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    外源性SHIP基因表达抑制生长因子介导的 K562细胞增殖及Akt磷酸化

    Published 2009-01-01
    “…【目的】 探讨SHIP基因对IL-3诱导K562细胞系增殖的抑制作用,阐明SHIP对K562细胞作用的机制65377;【方法】 将慢病毒质粒pReceiver-Lv31-FIV和pReceiver-Lv31-SHIP转染K562细胞;转染细胞与IL-3共培养,Western blot法检测K562细胞Akt磷酸化;观察转染野生型SHIP基因对K562细胞增殖的影响;末端脱氧核苷酸转移酶介导的dUTP缺失末端标记(TUNEL)法检测细胞凋亡65377;【结果】 重组慢病毒载体pReceiver-Lv31-FIV和pReceiver-Lv31-SHIP转染K562细胞,GFP阳性率为74.6%65377;野生型SHIP基因阻断了IL-3对K562细胞的增殖作用,对照组(K562/FIV)细胞增殖抑制率(3.26%)明显低于转染SHIP基因组细胞增殖抑制率(26.42%,P < 0.05);集落形成实验显示SHIP能显著抑制K562细胞集落形成能力[IL-3作用组K562/SHIP细胞形成集落为60.3 ± 6.6,明显低于IL-3诱导的K562/FIV组(91.7 ± 4.2)](P < 0.01)65377;细胞形态观察发现凋亡增加,Western blot检测发现转染SHIP基因组前凋亡酶pro-caspase-3降解增加,TUNEL法证实SHIP蛋白促进细胞凋亡65377;IL-3作用不同时间段(3 h, 6 h, 12 h),转染野生型SHIP组细胞增殖明显减弱,且Akt磷酸化水平均低于对照组(P < 0.05)65377;【结论】 SHIP基因负调控生长因子(IL-3)介导的K562细胞增殖及其蛋白激酶活化65377;…”
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    Experimental Study on the Effects of Controllable Parameters on the Healthy Operation of SF-2A Material Water-Lubricated Stern Bearing in Multi-Point Ultra-Long Shaft Systems of Ships by Xingshan Chang, Jie Liu, Xinping Yan, Feng Sun, Hanhua Zhu, Chengmin Wang

    Published 2024-12-01
    “…Effective control of the health operating condition of multi-support, ultra-long shaft system water-lubricated stern bearings is crucial for supporting the intelligent maintenance and health management of ships. This study investigates the failure modes of water-lubricated stern bearings and focuses on the critical failure modes of abnormal wear and high-temperature meltdown to analyze the mechanisms and influencing factors of these failures. …”
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