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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。

Caffeine - A derivative of coffee, is an efficient arouser of central nervous system capable to drive away fatigue, and improve renal circulation. Its stimulation on the cerebral cortex activates Neurotransmitter receptors in the cell membrane; the adenylyl cyclaseactivated on the other surface of the cell catalyzes Adenosine Triphosphate, forming Cyclic adenosine monophosphate, and thus set off series of bio-chemical reactions, like increase of passionate feel, prompt recovery from fatigue after working etc..

咖啡因—由于咖啡本身具有兴奋神经中枢,消除疲劳,增加肾脏血流量的作用,通过对大脑皮层的刺激,使神经递质作用于细胞膜受体,激活了膜另一侧的腺苷酸环化酶,被激活的腺苷酸环化酶催化三磷酸腺苷环化酶,被激活的腺苷酸环化酶催化三磷酸腺苷形成环磷酸腺苷,从而引起一系列生化反应,如增加愉快感和消除事后疲劳等。

It is postulated that IP induces the release of endogenous protective molecules that interact with cognate receptors to activate PLC through mediation of the chincough virus sensitive proteins. PLC hydrolyzes membrane phospholipid and produces diacylglyccerol,that,by working together with calcium hydronium,translocates PKC from cytoplasm to cell membrane and activates PKC.

推测缺血预处理细胞保护作用机制是:缺血预处理引起内源性保护物质释放,作用于细胞膜上的相应受体,通过百日咳病毒敏感性G蛋白的介导而激活磷脂酶,磷脂酶水解膜磷脂,产生二酰基甘油(diacylglyccerol,DAG),DAG和Ca2+协同作用于PKC,使其从胞浆转位到细胞膜并且被活化,PKC在膜上使底物蛋白磷酸化,引发一系列相关信号转导通路的激活,调控保护性基因的表达,从而提高细胞对缺血再灌注损伤的耐受性。

Secondly, the athletes should adopt the vibration training method or the strength training method with unstable supporting surface.Because these two methods can not only activate motion element which couldn\'t be activated in most of time,but also add up the harmonization of the nerve muscle and make the proprioceptor trained.Thirdly,we should make or choose special archery shoes which have slip-resistant sole and suitable degree of bend in the front and back,suiting for the competition ground and adding Up the stability,fourthly,we should properly pay attention to the stage of lifting.

因为这两种训练方法不仅可激活多数情况下不能激活的运动神经元使力量增加,而且可增加神经肌肉的协调性,同时也使本体感受器得到训练,从而增强对射箭动作的感觉能力;第三,为射箭运动员定制或选择有防滑块鞋底、前后上翘程度符合运动员脚型特点的射箭专用鞋,既可以适合比赛地面特点又能增加稳定性;第四,适当重视举弓阶段的训练。

Erve growth factor combined with its receptor, activated Ras - MAP kinase , mitogen - activated protein kinase kinase is the important regulating factor that make IkB kinase, IKK, phosphated, IkB kinase make the IκBα:(the subunit of NF -κB ) phosphated, the phosphated IkBα degraded, and p65 - p50 heterodimer can be formed, then the heterodimer translocated to nucleus and combined with the promoter domain or other consensus sequence.

GF与其受体相结合,最后可以激活Ras-有丝分裂激活的蛋白激酶途径,有丝分裂激活的蛋白酶激酶(MEKK1)是IγB激酶发生磷酸化的重要调节因子,IKK使NF-κB的亚单位IKBα发生磷酸化,磷酸化的IKBα发生降解,而最后留下p65-p50二聚体,该二聚体然后转位到细胞核内与κB基因的增强子区域或与他的顺式作用序列结合。

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。

Bitter compounds in saliva activate particular T2R/TRB isoforms activate gustducin heterotimers, activated α-gustducin stimulates PDE to hydrolyze cAMP, the decreased cAMP may disinhibit cyclic nucleotide-inhibited channels to elevate intracellular Ca2+.

唾液中的苦味化合物激活T2R/TRB同型体,这种激活导致味导素异聚体的激活,被激活的α-味导素又激活PDE,PDE水解cAMP,cAMP水平的降低使环核苷酸抑制的阳离子通道去抑制,从而使细胞内Ca2+升高。

Salty and sour directly transduction by apical channels that are non-gated channel or chemically-gated channel. Bitter compounds in saliva activate particular T2R/TRB isoforms which activate gustducin heterotimers, activated α-gustducin stimulates PDE to hydrolyze cAMP, the decreased cAMP may disinhibit cyclic nucleotide-inhibited channels to elevate intracellular Ca2+.

咸和酸直接通过顶部非门控或化学门控离子通道转导唾液中的苦味化合物激活T2R/TRB同型体,激活导致味导素异聚体的激活,被激活的α-味导素又激活PDE,PDE水解cAMP,cAMP水平的降低使环核苷酸抑制的阳离子通道去抑制,从而使细胞内Ca2+升高。

Bitter compounds in saliva activate particular T2R/TRB isoforms which activate gustducin heterotimers, activated α-gustducin stimulates PDE to hydrolyze cAMP, the decreased cAMP may disinhibit cyclic nucleotide-inhibited channels to elevate intracellular Ca2+.

唾液中的苦味化合物激活T2R/TRB同型体,这种激活导致味导素异聚体的激活,被激活的α-味导素又激活PDE,PDE水解cAMP,cAMP水平的降低使环核苷酸抑制的阳离子通道去抑制,从而使细胞内Ca2+升高。

Results showed that the activity of soil poly-phenol oxidases and acid phosphatase, and soil respiration were suppressed by Starane at 0.5 and 5 mgkg^(-1) dry soil, respectively, during the first several days of experiment, but were slight promoted thereafter. In contrast, treatment with Starane at 50 mgkg^(-1) stimulated at the beginning of experiment but inhibited following that time the activity of soil poly-phenol oxidases and acid phosphatase and soil respiration. Activity of urease was stimulated at the beginning but inhibited in the following days by Starane at 0.5 and 50 mgkg^(-1) dry soil, respectively. However, the pattern of stimulation of urease activity at first several days of experiment followed by reduction to the basil level was observed. With respect to invertase, its activity was constantly depressed in the presence of Starane.

结果表明使它隆在0.5mgkg^(-1)和5mgkg^(-1)质量分数时对土壤多酚氧化酶、酸性磷酸酶和呼吸强度的影响为轻微抑制-激活-恢复稳定的趋势,50mgkg^(-1)质量分数时为轻微激活-抑制-恢复稳定的趋势;使它隆在0.5mgkg^(-1)和50mgkg^(-1)质量分数时对土壤脲酶活性的影响为激活-恢复稳定的趋势,5mgkg^(-1)时则处于抑制-激活的趋势;各质量分数的使它隆浓度对土壤蔗糖酶和土壤全酚均为抑制作用,且质量分数越大抑制越强烈。

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