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ir损伤
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  i-r injury
     Conclusion:Previous to hepatic I-R, the pretreatment with lidocaine injected into hepatoduodenal ligament as a novel approach attenuates hepatic warm I-R injury of rats effectively, and alters some protein expressions of rat liver of I-R injury.
     结论 :肝十二指肠韧带内注射利多卡因预处理有效地减轻了大鼠肝脏随后的I R损伤 ,是一种保护面临I R损伤肝脏的新方法。 蛋白质组学研究可见 ,利多卡因预处理改变了肝脏I R后的蛋白质表达。
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     Conclusion Hemodilution may provent the lungs from I-R injury,which is better with hemodilution before ischemia.
     结论 血液稀释对肺I R损伤有预防保护作用 ,而缺血前稀释血液效果更明显
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  “ir损伤”译为未确定词的双语例句
     Results (1)IR injury stimulate the activation of Caspase-3, the Caspase-3 mRNA and cell apoptosis started to increase after ischemia reperfusion lasting for 4 h, lasting for 12 h Caspase-3 mRNA reached the peak. There was a positive correlation between Caspase-3 mRNA expression and cell apoptosis (r=0.9286,P<0.001).
     结果(1)IR损伤激发了Caspase-3的活化,交界区Caspase-3mRNA与心肌细胞凋亡在IR损伤8h后开始升高,12h达高峰,二者之间存在着明显的正相关性(r=0.9286,P<0.001)。
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     Methods Thirty-six SD rats were divided into three groups(n=12) at random: sham group,ischemia-reperfusion(IR) group and SM group.
     方法夹闭大鼠腹腔动脉、肠系膜上动脉40 m in,再灌注6 h制备胰腺IR损伤模型,取SD大鼠36只,随机分为3组(n=12):假手术组(Sham组)、缺血—再灌注组(IR组)、缺血—再灌注丹参保护组(SM组)。
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     IP may reduce IR injury of liver and its possible mechanism is to inhibite apoptotic hepatocytes by down-regulating caspase 3 activity.
     结论 IR损伤可激活Caspase3活性 ,促进肝细胞凋亡 ,从而加重肝脏损害 ,IP可明显减轻肝脏IR损伤 ,可能的机制之一是下调Caspase3的活性来抑制肝细胞调亡。
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     Conclusion EGb761 could induce HO-1 overexpression, through its antiinflammatory and antioxidative action to upregulate Bcl-2 and downregulate Bax,thus protect against cardiomyocyte apoptosis from IRI.
     结论EGb761能明显诱导心肌细胞内HO-1表达,并通过HO-1的抗炎、抗氧化等作用下调Bax表达,上调Bcl-2表达,从而显著抑制IR损伤后心肌细胞凋亡。
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     Methods Models of rabbits intestinal I/R injury was made. The effect of astragalus on the viscosity and malondialdehyde (MDA) in erythrocyte membrane, superoxide dismutase (SOD) in erythrocyte, oxidase (XO) in plasma were observed.
     ②方法 复制家兔I R损伤模型 ,检测给予黄芪后I R损伤家兔RBC膜微黏度的变化 ,同时检测RBC超氧化物歧化酶 (SOD)、RBC膜丙二醛 (MDA)含量及血浆黄嘌呤氧化酶 (XO)活性 ,并与I R组及假手术组比较。
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     , Ir.
     Ir.
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     , Ir.
     ,Ir.
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     In addition, renal histomorphological damage in either light or electronic microscope in IR group were evidently more serious than that in control group.
     IR组有明显的组织学损伤改变。
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     Duodenal injuries
     十二指肠损伤
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     The more severe the head injury is, the higher the values of FBG and HOMA-IR are in the patients with head injury.
     颅脑损伤程度越重,血糖和HOMA-IR越高。
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  i-r injury
However, there has been an ongoing debate upon the relative contribution of cardiomyocyte apoptosis to the myocardial infarct size after ischemia-reperfusion (I-R) injury.
      
We tested the hypothesis that blocking the death receptor pathway of apoptosis through genetic deletion of Fas receptors or Fas ligands would reduce myocardial infarct size caused by acute I-R injury.
      
The cellular mechanisms involved in the development of renal I-R injury have been targeted by several pharmacological interventions.
      
However, although showing promise in experimental models of renal I-R injury and ischemic ARF, they have not proved successful in the clinical setting (e.g., atrial natriuretic peptide, low-dose dopamine).
      
The extent of lipid peroxidation after ischemia-reperfusion (I-R) injury in rat kidney has been controversial.
      
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An in vivo porcine heart ischemia and reperfusion model was used to study the mechanisms of myocardial ischemia and reperfusion injury. The results showed1 In ischemic and reperfused myocardium, Na and Ca significantly increased and K declined.2 Chemiluminescence of coronary sinus blood during reperfusion was increased significantly. The fluidity of sarcolemma of myocardial celt in the ischemic zones was decreased. These results indirectly demonstrated increased free radical production during reperfusion and...

An in vivo porcine heart ischemia and reperfusion model was used to study the mechanisms of myocardial ischemia and reperfusion injury. The results showed1 In ischemic and reperfused myocardium, Na and Ca significantly increased and K declined.2 Chemiluminescence of coronary sinus blood during reperfusion was increased significantly. The fluidity of sarcolemma of myocardial celt in the ischemic zones was decreased. These results indirectly demonstrated increased free radical production during reperfusion and myocardial damage caused by free radicals.3 Using ESR technique, it was found that during ischemia and reperfusion, oxygen free radicals produced by WBC respiratory explosion increased. This demonstrated that WBC participates in myocardial ischemia and reperfusion injury and WBC is one of the sources for oxygen free radicals.

