• 布雷非德菌素一种高效细胞生长抑制剂。1958年第一次被报导之后几个研究小组一系列不同的生物化验中作为高效活性试剂。

    Brefeldin a is a potent inhibitor of cell growth first described in 1958, then independently "rediscovered" by several groups as a potent active in a broad range of bioassays.

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  • 目的探讨选择性非选择性环氧合酶-2抑制剂COX-2)对体外培养结肠癌细胞生长影响及其作用的信号传导通路

    Objective To evaluate the inhibiting effect of selective and non-selective cyclo-oxygenase-2(COX-2) inhibitor on growth of colon cancer cell lines in vitro and its signal transduction pathway.

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  • 研究小组总结认为,这些肿瘤细胞特殊EGFR突变确定了抑制剂分子可能可以减慢或者停止那些细胞生长

    The research team concluded that the particular EGFR mutation within tumor cells determines which inhibitor molecules are likely to be able to slow or stop the growth of those cells.

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  • 目的研究氧化酶- 2 (COX - 2)抑制剂腹膜间皮细胞(HPMC)转化生长因子- 1 (TGF - 1)表达影响

    Objective: to investigate the effects of cyclooxygenase-2 (COX-2) inhibitor on TGF-b1 expression in human peritoneal mesothelial cells (HPMC).

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  • 结论表皮生长因子受体抑制剂ag1487可对舌鳞细胞产生明显增殖抑制作用。

    Conclusion: Epidermal growth factor receptor inhibitor AG1487 may retard cell cycle, and then inhibit the proliferation of tumor cells.

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  • 目的了解表皮生长因子受体抑制剂AG1487细胞抑制增殖作用。

    Objective:To investigate the inhibitory effect of epidermal growth factor receptor inhibitor AG1487 on the proliferation of tongue cancer cells.

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  • 最近一项使用表皮生长因子受体抑制剂临床试验发现患者肿瘤细胞表达磷酸化化学转化水平很高- Akt对这种疗法没有反应Kwatra博士。”

    A recent clinical trial using an EGFR inhibitor found that patients whose tumors expressed high levels of phosphorylated - or chemically altered - Akt did not respond to treatment, Kwatra said.

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  • 结论选择性COX- 2抑制剂呈剂量时间依赖性抑制胃癌细胞生长这种作用可能依赖于对COX - 2表达抑制

    ConclusionsSCIs can inhibit cell proliferation in Bgc-823 cells in both concentration-dependent manner and time-dependent manner. The mechanism may be dependent on the inhibition of COX-2 expression.

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  • 结论选择性COX- 2抑制剂呈剂量时间依赖性抑制胃癌细胞生长这种作用可能依赖于对COX - 2表达抑制

    ConclusionsSCIs can inhibit cell proliferation in Bgc-823 cells in both concentration-dependent manner and time-dependent manner. The mechanism may be dependent on the inhibition of COX-2 expression.

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