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cerebral hypoxic ischemic injury
相关语句
  缺氧缺血性脑损伤
     4 Significance of β endorphin Activity on Acute Cerebral Hypoxic Ischemic Injury in Neonatal Rats
     新生大鼠急性缺氧缺血性脑损伤时β-内啡呔的变化
短句来源
     Objective To study the change of nitric oxide(NO) and the number of nerve cell apoptosis in neonatal cerebral hypoxic ischemic injury(CHI) in neonatal rats , and probe the possible mechanism of prevention and treatment effect of ganglioside(GM 1) on CHI.
     目的 研究新生大鼠缺氧缺血性脑损伤 (CHI)时一氧化氮 (NO)和神经细胞凋亡情况 ,探讨神经节苷脂(GM1)治疗新生大鼠CHI的作用和可能机制。
短句来源
     Objective:To probe sigificance of β endorphin(β EP)activity on acute cerebral hypoxic ischemic injury(CHI)in neonatal rats.
     目的探讨新生大鼠急性缺氧缺血性脑损伤(CHI)时β-内啡呔激活的病理生理意义。
短句来源
  “cerebral hypoxic ischemic injury”译为未确定词的双语例句
     Objective To study the effect of MK 801, the antagonist of NMDA receptor, on caspase 3 activation and apoptosis after cerebral hypoxic ischemic injury in neonatal rats.
     目的 探讨N 甲基 D 天冬氨酸 (NMDA)受体拮抗剂MK 80 1对新生大鼠缺氧缺血 (HI)后半胱天冬酶 3(Caspase 3)激活及凋亡的影响。
短句来源
     Conclusion:① the ratios of NAA/Cho,Lac/NAA,Lac/Cr,Lac/Cho,Lac/ (Cr+ Cho) were the most sensitive indicators of HIE,they quantitatively reflected the biochemical alterations of cerebral hypoxic ischemic injury.
     结论:①NAA/Cho、Lac/NAA、Lac/Cr、Lac/Cho和Lac/(Cr+Cho)是定量反映脑缺氧缺血生化改变的最敏感指标;
短句来源
     Protective function of ganglioside(GM_1) on cerebral hypoxic ischemic injury in neonatal rats
     新生大鼠缺氧缺血性脑损伤后神经节苷脂的保护作用
短句来源
     Methods Seven day old rat pups were injected with either 0.5 mg/kg MK 801 or normal saline immediately after cerebral hypoxic ischemic injury (HI). The pups were killed 24 h after the injection. Brain damage was evaluated using MAP 2 immunostaining.
     方法  7日龄新生大鼠在HI后即刻给予腹腔注射MK 80 10 .5mg/kg ,在HI后 2 4h取脑制作脑组织连续切片进行微管相关蛋白 2 (MAP 2 ) ,Caspase 3免疫组化染色及发夹寡核苷酸探针(HairpinProbe ,HPP)原位杂交 ,计算脑损伤面积及Caspase 3,HPP阳性细胞数。
短句来源
  相似匹配句对
     Endothelin and Cerebral Ischemic Injury
     内皮素与缺血性脑损伤
短句来源
     Cerebral ischemic injury and Akt
     脑缺血损伤与Akt研究的进展
短句来源
     Effectiveness of astragulus for cerebral ischemic injury
     黄芪治疗缺血性脑损伤的有效性
短句来源
     The Basic Study of Noninvasive Detecting the Ischemic/hypoxic Cerebral Injury
     缺血/缺氧脑损伤特征信息无创提取基础研究
短句来源
     Dexamethasone's Effect on Glutamate Receptor in Experimental Hypoxic Ischemic Cerebral Injury
     地塞米松对新生猪缺氧缺血性脑损伤时谷氨酸受体的影响
短句来源
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Institute of Medical Sciences, Nanjing Railway Medical College,Nanjing,210009.\;Objevtive To examine the effect of antioxidant (N acetyl L Cysteine, NAC) in neuronal apoptosis associated with cerebral hypoxic ischemic injury.Methods Terminal deoxynucleotidyl transferase mediated dUTP nick end labdciy (TUNEL) was used to detect DNA cleavage due to apoptosis in brain paraffin section from bypoxic ischemic neonatal rats, and the stained nuclei in cerebral cortex and hippocampus...

