细胞毒素的

Cellular and molecular mechanisms of Parkinson's disease: neurotoxins, causative genes, and inflammatory cytokines.

帕金森病的细胞和分子机制：神经毒素，致病基因和炎性细胞因子

The damage of hepatic kupffer cells function and intestine mucosae protective screen function caused cooperatively by ischemia, hypoxia, microcirculatory disarrangement, inflammatory mediators (O〓, OH〓 etc) and cytokines (TNF-α, IL-1, IFN-γetc), the functional damage easily results in bacterial translocation and endotoxemia, as the damage mitigates the clearance of bacteria and toxin.

缺血、缺氧、微循环障碍、炎症介质及细胞因子（TNF-α、IL-1、IFN-γ等）共同作用，使肝脏Kuppfer细胞和肠粘膜屏障功能受损，对内毒素清除能力减弱致内毒素血症，是肝功能衰竭的重要病生环节，亦是继发多脏器衰竭的始动因素，但ALF致病确切机制目前尚不十分清楚。

The p53 gene participated in the regulation of the apoptosis of granulose cells,Zearalenone can enhance the expression of p53 protein in granulose cells.

p53基因参与了小鼠卵巢颗粒细胞凋亡的调控，F-2毒素能增强卵巢颗粒细胞p53蛋白的表达。

Effect of tenuazonic acid on micronucleus and karyokinesis of Vicia faba root tip cells was investigated to evaluate its cytogenetic toxicity.

利用蚕豆根尖为材料，研究了链格孢菌毒素细交链孢菌酮酸对细胞微核和有丝分裂的影响，以评价其细胞遗传毒性。

This paper describes an inhibitory effert of GABA on the incorporation of￣3H-TdR into rat anterior pituitary cells in static primary monolayer cultures. The action was antagonizable by picrotoxin.

本实验利用原代细胞培养体系，观察到GABA对大鼠垂体前叶细胞的氚标胸苷（3H－TdR）基础掺入率有明显的抑制性效应，且可被印防己毒素所反转。

Objective To study the selective toxicity of immunotoxin on T cells and to determine its effect on hematopoietic progenitor cells.

目的 探讨抗T细胞免疫毒素(immunotoxin， IT)体外对脐血T细胞的清除效率及对造血干/祖细胞的影响。

In contrast to the wild strain, it improved the mosquitocidal toxicity,enlarged the mosquitocidal spectrum and provided a way to control the resistant mosquito.

另外，从苏云金杆菌野生株中克隆到一新的杀蚊毒素基因cyt2Ba7，其表达产物对昆虫细胞也具有溶细胞活性。

The tripartite cytolethal distending toxin induces cell cycle arrest and apoptosis in eukaryotic cells.

由三部分组成的细胞致死性扩张毒素诱发真核细胞周期停止和凋亡。

Aware of its central part in anthrax's lethality, many researchers have since focused on learning how the substance "intoxicates" cells— gets into them and disrupts their activities.

知道毒素是炭疽致死的主因之后，许多研究人员开始致力研究这个物质如何造成细胞的中毒——也就是，如何进入细胞并破坏细胞活性。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs.

结果： ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及［Ca2+］i浓度，以上作用可被ETA受体拮抗剂BQ123所完全抑制，被百日咳毒素部分抑制，而ETB受体拮抗剂BQ788则无效；②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用，钙通道拮抗剂硝苯地平可明显抑制ET-1介导的［Ca2+］i浓度增加，但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应；③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活，但可抑制ET-1介导的的［Ca2+］i浓度增加及心肌细胞肥大反应。

Plunder melds and run with this jewel!

掠夺melds和运行与此宝石！

My dream is to be a crazy growing tree and extend at the edge between the city and the forest.

此刻，也许正是在通往天国的路上，我体验着这白色的晕旋。