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damaged group
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  损伤组
    APP 17 mer peptide and Aβ 25 35 were synthesized by solid phase method and purified by HPLC. Human neuroblastoma cells SY5Y were segregated into 3 groups: normal control group, Aβ 25 35 (10 μmol/L) damaged group, and Aβ 25 35 (10 μmol/L) +APP17 mer peptide(10 μmol/L) for neuroprotection group.
    用固相法合成APP1 7肽、Aβ2 5 3 5,高效液相纯化 ,以人神经母细胞瘤株SY5Y为细胞模型 ,分为正常对照组、Aβ2 5 3 51 0 μmol/L损伤组和Aβ2 5 3 51 0 μmol/L加APP1 7肽 1 0 μmol/L保护组。
短句来源
    Compared with normal control group, Aβ 25 35 damaged group showed reduced cell count and MTT metabolic rate, increased LDH leakage rate, diminished axonal length and area of cell body, reduced NT 3 expression, increased concentration of cytosolic calcium(Ca 2+ ), but the addition of APP17 mer peptide normalized the foregoing changes.
    结果 :与正常对照组相比 ,Aβ2 5 3 5损伤组轴突长度和胞体面积均缩小 ,细胞计数减少 ,MTT代谢率降低 ,LDH漏出率升高 ,细胞内Ca2 + 浓度升高 ,而加入APP1 7肽保护后 ,可使上述指标恢复或接近正常。
短句来源
    METHODS:APP 17-mer peptide and Aβ25-35 were synthesized by solid phase meth od and purified by HPLC. Human neuroblastoma cells SY5Y were grouped into normal control group,Aβ25-35 damaged group and Aβ25-35+APP 17-mer peptide for neu roprotection group.
    方法:固相法合成APP17肽、Aβ25-35,高效液相纯化,以人神经母细胞瘤株SY5Y为细胞模型,分为正常对照组、Aβ25-3510μmol/L损伤组和Aβ25-3510μmol/L加APP17肽10μmol/L保护组。
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  damaged group
Low IQ patients performed like the brain-damaged group; high IQ children failed to benefit from reduction in stimulus competition and produced more bizarre and irrelevant responses.
      
Figure 9 shows that the severely damaged group has two subgroups, A and B.
      


A test of the judgement of linear orient-ation was given to 168 patients with braindamage.240 normal persons comprised a con-trol group.The results showed that:1)theperformance level was affected by age,sex and,in particular,education level;2)all thebrain damage groups had a lower performancelevel than the control group;the performan-ce level of the cerebral infarction group andthe brain tumor group was even worse thanthat of the brain injury group and heman-gioma group;3)the...

A test of the judgement of linear orient-ation was given to 168 patients with braindamage.240 normal persons comprised a con-trol group.The results showed that:1)theperformance level was affected by age,sex and,in particular,education level;2)all thebrain damage groups had a lower performancelevel than the control group;the performan-ce level of the cerebral infarction group andthe brain tumor group was even worse thanthat of the brain injury group and heman-gioma group;3)the mean error score wasfound to be higher for patients with right-hemisphere lesion than those for patientswith left-hemisphere lesion.

对200名正常人及168例脑损害病人分别进行了线方向判断测验的测查。发现在对照组中,年龄、性别、文化水平对测验成绩均有一定的影响,尤以文化水平的影响最为显著。各病种组与对照组比较,发现脑梗塞组与脑肿瘤组成绩比外伤组和血管畸形组为差。同时还发现所有病种组右脑损害患者分数均低于左脑损害患者。

The present work aims at adducing further proof of the neurotrophic effect of β amyloid (Aβ) precursor protein(APP) 319~335(APP17 mer peptide), through studying the effect of APP17 mer peptide on the neurotoxicity of Aβ, and thereby providing scientific evidence for the pathogenesis of AD and its treatment. APP 17 mer peptide and Aβ 25 35 were synthesized by solid phase method and purified by HPLC. Human neuroblastoma cells SY5Y were segregated into 3 groups: normal control group, Aβ 25 35 ...

