activation record

activation record的基本解释

-

现役记录

与activation record相关的网络例句 [注：此内容来源于网络，仅供参考]

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

In this thesis, two electrochemical activation methods and two activation solution were used to obtain four types of the activated GC electrodes. Effects of electrochemical activation procedure on the structure, the size, the distribution and the type of electron transfer site on electrode surface have been investigated. Application of electrochemical activation GC electrode has been exploited in electroanalysis of metal ions. Meanwhile, the essence structure and character of electron transfer site of sp2 hybridized carbon material have been explored.

在本论文研究中，通过采用酸性和碱性两种活化溶液，分别以两种不同的电化学活化方法，获得了四种不同的活化电极表面；调查了电化学活化方法对电极表面的电化学活性点的种类、尺度大小、结构以及分布的影响规律；拓展了电化学活化玻碳电极在电分析领域中的应用；探索了sp2杂化类碳材料电极在电子传导点的性质和结构上存在的本质共同点。

The spectral response performance of transmission-mode GaAs photocathode after high-temperature activation and low-temperature activation was measured by the use of on-line spectral response measurement technology, and the integral sensitivity and spectral response performance parameters of the GaAs photocathode after high-temperature activation and low-temperature activation were compared.

利用在线光谱响应技术，对透射式GaAs光电阴极在高温激活和低温激活后的光谱响应特性进行了测试，计算并比较了高温激活和低温激活后阴极的积分灵敏度和光谱响应特性参数。

与activation record相关的网络解释 [注：此内容来源于网络，仅供参考]

set up a record = make a record：创记录

break the record 破记录 | set up a record = make a record 创记录 | hold the record = keep the record 保持记录

activation analysis：活化分析

活化态;致活作用 activation | 活化分析 activation analysis | 活化能 activation energy

activation analysis：放射化分析

activation 活化 | activation analysis 放射化分析 | activation energy 活化能