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interfering effect
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  干预效果
    The Role of Oxidative Stress and TGFβ_1 in Hyperoxia-induced Lung Injury and the Interfering Effect of N- acetylcysteine on Them
    氧化应激及TGFβ_1在高氧肺损伤中的作用及NAC的干预效果
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    Objective To study the deposition of collagen Ⅰ and Ⅲ in hyperoxia induced lung injury in newborn premature rats and to observe the interfering effect of N-acetylcysteine (NAC) on it.
    目的探讨高氧性肺损伤新生未成熟大鼠肺纤维化过程中Ⅰ、Ⅲ型胶原的沉积情况,并观察N-乙酰半胱氨酸(NAC)的干预效果,以期为临床防治高氧性肺损伤后肺纤维化提供一条新的有效途径。
短句来源
    ObjectiveTo find a new effective method for the protection against hyperoxia-induced lung injury in clinic, exploring the effect of oxidative stress and cytokine in the pathogenesis of lung injury and observing the interfering effect of N- acetylcysteine (NAC) on them.
    目的:探讨高氧环境下氧化应激反应及细胞因子在肺损伤发生机制中的作用,并观察N-乙酰半胱氨酸(NAC)的干预效果,以期为临床防治高氧肺损伤提供一条新的有效途径。
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  interfering effect
A slight interfering effect of the poliovirus on the multiplication of ECHO-9 virus has been observed in suckling-mice.
      
An ionic binding of PLA2 to membrane may be alluded from the interfering effect of anionic phospholipids on the PLA2 action.
      
The interfering effect of different technological impurities on the accuracy of determining the concentration of DMAA is reduced to the minimum in the proposed version of the method.
      
Arsenite, arsenate, phosphate and sulfate show strong interfering effect at high anions to fluoride molar ratio in solution.
      
off-line), there is noconsensus on the exact effect of explicitdiscourse markers on text understanding; threedifferent findings are reported in theliterature: markers would have a facilitatingeffect, an interfering effect or no effect atall.
      
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Objective Many studies of recent years had demonstrated that the disorders of thrombic fibrinolytic system are a crucial inductor to the extracellular matrix (ECM) production and accumulation in renal tissues during chronic or progressive renal diseases, as well as to the renal damage of the thrombotic microangiopathy At the same time, the proliferation effect of rennin angiotensin system also plays an important role on these injuries Therefore, the investigation for the effects and interfering...

Objective Many studies of recent years had demonstrated that the disorders of thrombic fibrinolytic system are a crucial inductor to the extracellular matrix (ECM) production and accumulation in renal tissues during chronic or progressive renal diseases, as well as to the renal damage of the thrombotic microangiopathy At the same time, the proliferation effect of rennin angiotensin system also plays an important role on these injuries Therefore, the investigation for the effects and interfering mechanism of angiotensin converting enzyme inhibitor (ACEI) and AT1 receptor antagonist on renal damage has become to a significant researching target in this field recently The study here was designed to detect the mRNA and protein expressions of urokinase type plasminogen activator (uPA) and type 1 plasminogen activator inhibitor (PAI 1) in renal tissues of nephrotic young rats and the interfering effects of ACEI treatment Methods Sixty Wistar rats at 4 months old were chosen in this experiment, 45 rats as the nephrotic group were injected with adriamycin via tail vein for two times, and other 15 rats as the control group were injected with 0 9% saline Two weeks after the injections the nephrotic model was established, which was proved by the blood and urine parameters and the renal pathologic changes All rats were further randomly divided into untreated group, ACEI treated group and control group, 15 rats in each group After treated with ACEI for 12 weeks, the blood pressure, body weight, proteinuria and serum biochemical parameters were measured, respectively The renal morphologic changes were observed on PAS staining slides, the mRNA and protein expressions of PAI 1 and uPA were detected by Northern blot analysis and immunochemical staining Results The expressions of PAI 1 mRNA ( A =1 6) and protein [(65 3±10 2)%] in renal tissues in untreated group increased, but the expressions of uPA [mRNA A =0 4; protein expression (30 3±4 2)%] decreased significantly compared to the control group [PAI 1 mRNA A =0 5; protein (10 6±2 4)%, uPA mRNA A =0 7; protein (85 3±3 0)%] In contrast, PAI 1 mRNA ( A =0 9) or protein (20 7±6 5)% decreased and uPA [mRNA A =0 8; protein (93 1±5 1)% ] markedly increased after the treatment with ACEI ( P <0 01) Conclusions The unbalance of thrombic fibrinolytic system was an important pathophysiologic event during glomerulosclerosic and tubulointerstitial fibrotic lesions The increased expression of PAI 1 and the decreased expression of uPA might induce the efficiency of the endogenous fibrinolytic system ACEI treatment could prevent the accumulation of ECM, which may be mediated by PAI 1 and other cytokines in renal tissues