The present work aims at adducing further proof of the neurotrophic effect of β amyloid (Aβ) precursor protein(APP) 319~335(APP17 mer peptide), through studying the effect of APP17 mer peptide on the neurotoxicity of Aβ, and thereby providing scientific evidence for the pathogenesis of AD and its treatment. APP 17 mer peptide and Aβ 25 35 were synthesized by solid phase method and purified by HPLC. Human neuroblastoma cells SY5Y were segregated into 3 groups: normal control group, Aβ 25 35 (10 μmol/L) damaged group, and Aβ 25 35 (10 μmol/L) +APP17 mer peptide(10 μmol/L) for neuroprotection group. Cell count, MTT metabolic rate, LDH leakage rate, axonal length, area of cell body, NT 3 immunohistorychemical staining and concentration of cytosolic calcium(Ca 2+ ) were used as indicators. Compared with normal control group, Aβ 25 35 damaged group showed reduced cell count and MTT metabolic rate, increased LDH leakage rate, diminished axonal length and area of cell body, reduced NT 3 expression, increased concentration of cytosolic calcium(Ca 2+ ), but the addition of APP17 mer peptide normalized the foregoing changes. APP17 mer peptide is neurotrophic. It can diminished neurotoxicity of Aβ.

通过观察β 淀粉样肽 (Aβ)前体蛋白 (APP1 7)中 3 1 9 3 3 5肽段 (APP1 7肽 )对Aβ引起神经毒性作用的影响 ,进一步证实APP1 7肽的神经营养作用。用固相法合成APP1 7肽、Aβ2 5 3 5,高效液相纯化 ,以人神经母细胞瘤株SY5Y为细胞模型 ,分为正常对照组、Aβ2 5 3 51 0 μmol/L损伤组和Aβ2 5 3 51 0 μmol/L加APP1 7肽 1 0 μmol/L保护组。以细胞计数、噻唑蓝 (MTT)代谢率、LDH漏出率、细胞轴突长度、胞体面积、NT 3免疫细胞化学染色和细胞内游离钙离子(Ca2 + )浓度为观察指标。结果 :与正常对照组相比 ,Aβ2 5 3 5损伤组轴突长度和胞体面积均缩小 ,细胞计数减少 ,MTT代谢率降低 ,LDH漏出率升高 ,细胞内Ca2 + 浓度升高 ,而加入APP1 7肽保护后 ,可使上述指标恢复或接近正常。提示 :APP1 7肽具有神经营养和神经保护作用 ,可减轻Aβ引起的神经元损伤。

Objective To determine the change of behaviour and brain histochemistry of the aged rats with site-specificly destruction of the brain cholinergic neurons system by excitatory neurotoxin. And to study the brain damage mechanism by excitatory neurotoxin in Alzheimer's disease. Methods To destroy the right nucleus of Meynert of old rats' brain site-specificly with excitatory neurotoxin ibotenic acid (IBA) and N-methyl-D-asparate(NMDA), then for the damaged rats the learning ability and brain acetylcholinesterase...

