Objective:MicroRNA-155（miR-155） regulates T cell differentiation and *** has also been associated with HIV ***,it remains unclear whether miR-155 is related to the T cell response in HIV-infected individuals（e.g.,T...
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Objective:MicroRNA-155（miR-155） regulates T cell differentiation and *** has also been associated with HIV ***,it remains unclear whether miR-155 is related to the T cell response in HIV-infected individuals（e.g.,T cell activation and exhaustion）.Methods:We performed a cross-sectional study involving 121 HIV-1 infected patients with HAART and 43 HAART naive *** miR-155 levels in the peripheral blood were detected by quantitative reverse transcription-PCR.T cell immune activation,exhaustion,and homeostasis were detected by the expression of CD38,PD-1 and CD 127 via flow ***:The levels of miR-155 in the total peripheral blood mononuclear cells,CD4+,and CD8+ T cells from HIV-1 patients were increased（P < 0.01）.Discord controllers and HAART naive patients also exhibited a higher percentage of CD8+CD38 T cells and a lower percentage of CD4+CD127+ and CD8+CD127+ T cells（P < 0.05）.We also found higher levels of PD-1 expression on the CD4+ and CD8+ T cells of HTV-1 patients（P < 0.05）.Conclusion:Our findings suggest that miR-155 levels in the peripheral blood of HIV-1 patients are increased and associated with T cell ***,miR-155 is a potential biomarker of the immune response following HIV-1 infection.
Acute liver failure (ALF) is still an intractable disease associated with serious metabolic *** the dynamic changes of serum and faeces metabolites during the development of ALF would increase our understanding of phy...
Acute liver failure (ALF) is still an intractable disease associated with serious metabolic *** the dynamic changes of serum and faeces metabolites during the development of ALF would increase our understanding of physiological changes in normal and pathological states.
目的:在前期体外实验的基础上,进一步检测反义寡核苷酸Glut-1(Glut-1 AS-ODN)在体内对实体瘤的治疗效果,明确喉癌放射抵抗与Glut-1表达增高有关;并研究LY29400、wortmannin和apigenin等抑制剂阻滞PI3K/Akt信号通路,降低喉癌细胞中Glut-1表达,明确喉癌细胞中PI3K/Akt信号通路调控Glut-1表达对喉癌放射敏感性的影响及机制,为将来临床喉癌患者喉功能保留治疗提供坚实的理论基础。方法:在BALB/c-nude裸鼠建立了Hep-2喉癌细胞的移植瘤模型,分成对照组,LY294002组,wortman原nin组,反义Glut-1组,apigenin组,单纯10Gy照射组,LY294002组+反义Glut-1组,wortmannin组+反义Glut-1组,apigenin组+反义Glut-1组,LY294002组+反义Glut-1组+10Gy,wortmannin组+反义Glut-1组+10Gy,apigenin组+反义Glut-1组+10Gy,LY294002组+10Gy,wortmannin组+10Gy,检测各组瘤体的变化,并通过反义GLUT-1抑制Glut-1表达、LY29400、wortmannin和apigenin等抑制剂阻滞PI3K/Akt信号通路,分别通过实时RT-PCR、Western blotting各组GLUT-1、AKT、PI3K、CD133 m RNA以及蛋白的表达情况、TUNEL检测裸鼠瘤体组织的细胞凋亡水平。结果:反义GLUT-1、LY29400、wortmannin和apigenin等抑制肿瘤生长,并能增强X线对瘤体的抑制作用,分别通过抑制GLUT-1、AKT、PI3K、CD133表达以及增加细胞凋亡来增强X线的作用。结论:靶向抑制Glut-1及PI3K/Akt信号通路能提高喉癌致瘤裸鼠的放射敏感性
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