目的 探讨肾病幼年大鼠肾组织尿激酶型纤溶酶原激活物 (uPA)及其特异性抑制物(PAI 1)mRNA与蛋白质表达的特点 ,及予血管紧张素转换酶抑制剂 (ACEI)苯那普利治疗的影响。方法 采用阿霉素诱导的肾病大鼠为动物模型 ,予ACEI治疗 12周后测大鼠体重、血压、尿蛋白及血生化各项指标的变化 ,同时用Northern杂交及免疫组化染色等方法 ,检测肾组织uPA和PAI 1的mRNA及蛋白表达情况 ,并比较各组间的变化特点。结果 肾病大鼠肾组织PAI 1mRNA吸光度值为 1 6 ,蛋白质组化半定量为 (6 5 3± 10 2 ) % ,uPAmRNA吸光度值为 0 4 ,蛋白组化半定量为 (30 3± 4 2 ) % ;正常对照组PAI 1mRNA吸光度值为 0 5 ,蛋白质组化半定量为 (10 6± 2 4 ) % ,uPAmRNA吸光度值为0 7,蛋白组化半定量为 (85 3± 3 0 ) % ,两组两指标比较差异均有显著意义。经治疗后肾组织PAI 1mRNA吸光度值 0 9,蛋白组化半定量为 (2 0 7± 6 5 ) % ,趋于下降...

目的 探讨肾病幼年大鼠肾组织尿激酶型纤溶酶原激活物 (uPA)及其特异性抑制物(PAI 1)mRNA与蛋白质表达的特点 ,及予血管紧张素转换酶抑制剂 (ACEI)苯那普利治疗的影响。方法 采用阿霉素诱导的肾病大鼠为动物模型 ,予ACEI治疗 12周后测大鼠体重、血压、尿蛋白及血生化各项指标的变化 ,同时用Northern杂交及免疫组化染色等方法 ,检测肾组织uPA和PAI 1的mRNA及蛋白表达情况 ,并比较各组间的变化特点。结果 肾病大鼠肾组织PAI 1mRNA吸光度值为 1 6 ,蛋白质组化半定量为 (6 5 3± 10 2 ) % ,uPAmRNA吸光度值为 0 4 ,蛋白组化半定量为 (30 3± 4 2 ) % ;正常对照组PAI 1mRNA吸光度值为 0 5 ,蛋白质组化半定量为 (10 6± 2 4 ) % ,uPAmRNA吸光度值为0 7,蛋白组化半定量为 (85 3± 3 0 ) % ,两组两指标比较差异均有显著意义。经治疗后肾组织PAI 1mRNA吸光度值 0 9,蛋白组化半定量为 (2 0 7± 6 5 ) % ,趋于下降 ,uPAmRNA吸光度值为 0 8,蛋白组化半定量为 (93 1± 5 1) % ,趋于增高 (P <0 0 1)。结论 肾病病变进展中可出现纤溶系统的平衡紊乱 ,ACEI治疗可改善PA/PAI 1的异常表达 ,防止细胞外基质的异常沉积 ,阻止肾小球硬化和间质纤维化病变的进展

Objective To investigate the changes of tissue-type plasminogen activator (tPA) and 1-type plasminogen activator inhibitor (PAI-1) in blood and the total activity of plasminogen activators (PAs) in urine in children with Henoch-Sch*inlein purpura nephritis (HSPN),and the interfering effects of ACEI and low-molecular heparin therapy.Methods The subjects were 23 HSPN children,and 11 normal children as control group.The blood and urine samples were collected at different times before and after treatment,the...

Objective To investigate the changes of tissue-type plasminogen activator (tPA) and 1-type plasminogen activator inhibitor (PAI-1) in blood and the total activity of plasminogen activators (PAs) in urine in children with Henoch-Sch*inlein purpura nephritis (HSPN),and the interfering effects of ACEI and low-molecular heparin therapy.Methods The subjects were 23 HSPN children,and 11 normal children as control group.The blood and urine samples were collected at different times before and after treatment,the blood tPA and PAI-1 were detected by ELISA,and urinary total activity of PAs by fibrinogen plate method.Results The blood tPA level and urinary PAs activity decreased markedly,but the PAI-1 increased in the children with HSPN.There disorders were ameliorated significantly following the treatment of ACEI and heparin (P<0.01).Conclusion The unbalance of thrombo-fibrinolytic system appeared in HSPN.Elevated levels of PAI-1 and lowered levels of tPA can reduce the function of endogenous fibrinolytic system.Interfering treatment can prevent or quell those disturbances.

目的 探讨过敏性紫癜肾患儿外周血和尿液中组织型纤溶酶原激活物 (tPA)及 1型纤溶酶原激活物抑制物 (PAI 1)的活性和尿纤溶酶原激活物总活性 (PAs)的变化特点及予血管紧张素转化酶抑制剂 (ACEI)、低分子肝素治疗的影响。方法  2 3例紫癜肾儿童为研究对象 ,11名正常对照。分别于ACEI和低分子肝素治疗前、治疗后 1周、治疗后 2周取血、尿标本 ,用纤维平板法测定尿PAs活性 ,用酶联免疫吸附测定 (ELISA)法测定血tPA和PAI 1活性 ,以 x±s报道数据。 结果 紫癜肾患儿于治疗前血tPA水平和尿PAs总活性均明显低于正常对照组 ,而PAI 1水平则显著高于对照组 ,ACEI和肝素联合治疗后 ,随着治疗的持续可明显改善凝血纤溶系统平衡紊乱的趋势 (P <0 0 1)。结论 紫癜肾儿童血、尿凝血纤溶系统平衡紊乱 ,表现为凝血亢进和纤溶障碍 ,干预性治疗具有一定疗效

Objective Glucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood brain barrier (BBB) permeability Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported In this study, the roles of the total hydrosulfide group (TSH), non protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain...

