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白细胞生成

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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。

PTX at tenuates the ALI induced by LPS or sepsis in rat. The therapeutic effects of PTX include:improve oxygenation, at tenuate pulmonary edema formation, enhance animal survival in sepsis-induced ALI. The mechanisms may related with the effects of PTX inhibiting the chemotaxis, migration, activation of inflammatory leukocytes, diminishing the production of active oxygen, and inhibiting inflammatory cytokine release partly.

4PTX对大鼠内毒素性ALI及脓毒症性ALI均有一定的防治作用,主要表现在改善动脉血氧合,减轻肺水肿形成,提高脓毒症性ALI大鼠的存活率等方面,其机理可能与抑制白细胞趋化与激活,减少肺内白细胞渗出及活性氧产生,一定程度上抑制炎性细胞因子生成等有关。

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This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。

There is no differences of cell proliferation vitality between labeled and unlabeled NSCs.

双标记神经干细胞的增殖、分化活力与未标记神经干细胞相比无改变。