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One hand mechanical obstruct led to the increase of veinous resistance and the obstacle of microcirculation, the other hand the adhesive PMN was activated in excess, the white blood cells released a lot of enzymes, in which PMN-elastase can decompose the components of cell and many albumens, inclusive of immunoglobulin、alexin and fibrication. These components induced the injury of the pancreatic capillary vessels and cell and lysosome enzy made the tissue protein hydrolyze and produced unsaturated fatty acids, which destroyed the structure and function of cellar membrane. The inflammatory cellar factors activate other immunocytes to produce the injury and necrosis of tissue, which aggravated the pathological injury and led to shock、pyaemia and MODS. So ICAM-1 and LFA-1 played an important role in SAP. Frossard found that the expression of ICAM-1 in the rat model, especially in serum、pancreas and lung. All these showed ICAM-1 is an important factor in AP and concomitant lung injury.

胰腺小叶组织局部血管EC首先被激活,ICAM-1表达升高,与被激活的PMN表面表达的LFA-1相结合,"PMN-EC"相互作用加剧,一方面机械性阻塞毛细血管导致静脉阻力增加、微循环障碍;另一方面粘附的PMN过度吞噬或激活,当白细胞吞噬的颗粒不能被封闭隔离,连同细胞内的酶被释放出来,其中的PMN-elastase能够降解细胞基质中各种成分,水解多种蛋白,加重胰腺的毛细血管内皮细胞和腺泡的损伤;释放的溶酶体酶使组织蛋白水解,产生的不饱和脂肪酸引发脂质过氧化方应,破坏细胞膜的结构和功能;释放的炎性细胞因子,激发其他的免疫细胞的功能,导致进一步的组织损伤和坏死,加重SAP的病理损伤,最终导致休克、脓毒血症及多器官功能障碍等严重后果。

The endotoxin also named as lipopolysaccharide in the outer membrane of Gram-negative bacteria is the primary constituent of pathopoiesis. LPS which has extensive biological activity can induce severe inflammation in cascade and lead to sepsis、systemic inflammatory response syndromes、multiple system organ failure.

细菌壁外膜的内毒素又称脂多糖(lipopolysaccharide,LPS)是其主要致病成分,具有广泛的生物活性,能引起严重的炎症级联反应,是导致脓毒症、系统性炎症反应综合征、多脏器功能衰竭的主要致病因子。

By comparing the body weight, immune organs index and response of lymphocytes to ConA, to analyze the effect of QKL on immunological system of normal mouse. Delayed type hypersensitivity mouse model was established by stimulation with dinitrofluorobenzene. By comparing spleen index and swelling rate of pathogenetic ear, to illuminate the immunoregulation of QKL in vivo. Polymicrobial sepsis mouse model was induced by cecal ligation and puncture. The cumulative survival rate was observed in QKL and NS groups. Results: QKL had no influence on body weight and spleen index of normal mouse, but it could significantly decrease thymus index and inhibit the immune response of lymphocytes to ConA.

连续皮下注射QKL 5 d,通过检测小鼠体重、免疫器官指数和淋巴细胞对ConA刺激的反应,分析QKL对正常小鼠免疫功能的影响;采用二硝基氟苯诱发小鼠耳朵肿胀,发生接触性皮炎,建立DTH模型,通过比较QKL与NS对照对小鼠脾脏指数和发病耳肿胀抑制率评价QKL体内对小鼠的免疫调节功能;采用盲肠结扎穿孔术后引起的多细菌性腹膜炎,建立小鼠脓毒症模型,通过观察QKL对小鼠存活状况的影响,评价QKL的免疫调节作用。

One hand mechanical obstruct led to the increase of veinous resistance and the obstacle of microcirculation, the other hand the adhesive PMN was activated in excess, the white blood cells released a lot of enzymes, in which PMN-elastase can decompose the components of cell and many albumens, inclusive of immunoglobulin、alexin and fibrication. These components induced the injury of the pancreatic capillary vessels and cell and lysosome enzy made the tissue protein hydrolyze and produced unsaturated fatty acids, which destroyed the structure and function of cellar membrane. The inflammatory cellar factors activate other immunocytes to produce the injury and necrosis of tissue, which aggravated the pathological injury and led to shock、pyaemia and MODS. So ICAM-1 and LFA-1 played an important role in SAP. Frossard found that the expression of ICAM-1 in the rat model, especially in serum、pancreas and lung. All these showed ICAM-1 is an important factor in AP and concomitant lung injury.

胰腺小叶组织局部血管EC首先被激活,ICAM-1表达升高,与被激活的PMN表面表达的LFA-1相结合,&PMN-EC&相互作用加剧,一方面机械性阻塞毛细血管导致静脉阻力增加、微循环障碍;另一方面粘附的PMN过度吞噬或激活,当白细胞吞噬的颗粒不能被封闭隔离,连同细胞内的酶被释放出来,其中的PMN-elastase能够降解细胞基质中各种成分,水解多种蛋白,加重胰腺的毛细血管内皮细胞和腺泡的损伤;释放的溶酶体酶使组织蛋白水解,产生的不饱和脂肪酸引发脂质过氧化方应,破坏细胞膜的结构和功能;释放的炎性细胞因子,激发其他的免疫细胞的功能,导致进一步的组织损伤和坏死,加重SAP的病理损伤,最终导致休克、脓毒血症及多器官功能障碍等严重后果。

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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。

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我比喻得过头了。