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硬化的细胞

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The present study analysis whether CRP could directly induce inflammation in endothelial cells, analysis what kind of effects CRP provide on cellular signal transduction in endothelial cell by gene array, and isolate LDL by one step of density gradient centrifugation, generate E-LDL by degrading LDL with multiple enzymes, direct fluorescent labeling CRP and LDL, investigate whether CRP play as intermediator in atherosclerosis.

本课题目的在于探讨CRP在脂质参与的动脉粥样硬化形成中是否起到介质作用,主要通过检测直接CRP能否诱导内皮细胞炎症表现,基因芯片分析CRP对内皮系统的细胞信号转导通路的影响,探讨CRP参与调控内皮系统炎症过程的主要机制,并且通过一步法密度梯度离心分离LDL,复合酶处理生成E-LDL,直接荧光标记CRP和LDL,分析CRP介导脂质紊乱尤其是LDL代谢产物参与动脉粥样硬化早期形成的作用。

Aim To observe changes of peroxisome proliferator activated receptor γ mRNA, ATP-binding cassette transporter A1 (ABCA1) mRNA and CD36 mRNA in foam cells which come from the peritoneal macrophage of apolipoprotein E knock out mice with giant knotweed rhizome, hawthorn and both of them, and discuss possible mechanism of anti-atherosclerosis on gene level.

目的 观察中药虎杖、山楂配伍对载脂蛋白E基因敲除小鼠巨噬细胞源性泡沫细胞内过氧化体增殖物激活型受体γ、三磷酸腺苷结合盒转运子A1及CD36 mRNA表达的影响,从基因水平探讨虎杖和山楂配伍对动脉粥样硬化泡沫细胞形成的干预机制。

Wenxin capsule can promote endolethial cells releasing CO and synthesing 〓, enhance activity of HO, induce angiectasis through activating guanylic cyclase and adenglate cyclate of intracellar of vessel smooth muscle cell to enhance content of intracellar cGMP and AMP. 3. Wenxin capsule can inhibit releasing of platelet activiting factor 〓 which inhibit platelet aggregation and have antithrombosis function. 4. Wenxin capsule can promote activity of t-PA, reduce activity of PAI-1, strengthen fibrinolytic function, therefore inhibit fibrin disposition. 5. Wenxin capsule can inhibit synthesis of smooth muscle cellular DNA. Its function don't kill it directly but prevent transformation from period Go to peried S. 6. Wenxin capsule is an effective prescription of anti-coronary atherosclerosis atherosis. The results of image pattern analysis tastifies that area of lipid plaque in treating group reduce 54% and 58% in contrast with that in control group. The results of light, electro- microscopy show that structure of endolethial cell and smooth muscle cell in treating group is more integral than that in control group.

其作用机制之一是由于该药具有良好的调脂降脂作用,其不仅能明显降低血清LDL-c及升高HDL-c含量,且能有效阻止TC沉积于血管壁,从而保护内皮细胞结构完整;此外,温心胶囊尚具有明显的抗氧化作用,该药不仅能明显降低血浆LPO含量,且能提高SOD活性,同时其对血红素在细胞内代谢的调节作用也参与了抗氧化过程。2 温心胶囊能明显促进内皮细胞释放CO及合成〓,提高HO活性,通过激活血管平滑肌细胞内鸟苷酸环化酶及腺苷酸环化酶引起细胞内cGMP、AMP浓度增加而引起血管舒张。3 温心胶囊能明显抑制血小板激活因子〓的释放,从而抑制血小板聚集,抗血栓形成。4 温心胶囊能明显提高t-PA活性,降低PAI-1活性,增强纤溶功能,从而抑制纤维蛋白沉积。5 温心胶囊能明显抑制平滑肌细胞DNA合成,其抑制作用不是直接杀伤抑制,而是阻止细胞由Go期向S期转化。6 温心胶囊是抗冠状动脉粥样硬化的有效制剂,图象分析结果证实,该药治疗组脂斑面积比对照组缩小了54%和58%,光电镜结果显示内皮细胞及平滑肌细胞结构较为完整。

Since 1962, when Gross and Lapiere discovered the first MMPs-collagenase, man had discovered various of MMPs in succession, where MMP-2 has a strong degradational effect on extracellular matrix, it is secreted bymacrophage, smooth muscle cells and endothelial cells and so on.

