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细胞生成

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Sanchez ET ,Botella LM ,Velasco B ,et al. Synergistic cooperation between hypoxia and transforming growth factor2beta pathways on humanvascular endothelial growth factor gene expression. J Biol Chem ,2001,19,276:38527238535.[3] Blancher C,Moore JW,Talks kl,et al.Relationship of hyposia-inducible factor HIF-1alpha expression to vascular endothelial growth factor I nduction and hypoxia survival in human breast cancer cell lines.

肝细胞癌中缺氧诱导因子-1α、热休克蛋白70的表达】;综上所述,肝细胞癌发生后,由于血供不足诱导HIF-1α过度表达,应激状态下产生的HSP70通过减轻缺血性损伤,增加毛细血管的生成及减轻细胞凋亡等途径使肿瘤细胞的增殖、移行加快,促进恶性肿瘤的生长、浸润和转移,使肿瘤细胞在适应缺氧、能量代谢、细胞凋亡及转移中起重要作用。

The living cell of L428 cell has experienced from monoclonal to the multi-cell forming process,and presents a big cell around many small clone cell encystation phenomenon.finally,gigantic cells is dead in the life time.3.The cell counting result showed that the proportion of big cell or the H/RS type cell(diameter≥25um)is for(11.6±1.5)%in the L428 group,for(4.6±0.7)%in L428-MVC group and for(13.1±1.3)%in L428-EVC group,respectively.

经持续稀释成单个大细胞、单个小细胞的L428细胞,小细胞可分裂转化成大细胞,大细胞亦可生成小细胞;常见单个大细胞周围出现多个小细胞围绕的现象,在此过程中NF-kB一直持续活化。3。

Can accelerate the bone marrow cell from G1 phase into S phase when we measure it's Cell cycle, it make S phase rate was increased .thus it promoted DNA synthesize and repaired. Mice irradiated at dose of 5.5 Gy gamma-irradiation showed timed-related decreases and restores in peripheral blood picture at day 1 through day 21, the counts of WBC of these group had taken drug has various degree to increase than irradiation control group in day 1. Grugs failed to protected the peripheral blood cell at lowest point, but seems promote their rescovery.9803 treated group was distinct. At 7days after mice were radiated in 3.5 Gy. we observed drug can Significantly hold back the decreased number of hematopoietic progenitors colony forming radiation induced. These findings indicated 9803 have a certain radioprotective activity against gammer irradiation in mice.

给药组的 CFU-S 数量较照射对照组明显增加,3.5Gy 照后第七天观察给药9803组对小鼠骨髓造血组细胞集落生成能力的影响,给药组的造血祖细胞集落的形成能力强于照射对照组,并且9803组明显优于523组。5.5Gy 照射引起的小鼠的外周血细胞数量的降低以 WBC 发生最早,照后24小时给药组的 WBC 数量均比照射对照组有不同程度的升高,以9803各给药组最为明显,药物未能使照射引起的外周血细胞最低值升高,而有降低的趋势,但给药对照射后期外周血象的总体恢复有较好的促进作用。7.5Gy 照射后第七天测定小鼠骨髓细胞周期的测定中发现9803具有促进骨髓细胞由 G1期进入 S 期的效应,致使 G0/G1期细胞显著减少, S 期细胞比率显著增加,这利于促进 DNA 合成修复,即促进骨髓细胞增殖,骨髓细胞 DNA 含量给药组显著高于照射对照组。

Results In the medium and high dose F0 groups, it was observed that the atrophy and incrassation of seminiferous tubule, decrease of spermatogenesis, hyperplasia of interstitial tissue, especially in high dose groups spermatozoon abnormality and nucleolus concentration in the rats testis after DU ingestion for 14 months. The changes became more severe with the prolongation of DU ingestion. Such changes occurred in filial rats (F1) after DC ingestion for 5 months. In the medium and high dose F0 groups, it was observed that a little atrophy of kidney glomerulus, hyperplasia of interstitial tissue after DC ingestion for 14 months, and kidney glomerulus fibrosis happened after DC ingestion for 20 months, such changes occurred in filial rats (F1) after DC ingestion for 5 months In the medium and high dose F0 groups, splenic germinal center and periarterial lymphatic sheaths were hyperplasia , companies with lymphopoiesis after DC ingestion for 7 months, splenic white pulp became more small and sparse after DC ingestion for 20 months.

