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activation相关的网络例句

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与 activation 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。

In accordance with such external technology requirements and based on such presumable precondition that we've found a kind of atomic reciprocal PNT combination A which can be used as PNT activation source accelerating along certain orientation once activated by the so-called PNT activator B, and we can volitionally predominate the magnitude of acceleration and activation rate of PNT activation source by the control of action rate or strength of PNT activator to PNT activation source, the paper introduces macrostructure design of tyre model of PNT engine as following

针对这样的客观技术要求并基于这样的假定事实——"我们己发现一种可用于PNT应激物质源的原子态PNT惠合系α在激励信号β的作用下沿一定方向加速运动,而且我们可以通过直接调控激励信号β对原子态PNT惠合系α的工作强度来控制PNT惠合系α的被激励程度或被激加速度大小和激活率",本文着重介绍PNT引擎的宏观结构设计——PNT引擎之轮胎结构如下

The activated or leached process and their influence elements are studied by 1DREACT software package of coupled mass/heat transfer and chemical reaction dynamics of water-rock interaction, according to the geological and geochemical characters of fine disseminated gold deposits.(1) Water-rock reaction time is not the important influence element of activating gold;(2) At first, activating capability of hydrothermal solution increases with the increasing of total sulfur activity; after lga〓≥-4, the content of activated gold in solution is mainly related to original content of gold in wall rock, and does not visibly dependent on total sulfur activity.(3) It is a complicated nonlinear process of influence of activating gold capacity of hydrothermal solution with the change of temperature, in general, 220 ℃ is most favorable to gold activation.(4) The influence of oxygen fugacity on gold activation has a multiple functions coupling nonlinear effect, in general, Igfo〓=-41 is most favorable to gold activation.(5) Solubility of gold in fluid decreases with the increasing of velocity of flow, the product of velocity and aurous solubility reaches maximum when velocity is 0.2~0.5m〓m〓. yr〓, i. e. this scope of velocity is most favorable to gold activation.

利用1DREACT水-岩相互作用反应-输运耦合动力学软件包,根据微细浸染型金矿床地质地球化学特征,计算机模拟研究了金的活化、浸取过程及其影响因素,发现:(1)金活化过程中水-岩反应时间不是其主要制约因素;(2)热液对金的活化能力开始随总硫活度的增高而增高,当lg a〓≥-4后,热液中活化金的含量将主要与围岩中金的初始丰度有关,而对总硫活度无明显依赖关系;(3)温度对热液浸金能力的影响是一个复杂的非线性过程,总体而言,220℃最有利于金的活化;(4)氧逸度对金活化的影响呈现出一种多因素叠加的非线性效应,总体而言,lgfo〓=-41最有利于金的活化与浸取;(5)流体中金的浓度随流体流速的加快而降低,流速与金浓度的乘积在流速为0.2~0.5m〓m〓。yr〓时达到极大,即0.2~0.5m〓m〓。yr〓的流速范围最有利于本类矿床的金的活化。

Through above study, the theoretical analysis of the inherent fault tolerance of feed-forward neural networks has been extended from hard-limit activation functions to differentiable activation functions; 2. By using above method, fault tolerance of discrete Hopfield feedback neural networks have been also analyzed. It means that the above method can be applied not only for feed-forward neural networks but also for feedback neural networks; 3. For the feed-forward neural network with the Sigmoid activation function, Chebyshev Inequality method was presented.

这项研究将以前仅限于对硬限幅作用函数前向神经网络固有容错性能的理论分析推广到具有可微作用函数的前向神经网络; 2 针对离散型Hopfield反馈神经网络,利用上面提出的方法,对其同样进行了容错性分析,得出许多有用的结论和计算公式,说明上面提出的方法不仅适用于前向神经网络,同时也适用于反馈神经网络; 3 针对具有Sigmoid作用函数的前向神经网络提出了一种切比雪夫不等式法。

The ideal activation process parameter as follow: The nickel sulfate hexahydrate concentration 15g·L~(-1);The Sodium borohydride concentration 15g·L~(-1); The Sodium hydroxide concentration 10-15 g·L~(-1);Hydrochloric acid concentration 10-15 g·L~(-1);The activation time in A solution 9min, the activation time in B solution 90s.

理想的活化工艺参数为:硫酸镍15g·L~(-1),硼氢化钠15g·L~(-1),氢氧化钠10-15 g·L~(-1),盐酸10-15 g·L~(-1),A液中活化的时间控制在9min左右为最佳,B液中活化的最佳时间为90s。

The ideal high temperature nickel activation process parameter as follow: Nickel acetate concentration 70g·L~(-1);Sodium hypophosphite concentration 70 g·L~(-1);Soakage temperature 40℃;Soakage time 5min ;activation time 30min;Activation temperature 170℃.

理想高温镍活化工艺参数为:乙酸镍浓度70g·L~(-1),次磷酸钠浓度70 g·L~(-1),浸渍温度40℃,浸渍时间5 min,活化时间30min,活化温度170℃。

Forty-eight hours after transfection, cells were harvested to determine luciferase activity by illuminometer. In the presence of RU486 a 40-fold maximum activation of the luciferase reporter gene was observed in cultured cells, whereas in the absence of RU486, no significant activation was observed. There was a positive correlation between the luciferase activation and RU486 concentration in a definite range. The results showed that the RU486-inducible regulatory vector was successfully constructed, which can be used to regulate the expression level of genes of interest in appropriate time by the inducer RU486. This inducible expression vector provides a platform for the research of gene regulation and gene therapy.

加入诱导剂RU486后,可以诱导表达荧光素酶,并在一定范围内两者呈正比,最高可以实现荧光素酶的40余倍的表达,而没有RU486时,几乎没有报告基因的表达,表明RU486诱导调控载体构建成功,可实现对目的基因的表达时间和表达水平的精确调控,为进一步的基因调控研究和和基因治疗提供了良好的工具。

Diagnosis was made through thromboctye aggregative activation,blood coagulative activation, thrombosis combined with fibrinolysis activation detection,venous doppler ultrasound scan and phlebography.

诊断通过血小板激活,血液凝固激活和血栓形成伴有的纤维溶解激活的检测及静脉多普勒扫描和静脉造影。

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