应用小型猪在体心脏缺血再灌注(IR)模型,探讨心肌IR损伤机制。发现心肌IR后有下列变化:①心肌细胞内钙、钠增多,钾减少。②心肌细胞膜流动性降低及冠状窦静脉血化学发光增强,间接显示自由基产生增多。③白细胞激活后产生氧自由基的反应增强,提示白细胞可能参与IR损伤机制。

Objective:To investigate the injury mechanism concerning acute lung injury associated with local intestinal ischemiareperfusion(IR).Methods:Animal model of intestinal IR injury was produced by occluded superior mesenteric artery for 60 minutes and reperfused for 90 minutes.Samples of serum and alveolus lavage fluid were collected before and after injury and tested for calcitonin gene related protein (CGRP) and 6ketoprostaglandin F 1α (6ketoPGF 1α ) levels by radioimmunoassay(RIA).Simultaneously,leukocyte...

Objective:To investigate the injury mechanism concerning acute lung injury associated with local intestinal ischemiareperfusion(IR).Methods:Animal model of intestinal IR injury was produced by occluded superior mesenteric artery for 60 minutes and reperfused for 90 minutes.Samples of serum and alveolus lavage fluid were collected before and after injury and tested for calcitonin gene related protein (CGRP) and 6ketoprostaglandin F 1α (6ketoPGF 1α ) levels by radioimmunoassay(RIA).Simultaneously,leukocyte aggregation and tissue injury of lung were examined under light microscopy (LM) and electron microscopy (EM).Results:Animals subjected to IR died within 4 hours,but those in shamoperating group without I R all survived within 24 hours of reperfusion.Using LM and EM,it was found that number of inflammatory leukocytes and inflammatory secretion obviously increased in lung tissue,which resulted in the pulmonary alveolus collapse and alveolar walls thickening.Furthermore,levels of 6ketoPGF 1α in alveolus lavage fluid after IR injury were higher than that of sham operating group.However,levels of CGRP in plasma after intestinal IR were obviously increased compared with baseline values.Treatment with phospholipase A 2 PLA 2 inhibitor or cycloxgenase inhibitor and lipooxygenase inhibitor attenuated acute lung injury,and it could prolonged the survival time of animals,decreasing levels of leukocytes in lung obviously,and making different effects to 6ketoPGF 1α and CGRP.Conclusions:PLA 2 activation and its metabolites release appear to be strongly involved in the acute lung injury following in testinal IR injury.

目的:探讨肠缺血再灌注(IR)损伤对远隔器官肺脏的损伤机制。方法:采用大鼠肠系膜上动脉夹闭造成肠IR损伤模型,收集动物损伤前后血和肺组织灌注液,利用放射免疫分析法测定样品中降钙素基因相关肽(CGRP)及6酮前列腺素F1α(6ketoPGF1α)含量,同时经光镜和电镜观察肺局部白细胞浸润及组织损伤情况。结果:IR损伤组动物4小时后全部死亡,而假手术组动物在24小时内全部存活。肺部光镜和电镜发现损伤后肺小血管和介质中白细胞明显增多,肺泡内炎性分泌物增加,肺泡腔关闭,肺泡壁明显增厚。IR损伤后,肺灌洗液中6ketoPGF1α明显高于假手术组,而血中CGRP明显高于伤前水平;使用磷脂酶A2(PLA2)抑制剂或其代谢产物合成的阻断剂可以明显延长动物存活时间,并明显减少肺内白细胞的数量,同时还对6ketoPGF1α和CGRP有不同的影响。结论:PLA2激活及其代谢产物的释放在肠IR急性肺损伤中发挥重要作用。

AIM and METHOD:On the model of limb ischemia-reperfusion(IR),the effect of ischemic preconditioning(PC)were observed.RESULTS: After the rats' limb were subjected to IR,hypotension occurred and enzymes leaved out from the cytoplasma and lysosomes.In the plasma and tissue the malondialldehyde(MDA,the metabolite of lipid peroxides) content increased significally.The edema of tissue and overload of calcium in skeletal muscular mitochondria occured.At the same time,it was found that the capillary permeability increased...

AIM and METHOD:On the model of limb ischemia-reperfusion(IR),the effect of ischemic preconditioning(PC)were observed.RESULTS: After the rats' limb were subjected to IR,hypotension occurred and enzymes leaved out from the cytoplasma and lysosomes.In the plasma and tissue the malondialldehyde(MDA,the metabolite of lipid peroxides) content increased significally.The edema of tissue and overload of calcium in skeletal muscular mitochondria occured.At the same time,it was found that the capillary permeability increased and the neutrophil infiltrated into limb tissue.In the plasma,the endothelin level also increased .However,treatment with PC to IR rats can alleviate there changes as mentioned above.CONCLUSION: PC protected rats from limb IR injury and the protective action on capillary bed is one of the protective mechanisms of PC. .

目的和方法在大鼠肢体缺血再灌注(IR)损伤模型上观察了缺血预处置(preconditioning,PC)的影响。结果:发现PC可以明显减轻IR引起的血压降低,血浆乳酸脱氢酶、组织蛋白酶D活性及脂质过氧化产物丙二醛含量的升高;并抑制骨骼肌组织水肿及骨骼肌细胞线粒体钙超载的发生。同时还观察到,PC对IR时肢体微血管通透性升高、中性粒细胞浸润及血浆内皮素水平增高均有抑制作用。结论:PC对大鼠IR肢体有保护作用,其保护机理之一与其对血管床的保护作用有关。

 
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