induced charge

induced charge的基本解释

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[化] 感生电荷

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

Take charge take in charge take charge of under the charge of charge for trouble charge of quarters charge off charge oneself with charge to charge with charges forward

记在某人帐上再发起冲锋，重新进攻；重新进行抨击，重新提出讨论向受话人收取电话费控告某人并发誓该项控告属实控告某人并发誓该项控告属实负责；掌管，接办；失去控制，出了毛病负责照料，引为己责；由警察拘留负责，看管在。。。

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。

Results Qidan Granules could relieve the pain caused by glacial acetic acid and heat stimuli; significantly inhibit the oxytocin-induced dysmenorrheal in mice; It also showed obvious inhibitory effects on the increased capillary permeability induced by glacial acetic acid, carrageen-induced toe edema in rats and dimethylbenzene-induced ear swelling in mice, and cotton pellet-induced granuloma formation in rats. It could also significantly inhibit oxytocin-induced dysmenorrhea in mice.

结果 奇丹颗粒能明显抑制乙酸和热刺激所致的小鼠疼痛反应；对缩宫素所致实验性痛经小鼠具有良好的镇痛作用，对乙酸所致小鼠腹腔毛细血管通透性增高以及大鼠角叉菜胶足趾肿胀、二甲苯所致小鼠耳廓肿胀、大鼠棉球肉芽肿等急慢性炎症模型均有明显抑制作用。

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

induced charge：感应电荷

induced air flotation 加气浮选 | induced charge 感应电荷 | induced convection 诱导对流

induced charge：感生电荷

indirectly heated cathode 旁热式阴极 | induced charge 感生电荷 | induced current 感生电流

induced charge：應電荷 =感生電荷

induced anisotropy 引致異向性 =感生各向異性 | induced charge 應電荷 =感生電荷 | induced electric field 應電場 =感生電場

induced charge：感生電荷;感應電荷

感生電流;感應電流 induced current | 感生電荷;感應電荷 induced charge | 感抗 inductive reactance

collision induced charge inversion：碰撞诱发电荷反转

collision gas cell 碰撞气室 | collision induced charge inversion 碰撞诱发电荷反转 | collision induced decomposition 碰撞诱发分解