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Bid的相关文献在1996年到2022年内共计97篇,主要集中在肿瘤学、药学、内科学 等领域,其中期刊论文89篇、专利文献8篇;相关期刊71种,包括齐鲁护理杂志、中国实验诊断学、国际呼吸杂志等; Bid的相关文献由276位作者贡献,包括张昶、赵文海、陈乃玲等。

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期刊论文>

论文:89 占比:91.75%

专利文献>

论文:8 占比:8.25%

总计:97篇

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Bid

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  • 张昶
  • 赵文海
  • 陈乃玲
  • 陈昊
  • 白莉
  • 万慧芳
  • 任立明
  • 何振华
  • 何有文
  • 余乐涵
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    • 孙赟珑; 曲庆
    • 摘要: 酸类气体(例如乙酸)的极性很强,在分析定量的过程中面临诸多问题,采用岛津公司的BID检测器,利用不同浓度[(10~1000×10^(-6))(摩尔分数)]的乙酸标准气,对乙酸的吸附性、进样重复性、定量线性、检测限、分析条件等方面进行了深入探讨,为酸类气体的分析提供一定的指导方法。
    • 石晓虹; 李佳欣; 纪海茹; 任立群; 齐洁敏
    • 摘要: 目的 检测凋亡相关因子B i d在胃腺癌组织中的差异性表达,同时分析临床意义.方法 60例胃腺癌组织为实验组,55例正常胃黏膜上皮组织为对照组,联合免疫组化SP法、蛋白印记(Western blot)及实时荧光定量PCR(qRT-PCR)技术综合检测Bid蛋白及mRNA的表达情况.结果 与对照组相比,Bid蛋白在胃腺癌组织中的阳性表达水平及mRNA的相对表达量减少,组间比较差异均有统计学意义(P<0.05).在蛋白水平及基因水平上,胃腺癌组织中Bid因子的表达水平与淋巴结转移、肿瘤分化程度、临床TNM分期及浸润深度情况密切相关(P<0.05).结论 凋亡相关因子B i d在胃腺癌的发生、发展过程中起重要作用,并有可能成为治疗胃腺癌患者的新靶点.
    • 蒋鹏飞; 彭俊; 吴大力; 彭清华
    • 摘要: 目的:探讨蛴螬提取物对兔光损伤视网膜变性Caspase-8、Bax、Bid、Caspase-3 mRNA表达的影响.方法:将30只雄性实验性兔随机平均分为空白组、模型组、蛴螬低剂量组、蛴螬中剂量组和蛴螬高剂量组.除空白组外,其余4组均建立光损伤视网膜变性模型,在给药14 d处死后取材采用RT-qPCR法测定Caspase-8 mRNA、Bax mRNA、Bid mRNA、Caspase-3 mRNA的表达水平.结果:与模型组比较,蛴螬低、中、高剂量组的Caspase-8 mRNA、Bax mRNA、Bid mRNA、Caspase-3 mRNA相对表达量降低,差异具有统计学意义(P0.05).结论:蛴螬通过抑制Caspase-8 mRNA、Bax mRNA、Bid mRNA、Caspase-3 mRNA的表达,抑制细胞凋亡受体信号通路来发挥保护视网膜作用,中、高剂量组效果较好.
    • 彭俊; 王英; 蒋鹏飞; 刘家琪; 潘坤; 周亚莎; 徐剑; 彭清华
    • 摘要: 目的 观察枸杞加丹参对视网膜色素变性大鼠视网膜Bcl-2、Bid表达的影响.方法 实验对象分五组.空白组:RCS (rdy+/+,p+/+)大鼠,8只,雌雄均4只,灌胃生理盐水;将RCS(rdy-/-,p-/-)雌性及雄性大鼠均随机分为4组,分别为:模型组、枸杞组、丹参组和枸杞加丹参组(杞参组),每组雌雄均4只,共8只,分别给予灌胃生理盐水、生理盐水、枸杞、丹参、枸杞加丹参.灌胃28天后,免疫组化、Real-time PCR、WB检测各组RCS大鼠视网膜Bcl-2、Bid的相对表达量.结果 ①免疫组化检测显示:RCS (rdy-/-,p-/-)杞参组大鼠视网膜上Bcl-2蛋白阳性表达较RCS(rdy-/-,p-/-)大鼠模型组明显增多;RCS(rdy-/-,p-/-)杞参组大鼠视网膜上Bid蛋白阳性表达较RCS(rdy-/-,p-/-)大鼠模型组明显减少,但较RCS (rdy+/+,p+/+)大鼠空白组多.②RT-qPCR检测显示:RCS (rdy-/-,p-/-)杞参组Bcl-2 mRNA相对表达量明显高于RCS (rdy-/-,p-/-)模型组,差异有统计学意义(P<0.05),且接近RCS (rdy+/+,p+/+)大鼠空白对照组.RCS(rdy-/-,p-/-)杞参组Bid mRNA相对表达量明显低于RCS (rdy-/-,p-/-)模型组,差异有统计学意义(P<0.05),且接近RCS(rdy+/+,p+/+)大鼠空白对照组.③WB检测显示:RCS(rdy-/-,p-/-)杞参组Bcl-2蛋白相对表达量明显高于RCS(rdy-/-,p-/-)模型组,差异有统计学意义(P<0.05),且接近RCS(rdy+/+,p+/+)大鼠空白对照组.RCS(rdy-/-,p-/-)杞参组Bid蛋白相对表达量明显低于RCS(rdy-/-,p-/-)模型组,差异有统计学意义(P<0.05),且接近RCS(rdy+/+,p+/+)大鼠空白对照组.结论 视网膜色素变性经典动物模型RCS(rdy-/-,p-/-)大鼠视网膜组织中Bcl-2表达下降、Bid表达上升;枸杞加丹参灌胃促进RCS(rdy-/-,p-/-)大鼠视网膜抗凋亡因子Bcl-2表达上调,同时,下调促凋亡因子Bid表达,在抗线粒体凋亡途径上减轻视网膜色素变性大鼠的视网膜细胞凋亡,从而保护视功能.
    • 汪旭伟; 马沛; 王建伟; 陈玉星