Objective To determine the change of behaviour and brain histochemistry of the aged rats with site-specificly destruction of the brain cholinergic neurons system by excitatory neurotoxin. And to study the brain damage mechanism by excitatory neurotoxin in Alzheimer's disease. Methods To destroy the right nucleus of Meynert of old rats' brain site-specificly with excitatory neurotoxin ibotenic acid (IBA) and N-methyl-D-asparate(NMDA), then for the damaged rats the learning ability and brain acetylcholinesterase (AchE) activity was measured by Y-maze and spectrophotography method, and the expression of brain neuropeptide: β-amyloid peptide precursor (β-APP), somatostatin (SOM) and substance P (SP) were determined using immunohistochemistry method.Results Compared with the control group, the old rats undergoing brain damage show that their learning ability and the brain acetylcholinesterase activity is lower notably (all are P<0.05), in their brain frontal cortex and hippocampus the β-APP expression is higher but SOM positive neurons is less, and the SP expression is higher only in IBA andβ-AP 25-35 co-damaged and NMDA damaged groups , but not in IBA damaged , than that in control group significantly (all are P<0.01). Conclusions The old rats injured the brain Meynert nucleus with IBA and NMDA site-specificly display the damage of the brain cholinergic system and the learning desfunction. In addition they showed that β-APP is overexpressed and SP expression is higher significantly, that may be related to β-AP deposition in brain, the neuropeptide SOM expression is lower may cause to reduce their learning ability. The aforesaid characteristics of this AD animal model are similar to some AD patients' clinical and pathologic features.

目的 探讨兴奋性神经毒素定位损伤脑胆碱能神经元的老化大鼠行为及脑组化改变 ,及在 AD发病中兴奋性毒素脑损伤的机制。方法 分别用兴奋性毒素鹅膏蕈氨酸 (IBA)、N-甲基 - D-天冬氨酸 (NMDA)定位损伤老化大鼠脑右侧 Meynert核。用 Y型迷宫法和分光光度法检测损伤大鼠学习能力和脑胆碱酯酶 (Ach E)活性改变 ,并用免疫组化染色法测定损伤动物脑神经肽 :β-淀粉样肽前体 (β- APP)、生长抑素 (SOM)及 P物质(SP)的表达。结果 脑损伤大鼠与对照组比较 ,表现学习能力及脑胆碱酯酶活性显著降低 (均 P<0 .0 5) ;鼠脑额叶皮层和海马区显示β- APP的表达明显升高 ;而生长抑素阳性神经元数量则显著减少。用 IBA及 β- AP2 5- 3 5同时或 NMDA损伤鼠脑时 ,可显示脑皮质区 P物质过表达 (均 P<0 .0 1 ) ;用IBA单独注射时 ,SP表达无显著改变。结论 以 IBA、NMDA定位损伤老化大鼠脑 Meynert核后 ,显示鼠脑胆碱能系统损伤 ,学习能力障碍 ,β- APP、P物质表达明显增多 ,可能与脑中 β- AP的沉积有关。神经肽 SOM表达降低可能致动...

目的 探讨兴奋性神经毒素定位损伤脑胆碱能神经元的老化大鼠行为及脑组化改变 ,及在 AD发病中兴奋性毒素脑损伤的机制。方法 分别用兴奋性毒素鹅膏蕈氨酸 (IBA)、N-甲基 - D-天冬氨酸 (NMDA)定位损伤老化大鼠脑右侧 Meynert核。用 Y型迷宫法和分光光度法检测损伤大鼠学习能力和脑胆碱酯酶 (Ach E)活性改变 ,并用免疫组化染色法测定损伤动物脑神经肽 :β-淀粉样肽前体 (β- APP)、生长抑素 (SOM)及 P物质(SP)的表达。结果 脑损伤大鼠与对照组比较 ,表现学习能力及脑胆碱酯酶活性显著降低 (均 P<0 .0 5) ;鼠脑额叶皮层和海马区显示β- APP的表达明显升高 ;而生长抑素阳性神经元数量则显著减少。用 IBA及 β- AP2 5- 3 5同时或 NMDA损伤鼠脑时 ,可显示脑皮质区 P物质过表达 (均 P<0 .0 1 ) ;用IBA单独注射时 ,SP表达无显著改变。结论 以 IBA、NMDA定位损伤老化大鼠脑 Meynert核后 ,显示鼠脑胆碱能系统损伤 ,学习能力障碍 ,β- APP、P物质表达明显增多 ,可能与脑中 β- AP的沉积有关。神经肽 SOM表达降低可能致动物学习能力下降。该 AD模型动物表现 AD类似临床和病理特征。

 
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