• 甲状腺结节伴微钙化患者5年内发生恶变的临床研究
  • Effect of lenti-siRNA against BRD4 on energy metabolism in non-small cell lung cancer A549 cells by inhibiting SHH pathway
  • 何志伟.甲状腺结节伴微钙化患者5年内发生恶变的临床研究[J].内科急危重症杂志,2019,25(5):407-409
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    DOI:10.11768/nkjwzzzz20190516
    中文关键词:  甲状腺结节伴钙化  微钙化  恶变  甲状腺激素
    英文关键词:BRD4  SHH  Non-small cell lung cancer  Energy metabolism
    基金项目:上海市卫生和计划生育委员会科研项目(No:201540289)
    作者单位E-mail
    何志伟 上海邮电医院 hezhiweimv@163.com 
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    中文摘要:
          目的:探讨甲状腺结节伴钙化患者甲状腺激素与5年内发生恶变的相关性。方法: 采用多普勒超声检查仪对427例甲状腺结节伴钙化患者(观察组)和1147例单纯甲状腺结节患者(对照组)定期随访约5年,观察2组患者甲状腺结节恶变情况,并比较2组患者甲状腺激素水平。结果:观察组中有51例(11.94%)患者发生恶变,对照组中有58例(5.06%)患者发生恶变,观察组恶变发生率明显高于对照组(P<0.01);观察组患者结节恶变发生在随访后的25.0~75.0个月,恶变中位时间48.5个月,对照组发生在随访后40.0~81.5个月,中位时间66.5个月。观察组恶变时间明显短于对照组(P<0.01)。在观察组51例发生恶变的患者中,有48例为微钙化,占94.12%,剩下3例为粗大钙化。2组中,恶变与未恶变患者,在随访前后甲状腺激素(FT3、FT4和TSH)水平均无显著差异(均P>0.05),患者甲状腺激素与恶变无明显相关性(r=0.217,P>0.05)。结论: 健康人群中甲状腺结节伴钙化恶变发生率要高于无钙化的单纯甲状腺结节患者,绝大部分为微钙化,且恶变的发生与甲状腺激素水平无关。
    英文摘要:
          Objective: To investigate the effect of lenti-siRNA against BRD4 on energy metabolism in non-small cell lung cancer A549 cells by SHH pathway. Methods: The expression of BRD4 in A549 and HLF-1 cells was detected by RT-qPCR. After BRD4 siRNA was transferred into A549 cells, the effects of BRD4 siRNA on the growth and proliferation of A549 cells were detected by CCK8 and cell cloning assays. The effects of BRD4 siRNA on the glucose uptake and lactic acid production of A549 cells were detected by 2-NBDG and lactic acid test kit. The expression levels of SHH, GLI1 mRNA and protein were detected by RT-qPCR and Western blotting respectively. Results: The expression of BRD4 mRNA was up-regulated in A549 cells (P<0.05), and BRD4 siRNA inhibited the proliferation, cloning, glucose intake and lactic acid production of A549 cells (P<0.05), and promoted the significant down-regulation of mRNA and protein expression of SHH and GLI1 genes (P<0.05). Conclusion: The lenti-siRNA against BRD4 could reduce the level of energy metabolism in non-small cell lung cancer A549 cells by inhibiting the SHH pathway.