    • 摘要: Objective To investigate the effect of miR-26 on the regulation of BID protein and its effect on prolifera-tion and invasion of colon cancer cells.Methods The expressions of miR-26 in colon cancer tissues and colon cancer cells were detected by qPCR. The relationship between miR-26 and clinicopathological staging of colon cancer was ex-amined. Immunofluorescence was used to detect the transfected efficiency of miR-26-inhibitor in colon cancer cells. MTT assay was used to detect the effect of miR-26 on the proliferation of colon cancer cells. Transwell invasion assay was used to detect the effect of miR-26 on the invasion of colon cancer cells.Results The expression of miR-26 in colon cancer tissue was higher than that in normal tissue. The expression of miR-26 was significantly increased with the patho-logical stage of colon cancer. Silencing miR-26 could improve the expression of BID. Silencing miR-26 could inhibit proliferation and invasive ability of colon cancer cells.Conclusion miR-26 is up-regulated in colon cancer, and miR-26 can regulate the expression of BID and affect the proliferation and invasion of colon cancer cells.%目的 探讨miR-26对BID蛋白的调控作用及在结肠癌细胞中对其增殖和侵袭能力的作用.方法 qPCR检测结肠癌组织和结肠癌细胞中miR-26的表达情况;探讨miR-26和结肠癌临床病理参数之间的关系;免疫荧光检测miR-26-inhibitor在结肠癌细胞中的转染效率;双荧光素酶实验检测miR-26和BID的关系;MTT实验检测沉默miR-26对结肠癌细胞增殖能力的影响;Tran-swell侵袭实验检测沉默miR-26对结肠癌细胞侵袭能力的影响.结果 miR-26在结肠癌组织中表达水平较高;随着结肠癌的病理分期升高,miR-26的表达相应升高;沉默miR-26可以有效上调BID的表达;沉默miR-26可以抑制结肠癌细胞的增殖和侵袭能力.结论 miR-26在结肠癌中表达上调,同时miR-26可以调控BID的表达影响结肠癌细胞增殖和侵袭能力.
    • 王书乐; 成祥; 陈国柱; 赵名; 于晓妉
    • 摘要: Objective To explore the mechanism by which tumor necrosis factor alpha(TNF-α) induces RIP1 kinase-dependented apoptosis in L929-A fibroblastoma cells.Methods The sub-mitochondrial localization of receptor-interacting protein 1(RIP1),caspase-8 and Bid proteins was detected by dose-gradient trypsin digestion and Western blotting.The levels of reactive oxygen species (ROS),intracellular calcium concentration,mitochondrial membrane potential (MMP),and cellular adenosine triphosphate(ATP) content were determined by fluorescent probe labeling and flow cytometry assay.The mitochondrial respiratory chain complex Ⅰ and Ⅲ activities were detected by commercial kits.Nec-1,A RIP1 kinase specific inhibitor,and RIP1-/-or Bid-/-L929-A cells were used to detect the roles of RIP1 kinase and Bid protein in cell death.Results RIP1,caspase-8 and Bid proteins were co-located in the outer membrane of mitochondrial.TNF-α exposure for 3 h could induce Bid cleavage,inhibit mitochondrial respiratory chain