Objective Glucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood brain barrier (BBB) permeability Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported In this study, the roles of the total hydrosulfide group (TSH), non protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain edema in infant rats and the interfering effects of dexamethasone (DEX) and IVIG were investigated Methods In 35 infant rats, 10 mg/kg lipopolysaccharide (LPS) was intraperitoneally injected The same volume of normal saline was injected to 24 control rats Ten mg/kg DEX and 400 mg/kg IVIG were intravenously injected respectively to 36 and 24 infant rats instantly following LPS injection The TSH, NPSH and MDA concentrations and the brain Evans blue contents were detected at different time in the brain tissue The brain water content was measured by drying method Results The brain water, EB and MDA contents after endotoxin injection were significantly higher than those of control group, while the brain TSH, NPSH content were significantly lower than those of control group ( P <0 05 or P <0 01); After treatment with DEX or IVIG, the brain EB, MDA and water content significantly decreased with the peak at 6 h ( P <0 05 or P <0 01), TSH and NPSH significantly increased compared with LPS group However, the NPSH content in IVIG treatment group did not change significantly ( P >0 05) Conclusion Free radicals play a role in the brain edema induced by LPS in infant rats The primary results suggested that DEX and IVIG have therapeutic effect for the endotoxin induced brain edema by affecting the free radicals

目的 探讨总巯基 (TSH)、非蛋白巯基 (NPSH)及丙二醛 (MDA)等自由基在幼年鼠内毒素性脑水肿发病机理中的作用以及地塞米松 (DEX)、IVIG对其干预作用。方法 Wistar鼠 1 2 0只 ,对照组 :2 4只 ,1mg/kg生理盐水腹腔注射 ;单纯内毒素 (LPS)组 :36只 ,1 0mg/kgLPS腹腔注射 ;地塞米松治疗组 (DEX组 ) :36只 ,LPS 1 0mg/kg腹腔注射后 ,立即从尾静脉给予DEX 1 0mg/kg;免疫球蛋白治疗组 (IVIG组 ) :共 2 4只 ,LPS 1 0mg/kg腹腔注射后 ,立即从尾静脉给予IVIG 40 0mg/kg。于不同时间用常规生化方法测定脑组织匀浆中MDA、TSH、NPSH和伊文思蓝 (EB)含量。用干湿法测定脑组织含水量。结果 LPS组脑含水量、EB含量及MDA含量均明显高于对照组 ,而TSH和NPSH含量明显低于对照组 (P <0 0 5或P <0 0 1 ) ;DEX组和IVIG组脑含水量、EB含量及MDA含量与LPS组相比则有明显降低 ,以 6h更明显 (P <0 0 5或P <0 0 1 ) ,而TSH和NPSH含...

目的 探讨总巯基 (TSH)、非蛋白巯基 (NPSH)及丙二醛 (MDA)等自由基在幼年鼠内毒素性脑水肿发病机理中的作用以及地塞米松 (DEX)、IVIG对其干预作用。方法 Wistar鼠 1 2 0只 ,对照组 :2 4只 ,1mg/kg生理盐水腹腔注射 ;单纯内毒素 (LPS)组 :36只 ,1 0mg/kgLPS腹腔注射 ;地塞米松治疗组 (DEX组 ) :36只 ,LPS 1 0mg/kg腹腔注射后 ,立即从尾静脉给予DEX 1 0mg/kg;免疫球蛋白治疗组 (IVIG组 ) :共 2 4只 ,LPS 1 0mg/kg腹腔注射后 ,立即从尾静脉给予IVIG 40 0mg/kg。于不同时间用常规生化方法测定脑组织匀浆中MDA、TSH、NPSH和伊文思蓝 (EB)含量。用干湿法测定脑组织含水量。结果 LPS组脑含水量、EB含量及MDA含量均明显高于对照组 ,而TSH和NPSH含量明显低于对照组 (P <0 0 5或P <0 0 1 ) ;DEX组和IVIG组脑含水量、EB含量及MDA含量与LPS组相比则有明显降低 ,以 6h更明显 (P <0 0 5或P <0 0 1 ) ,而TSH和NPSH含量分别在各时间点上比LPS组明显增高 ,但IVIG对NPSH含量影响与LPS组相比差异无显著性 (P >0 0 5)。结论 自由基参与了幼年鼠内毒素性脑水肿的发生发展 ,初步证实地塞米松和静注免疫球蛋白通过影响自由基 ,具有治疗幼年鼠内毒素性脑水肿的作用

 
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