阻断剂

Our results suggest that COX-2 activity is involved in ethanol-induced HCV-RNA and NS5A protein expression, because acetylsalicylic acid, a COX-1/2 inhibitor, blocked this induction and downregulated COX-2 protein expression and activity.

研究结果表明，环氧合酶-2活性，涉及酒精介导的丙型肝炎病毒核酸及ns5a区蛋白表达，因为环氧合酶-1 / 2抑制剂——乙酰水杨酸，可阻断这种诱导机制，并下调环氧合酶-2蛋白的表达和活性。

First, the individuals who would be most likely to benefit need to be identified, writes editorialist Sanford Markowitz, MD, PhD, from Case Western Reserve University, in Cleveland, Ohio. Then, it needs to be shown that certain persons reproducibly demonstrate high COX-2 expression in independent adenomas or cancers, because of genetic predisposition or environmental exposures. And third, the work of Dr. Chan and colleagues needs to be extended by demonstrating that prevention of colon adenomas by aspirin or COX-2 inhibitors also involves blocking the development of the highest COX-2–expressing lesions, he says.

俄亥俄州克里夫兰Case Western Reserve大学的Case Western Reserve医师表示，首先，必须要拿找出最能受益的一群病患；接著，必须要能证实部分病患的独立腺瘤或癌症，因为基因及环境的影响，会一再地是高度表现COX-2的；第三，Chan医师与其同事的研究，需要透过aspirin或是COX-2抑制剂可以预防大肠腺瘤的作用，也牵涉到阻断COX-2表现病灶的生成。

Naltrexone and nalmefene are antagonists of opioid receptors, and they can suppress inflammation with blocking the opioid receptors.

纳美芬与纳美芬酮是一种类鸦片受体的对抗剂，可以透过阻断类鸦片受体来达到抗发炎效果。

The effect of progesterone could be potentiated by GABA A receptor agonist muscimol and antagonized by GABA A receptor antagonists bicuculline and picrotoxin as well as GABA B receptor agonist baclofen. The effect of progesterone and the actions of these drugs mainly manifested in the concentration range of progesterone 0 01～0 05 μmol/L.

该作用可被氨基丁酸A受体激动剂蝇蕈醇加强，被氨基丁酸A受体拮抗剂荷包牡丹碱和印防己毒素以及氨基丁酸B受体激动剂巴氯芬阻断，而且孕酮的效应以及各药物对其的影响均集中在0.01～0.05 μmol/L孕酮浓度中较为明显。

The results showed that UK14300 3×10~(-6 mol/L, a potent #alpha#_(2)-adrenoceptor agonist,significantly inhibited both basal and endotoxin-induced CGRP release by 22%-42%,while specific antagonist of #alpha#_(2)-adrenoceptor yohimbine 10~(-5 mol/L blocked the effect of UK14304 completely.

结果发现，α_(2)-受体激动剂UK143043×10~(-6mol／L可以显著抑制CGRP的基础释放和内毒素(1～5μg／ml)刺激后的释放，抑制幅度为22％～42％；用α2-受体拮抗剂Yohimbine(10－5mol／L)可以完全阻断UK14304的作用。

However, Treatment with NMDA resulted in Giα2 phosphorylation. This phosphorylation could reversed by APV or chelerythrine chloride .

但NMDA可明显增加细胞内Giα2的磷酸化水平，这一作用可被NMDA受体的拮抗剂以及PKC抑制剂所阻断。

Tetrodotoxin selectively blocks the neuromuscular electrical activity, producing the effect of nondepolarizing curine and leading to failure of the respiratory drive without compromising the respiratory center.

河豚毒选择阻断神经与肌肉的电生理活动，呈非去极化型箭毒碱样作用，致呼吸动力障碍，与呼吸中枢无关，M胆碱能受体阻滞剂阿托品及中枢兴备剂均无明确使用指征，维持有效通气等综合治疗可达到满意疗效。

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。

AMs that collected, pured and cultured with contine method were stimulated by LPS of different concentration(0μg/ml,0.01μg/ml,0.1μg/ml,1μg/ml,10μg/ml) for 60min or by 1μg/ml LPS for different time stage (0min,5min,15min,30min,60min,120min) to observe the dynamic change of NF-кB intranuclear level and NO production, from which the best concentration and time point of LPS stimulation were selected. In the study, all AMs were divided into 4 groups: control group, group stimulated with LPS, group interrupted by Cal C and group inhibited by PDTC. The following parameters were measured: NF-кB level in nuclear protein extraction of AMs detected with sandwich ELISA, Inter-nuclear transposition of NF-кB observed with immunocytochemistry staining, NO content in cell culture medium quantitied with nitric acid reductase assay, Morphologic change of AMs in apoptosis observed with acridine orange staining and fragmentation at genome DNA of AMs detected with apoptotic electrophoresis assay.

分离、纯化及培养大鼠肺巨噬细胞；以不同浓度的LPS(0μg/ml，0.01μg/ml，0.1μg/ml，1μg/ml，10μg/ml)和不同作用时间(0min，5min，15min，30min，60min，120min)分别刺激小室培养的细胞单层，观察NF-κB的核内浓度及NO合成量的动态变化，选择LPS的最佳用量和作用时间；然后分成四组实验，设正常对照组，LPS处理组，特异性PKC抑制剂阻断组，NF-κB抑制剂阻断组；收集培养的单层细胞及培养液；采用夹心ELISA法定量测定细胞核提取物中的NF-κB水平；免疫组化法检测NF-κB的核内移位变化；硝酸还原酶法测定细胞培养液中NO含量；吖啶橙染色观察凋亡细胞的形态学变化，凋亡电泳实验检测细胞凋亡后基因组DNA的断裂情况。

The result using inhibitors of Ca〓 channels supported above observation. When Ca〓 channels in plasma membrane were blocked by LaCl〓, verapamil or nifedipine, and the Ca〓 channels in endomembranes opened naturally, extracellular CaM couldn't induce 〓 increase. When Ca〓 channels in endomembranes were blocked by ruthenium red and the Ca〓 channels in plasma membrane opened naturally, extracellular CaM induced Ca〓 increase in guard cells, but the extent of Ca〓 increase was lower than that of control.

使用质膜Ca〓通道抑制剂LaCl〓、异博定、尼群地平及细胞内Ca〓通道抑制剂钌红的结果支持这种推测：在质膜Ca〓通道被阻断、细胞内Ca〓通道仍正常开放的情况下，保卫细胞〓不能被CaM诱导增加；细胞内Ca〓通道被抑制、质膜Ca〓通道正常开放的条件下，细胞外CaM诱导保卫细胞内〓升高的幅度不能达到不使用Ca〓通道抑制剂的水平。

I didn't watch TV last night, because it .

昨晚我没有看电视，因为电视机坏了。

Since this year, in a lot of villages of Beijing, TV of elevator liquid crystal was removed.

今年以来，在北京的很多小区里，电梯液晶电视被撤了下来。