结果 F0代的中、高剂量组大鼠摄入贫铀14个月后可见雄性的精曲小管萎缩,管壁增厚呈空虚网状,生精细胞层次减少,间质细胞增生,但仍见有精子生成;高剂量组可见到精子呈异型性改变,细胞核浓缩深染,且随着摄入时间延长改变愈趋明显;F1代大鼠摄入贫铀5个月后就有上述改变且更为严重。F0代中、高剂量组大鼠摄入贫铀14个月后肾小球轻度萎缩,间质增生明显,20个月时肾小球萎缩纤维化;F1代大鼠摄入贫铀5个月后就有上述改变。F0代中、高剂量组摄入贫铀7个月时脾脏生发中心和淋巴鞘增生,淋巴母细胞增生活跃,20个月时脾小体减少,生发中心稀疏;F1代大鼠摄入贫铀早期和晚期有类似改变。F0和F1代高剂量组摄入贫铀早期肝脏有炎症细胞浸润,晚期骨髓有核细胞减少,脂肪细胞增加。

Aside from pancreatic enzymes activiation and autodigestive process, recent investigations have established that the upregulation of inflammatory mediator are believed to be the critical steps in the progression of mild pancreatitis to severe pancreatitis. Tumor necrosis factor-, ThyomboxaneA2 ,ProstaglandinsI2 are all important inflammatory mediator. TNF-( is one of cytokines. It is important to the over-production of ICAM-1,VCAM-1, TXA2 andPGI2. The ICAM-1 and VCAM-1 mediate both leukocytes adhesion and migration through the endothelium into tissues to connect with injuried target cells. The TXA2 and PGI2 are the production of arachidonic acid. They are responsible for the tissue ischaemia.

肿瘤坏死因子(Tumor necrosis factor-, TNF-、血栓素A2(ThyomboxaneA2,TXA2),前列环素(ProstaglandinsI2,PGI2)均是炎症反应中重要的炎性介质,其中肿瘤坏死因子-是非常重要的细胞因子之一,它由活化的单核细胞产生,在细胞间黏附分子(Intercellular adhesion molecule-1,ICAM-1)及血管细胞黏附分子(Vascular cell adhesion molecule-1,VCAM-1的表达、血栓素A2及前列环素过量生成方面起着重要的作用,前两者是介导白细胞与内皮细胞黏附,迁移于组织并与受损的靶细胞相结合的主要媒介,是炎症反应中的重要介质,后两者是花生四烯酸的代谢产物,亦是重要的炎性介质,参与构成血液循环障碍。

From the outside to the inside , the body skin is divided into the stratum corneum , stratum lucidum , stratum granulosum , stratum spinosm and stratum basale , after through stratum corneum , stratum lucidum , stratum granulosum , stratum spinosm EGF can reach the stratum basale: accelerate the basal cells prpliferation and differentiation , reverse matured cells' differentiation to make stem cells that will form a " stem cells island " with a certain amount , which accelerate the generation of new cellls , make senescent cells keratinize and shed rapidly , make broken and denatured collagen fibers and elastic fibers repaired , so the skin's elasticity increase , and the wrinkles calm down or disappera gradually .

体表皮由外及里共分为角质层、透明层、颗粒层、棘细胞层、基底层,EGF可以通过透明层、颗粒层、棘细胞层深入肌肤基底层,加速基底层细胞增殖分化,将已经分化成熟的细胞逆分化成干细胞,当达到一定量时,便会形成&干细胞岛&,加速新细胞的生成,让衰老细胞快速角化、脱落,已断裂、变性的胶原纤维和弹性纤维得到修复,皮肤弹性增加,皱纹逐渐平复、消失。

VEGF can specifically increase the dividing, proliferation and movement of endotheliocyte, as well as the permeability of tumor vessels, making it a crucial angiogenic factor in research.

血管的生成机制中,血管内皮生长因子(vascular endothelial growth factor,VEGF)是重要的直接作用于血管内皮细胞的生长因子,可以特异性地促进内皮细胞分裂、增殖、移动,增加血管的通透性,在血管形成中起重要作用,是目前特别受重视的血管生成因子之一。

Aβ(β-amyloid peptide) induce neuronal cell damage by increasing the generation of ROS. Therefore, we further assessed the effects of test compounds on living cells. Esculetin was the most potent agent at protecting cells against Aβ induced cell cytotoxisity via inhibiting the generation of ROS or ROS scavenging among the tested coumarin derivatives.

由於Aβ肽造成神经细胞伤害涉及自由基的过度生成,因此我们将上述结构-活性关系结论进一步应用在活体细胞实验的表现,结果显示esculetin可以透过抑制自由基生成或自由基清除作用而降低Aβ所引发的细胞毒性。

Suicide genes can convert the drug into toxical metabolic product, cytokines can enhance the antineoplastic and immunologic responses, angiogenesis inhibitors can inhibit the development of new vessels, and apoptosis related factors can induce the apoptosis of tumor cells.

自杀基因能将药物转化为毒性代谢产物,细胞因子能增强抗肿瘤免疫效应,血管生成抑制因子能抑制血管生成,凋亡相关分子能诱导细胞凋亡,这些基因在前列腺癌的基础和临床研究中均表现出一定的肿瘤生长抑制作用。

The capacity of endothelial cells to recognize and migrate in response to the extracellular matrix depends on one or more members of the integrin family of cell adhesion receptors.

血管新生的过程依赖于参与血管生成的细胞因子和细胞粘附的协同作用,整合素是一组细胞表面受体,介导细胞-细胞间、细胞-基质间的相互作用,对内皮细胞的粘附、迁移、增殖起重要作用。

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呼气,收缩臀部肌肉;拱起身体,尽量抬起头来,右腿伸直朝向天花板(膝微屈,以避免肌肉紧张)。

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