关性。方法...目的:探讨弥漫大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)患者治疗前血清β2微球蛋白(β2-microglobnlin,β2-MG)和内皮细胞生长因子(vascular endothelial growth factor,VEGF)蛋白表达与Bcl-6和Ki-67表达的临床相关性。方法:2011-09-08-2013-02-16江苏省肿瘤医院初治49例DLBCL患者行CHOP方案化疗,Luminex液相芯片法检测治疗前血清VEGF和β2-MG蛋白表达水平,常规免疫组化法检测Bcl-6和Ki-67表达。结果:VEGF蛋白高表达合并Bcl-6高表达者多见于年龄>60岁的老年患者,阳性率为53.8%(7/13),P=0.048;合并Ki-67高表达者的各项临床特征间差异均无统计学意义,P>0.05。VEGF蛋白高表达合并Ki-67高表达者能获得更佳的疗效,P=0.008;完全缓解(CR)患者阳性率为4/7,部分缓解(PR)患者阳性率为50.0%(8/16)。β2-MG蛋白高表达合并Bcl-6和Ki-67高表达与各项临床特征间差异无统计学意义,P>0.05。结论:VEGF蛋白高表达合并Ki-67高表达与治疗疗效密切相关,两者同时高表达时DLBCL患者对CHOP治疗方案的敏感度高,治疗疗效好。β2-MG和VEGF蛋白表达结合临床常规免疫组化检测有望成为DLBCL临床诊断和治疗方案选择的新方法。展开更多
基金Foundation Research Project of National defence(B0920110051)
文摘1 Introduction In the last decades,the furazan fused ring compounds have been paid much more attention owing to their characteristics,such as high density,high specific volume and high nitrogen content.A novel energetic compound based on furazan fused ring,6-nitroimino-4,8-dinitro-5,6,7,8-tetrahydro-4H-imidazo furazano pyrazine(NIFDNP),was firstly designed and its properties of physico-chemical and detonation were calculated by Gaussian 09 program[4] and VLW method[5].Using glyoxal
文摘目的:S100钙结合蛋白A9(S100A9)激活核因子κB(NF-κB)促进小胶质细胞toll样受体7(TLR7)的表达和炎症因子释放的作用及其机制研究。方法:CCK-8实验检测BV2小胶质细胞的增殖率;转录组测序并结合GO分析、KEGG富集分析和STRING数据库对差异基因(DEGs)进行比对并从差异表达基因中筛选出目标基因;Real time RT-PCR验证TLR7的表达;免疫荧光染色检测CD68、CD206的表达;Western Blot检测CD68、CD206、TLR7、p65、p-p65的表达;ELISA检测白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达。结果:中等浓度的S100A9对小胶质细胞无增殖抑制效应;实验组CD68蛋白的表达水平较对照组明显增加,而CD206蛋白的表达水平明显下降,提示S100A9促进BV2小胶质细胞向促炎型激活;Toll样受体4(TLR4)的抑制剂TAK-242明显抑制S100A9刺激BV2小胶质细胞后TNF-α和IL-6的表达水平;TLR4/NF-κB通路激活促进TLR7蛋白表达。结论:中等浓度的S100A9可以促进小胶质细胞向促炎型极化,通过激活TLR4/NF-κB通路促进TLR7表达和包括TNF-α和IL-6在内的多种炎症因子的释放,S100A9具有明显的促炎作用。
文摘目的:探讨弥漫大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)患者治疗前血清β2微球蛋白(β2-microglobnlin,β2-MG)和内皮细胞生长因子(vascular endothelial growth factor,VEGF)蛋白表达与Bcl-6和Ki-67表达的临床相关性。方法:2011-09-08-2013-02-16江苏省肿瘤医院初治49例DLBCL患者行CHOP方案化疗,Luminex液相芯片法检测治疗前血清VEGF和β2-MG蛋白表达水平,常规免疫组化法检测Bcl-6和Ki-67表达。结果:VEGF蛋白高表达合并Bcl-6高表达者多见于年龄>60岁的老年患者,阳性率为53.8%(7/13),P=0.048;合并Ki-67高表达者的各项临床特征间差异均无统计学意义,P>0.05。VEGF蛋白高表达合并Ki-67高表达者能获得更佳的疗效,P=0.008;完全缓解(CR)患者阳性率为4/7,部分缓解(PR)患者阳性率为50.0%(8/16)。β2-MG蛋白高表达合并Bcl-6和Ki-67高表达与各项临床特征间差异无统计学意义,P>0.05。结论:VEGF蛋白高表达合并Ki-67高表达与治疗疗效密切相关,两者同时高表达时DLBCL患者对CHOP治疗方案的敏感度高,治疗疗效好。β2-MG和VEGF蛋白表达结合临床常规免疫组化检测有望成为DLBCL临床诊断和治疗方案选择的新方法。