自从 1962年 Gross和 Lapiere发现第一种基质金属蛋白酶一胶原酶以来,人类陆续发现了很多种基质金属蛋白酶,其中的MMP—2对细胞外基质具有极强的降解作用,它由巨噬细胞、平滑肌细胞以及内皮细胞等分泌,在动脉粥样硬化斑块中憎多时降解纤维帽及基底膜的胶原等基质成分,是使纤维帽变薄及加速动脉粥样硬化的重要因素之一。

Cases healthy subjects served as control. In addition, density of glomerular matrix membrane and quantity of cell in glomeruli were measured with CMIAS image analysis system by computer. Global sclerosis, cellular crescents, fiber or fibrocellular crescents were measured with Memphis scope. Tubulointerstitial lesions were examined with semi-quantitative grades (including O-III grades).Results Compared to normal control, there was a significant increase of urinary TGF-betaK IL-6 and Col-lV levels in patients with IgAN (p. 01). There were also significantly positive correlation between the levels of urinary TGF-betaK Col-IV and density of glomerular matrix membrane ., interstitial fibrosisp.

采用酶联免疫吸附法测定尿TGF-β1(Transforming growth factor-β1)、尿IL-6(interleukin-6)和尿Col-Ⅳ(type Ⅳ Collagen);采用免疫组织化学法检测肾组织TGF-β1、Col-Ⅳ表达;应用CMIAS多功能真彩色病理图像分析系统对肾小球基质基底膜面密度和细胞个数进行半定量测定;对球性硬化、节段硬化、细胞新月体及纤维或纤维细胞新月体所占肾小球百分数和肾小球IgA沉积免疫荧光强弱的判断采用Memphis法进行评分;肾小管间质病变程度采用光镜下半定量分级法(包括0-Ⅲ级)。

Leucocytic differentiation antigen 40 sign-al access participates in regulation of inflammatory reaction accommodation of major cell component (vascular endothelial cell、vascular smooth muscle cell and macrophage), it is playing critical role in AS process, participates ather-osclerotic occurrence and development ,reside in atherosclerotic plaque cell thro-ugh CD40-CD40L interaction, induce activate by itself , express and secrete profit to happen immune response、inflammatory reaction、hemagglutination t-hrombogenic proteo-cytokine.

白细胞分化抗原40 (CD40)信号通路参与了动脉粥样硬化斑块内主要细胞成分(血管内皮细胞、血管平滑肌细胞以及巨噬细胞)炎症反应的调节,其在AS进程中扮演着关键性的角色,参与了动脉粥样硬化的发生和发展;存在于AS斑块内的细胞通过CD40-CD40L相互作用,导致自身活化,表达和分泌了有利于免疫应答发生、炎症反应、血凝和血栓形成的蛋白质细胞因子,如激活在AS斑块中的关键性细胞成分如黏附分子、炎症因子、基质金属蛋白酶等的产生,导致斑块的不稳定和破裂,而最终导致粥样硬化斑块病变的恶化。

In this study, we evaluated pathology, cytoplasmic factor and the phenotypic transition of primary kidney cells in the glomerulosclerosis rats, to explore the mechanism of the glomerulasclerosis and the effects of Shenshuning of smoothing shaoyang and treating both the primar...

本研究从肾脏病理、细胞因子网络和肾脏固有细胞的表型转化方面等探讨肾小球硬化的病理机制和疏利少阳标本兼治法之肾疏宁对阿霉素肾小球硬化大鼠的作用和作用机理。

In the experimental group (transplanted with embryonic arcuate nucleus), the endothelial cells remained intact, and connected tightly with subendothelial tissue, occasionally twisted nucleus could be seen.

实验证明,在被毁损弓状核区重新植入胚鼠弓状核细胞后对动脉粥样硬化有明显恢复作用,从而证实下丘脑弓状核对动脉粥样硬化的形成具有重要调控作用。

The results showed that though testosterone or 17-β-estradiol did not affect the expression of these AM in unstimulated HUVEC, both of them transiently increased the expression of E-selectin and VCAM-1 in TNF-α-stimulated HUVEC.

近几年研究发现,粥样硬化与炎症及免疫反应有关,TNF-α等细胞因子可以通过刺激血管内皮细胞粘附分子的表达及血管平滑肌细胞的增殖等而在粥样硬化的形成中起重要作用。

This model suppled a reliable pathological cell tool for the study of atherosclerosis .

本实验从离休细胞培养方面探寻建立小鼠巨噬细胞源性泡沫细胞的可能性,为动脉粥样硬化的形成机理分析和防治研究提供了一种可靠的病理细胞模型。

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The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

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