complex Ⅲ activity and reduce MMP.Following these changes and after TNF-α exposure for 6-12 h,the intracellular calcium concentration and ROS were increased,whereas the ATP concentration was decreased,and the cells were killed.Inhibiting RIP1 kinase or knockdown RIP1 or Bid protein could suppress all the cytotoxic effects of TNF-α.Conclusion TNF-α treatment can result in RIP1 kinase-mediated Bid cleavage and inhibit mitochondrial respiratory chains and cell energy metabolism,which ultimately leads to the death of L929-A cells.%目的 探讨肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)诱导L929-A细胞发生受体相互作用蛋白激酶1(receptor-interacting protein 1,RIP1)依赖性凋亡的分子机制.方法 通过胰蛋白酶浓度梯度消化及蛋白质印迹法检测RIP1、胱天蛋白酶8(caspase-8)和Bid蛋白的表达和线粒体定位;利用荧光探针标记法检测TNF-α处理后L929-A细胞内的活性氧(reactive oxygen species,ROS)水平、胞内钙离子浓度、线粒体膜电位(mitochondrial membrane potential,MMP)及三磷酸腺苷(adenosine triphosphate,ATP)浓度,应用试剂盒检测线粒体呼吸链复合体Ⅰ、Ⅲ的活性变化;采用RIP1激酶特异性抑制剂坏死抑素1(necrostatin-1,Nec-1)和Bid基因敲除的L929-A细胞评估RIP1激酶活性和Bid蛋白在介导细胞死亡中的作用.结果 RIP1、caspase-8和Bid蛋白均定位在线粒体外膜上;TNF-α处理后3 h即可诱导Bid剪切,伴随Bid剪切,线粒体呼吸链复合体功能检测显示复合体Ⅲ的活性受到抑制,MMP下降.TNF-α处理后6~12 h细胞内ROS升高、钙离子浓度上升、ATP浓度降低;抑制RIP1激酶活性或敲低Bid蛋白可完全拮抗TNF-α诱导的细胞毒性.结论 TNF-α通过诱导RIP1激酶活性依赖的Bid剪切,继而抑制线粒体呼吸链和细胞能量代谢,诱导细胞死亡.
    • 王方
    • 摘要: 目的观察TIPE2过表达对小细胞肺癌H446细胞凋亡相关分子BID的影响。方法建立TIPE2过表达的H446小细胞肺癌细胞株,利用荧光显微成像技术和Western Blot技术分别检测TIPE2过表达情况和细胞凋亡相关分子BID的变化。结果 TIPE2质粒稳转H446细胞高表达TIPE2基因和绿色荧光蛋白。TIPE2过表达的H446细胞促凋亡分子BID表达增多,显微镜观察细胞凋亡明显。结论过表达TIPE2基因引起BID上调,并促进小细胞肺癌H446凋亡。
    • Babak Nikpour; Ahmed Senouci; Neil Eldin
    • 摘要: Unbalanced bidding is a cash flow management strategy that is recognized as an illegal/disqualifying practice by public owners;and unethical practice by most private owners. This practice provides the awarded bidder with unjustified advantages at the expense of the owner. Unfortunately, limited tools and techniques are currently available to identify and detect unbalanced bids during the evaluation process. This paper presents an innovative detection tool to identify unbalanced bids in unit price contracts during the bid evaluation process. The proposed technique develops BMDI graphs to visualize total markup variation patterns during the project lifetime to detect unbalanced bids. The proposed method also uses Monte Carlo simulation to take in consideration the impact of cost uncertainties and risks. An illustrative example was presented to show the capabilities and features of the proposed method in determining the status of submitted bids during the evaluation process.
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