Institute of Medical Sciences, Nanjing Railway Medical College,Nanjing,210009.\;Objevtive To examine the effect of antioxidant (N acetyl L Cysteine, NAC) in neuronal apoptosis associated with cerebral hypoxic ischemic injury.Methods Terminal deoxynucleotidyl transferase mediated dUTP nick end labdciy (TUNEL) was used to detect DNA cleavage due to apoptosis in brain paraffin section from bypoxic ischemic neonatal rats, and the stained nuclei in cerebral cortex and hippocampus were observed and counted. Results Brain samples of hypoxic ischemic neonatal rats pretreated with antioxidant exhibited significantly decreased numbers of positive statined neclei compared to untreated brain tissue. Conclusion Antioxidant (NAC) inhibits effectively neuronal cell apoptosis associated with cerebral hypoxia ischemia in the neonatal rat; Oxidative stress is implicated in the mechanism of neonatal hypoxic schemic neuronal damage. (Original article on page 260)

目的 研究抗氧化剂 (NAC)对缺氧缺血脑损伤引起的神经细胞凋亡的作用。方法 利用新生大鼠缺氧缺血脑损伤的动物模型 ,通过末端转移酶介导的原位缺口标记 (TUNEL)法 ,检测并比较在有或无药物保护下脑皮质、海马中神经细胞凋亡的程度。结果 抗氧化剂(NAC)处理显著减少缺氧缺血脑组织中凋亡阳性细胞数。结论 抗氧化剂 NAC可有效抑制缺氧缺血脑损伤引起的神经细胞凋亡 ;氧化张力在缺氧缺血脑损伤的形成机制中可能起重要作用

Objective:To probe sigificance of β endorphin(β EP)activity on acute cerebral hypoxic ischemic injury(CHI)in neonatal rats.Method:Perinatal cerebral hypoxia ischemia rat model were prepared by permanent ligations of right common carotid artery combined with a temporary systemic hypoxia(inhaling 8%O 2+92%N 2)at 37℃ in 6 day old SD rats,changs of β EP contents in plasma,pituitary,contex and thalamus were determined by radioimmunoassay.Result:The concentration of β Epin CHI...

Objective:To probe sigificance of β endorphin(β EP)activity on acute cerebral hypoxic ischemic injury(CHI)in neonatal rats.Method:Perinatal cerebral hypoxia ischemia rat model were prepared by permanent ligations of right common carotid artery combined with a temporary systemic hypoxia(inhaling 8%O 2+92%N 2)at 37℃ in 6 day old SD rats,changs of β EP contents in plasma,pituitary,contex and thalamus were determined by radioimmunoassay.Result:The concentration of β Epin CHI neonatal rats were significantly higher in plasma,pituitary,contex and thalamus than those in the control group respectively( P <0 05 OR 0 01).(after cerebral ischmia:at 0 minute,343 5±47 2 vs 123 8±37 2ng·L -1 in plasma,10 3±1 1 vs 4 1±0 8ng·g -1 inpituitary,13 4±1 1 vs 10 3±0 8ng·g -1 in cortex,60 6±0 7 vs 41 0±6 5 in thalamus;at 1 hour,410 4±53 8 vs 118 9±28 6ng·L -1 in plasma,11 4±1 7 vs 4 3±0 9ng·L -1 in pituitary,17 3±3 6 vs 11 7±0 9ng·L -1 in cortex,73 2±3 3 vs 43 8±7 2ng·L -1 in thalamus).Result:These preliminary results suggest that the CHI of neonatal rat might relate to the increaseof β EP in plasma,pituitary,thalamus and cortex,β EP might take part in the pathophyiological process and mechanisms of CHI in new bron rats. [

目的探讨新生大鼠急性缺氧缺血性脑损伤(CHI)时β-内啡呔激活的病理生理意义。方法采用结扎右侧颈总动脉合并吸入低氧的混合气体制作的新生大鼠CHI动物模型,用放射免疫测定法测定大鼠大脑皮质、丘脑、垂体和周围血浆中β-EP的含量。结果新生大鼠CHI后即刻和1h后大脑皮质、丘脑、垂体和周围血浆中ir-β-EP含量显著高于对照组,差异有显著性(P<0.05或0.01)。结论新生大鼠急性CHI后β-EP释放增加,它可能参与新生大鼠CHI的病理过程,与CHI的发生发展有密切关系

Objective To study the change of nitric oxide(NO) and the number of nerve cell apoptosis in neonatal cerebral hypoxic ischemic injury(CHI) in neonatal rats , and probe the possible mechanism of prevention and treatment effect of ganglioside(GM 1) on CHI.Method Neonatal SD rats of 6 days were divided into three groups, namely normally control group, CHI group and ganglioside treated group. Perinatal cerebral hypoxic ischemiac rat models were prepared by permanent ligation...

Objective To study the change of nitric oxide(NO) and the number of nerve cell apoptosis in neonatal cerebral hypoxic ischemic injury(CHI) in neonatal rats , and probe the possible mechanism of prevention and treatment effect of ganglioside(GM 1) on CHI.Method Neonatal SD rats of 6 days were divided into three groups, namely normally control group, CHI group and ganglioside treated group. Perinatal cerebral hypoxic ischemiac rat models were prepared by permanent ligation of right common carotid artery combined with a temporary systemic hypoxia (inhaling 8 % 2+92 %N 2). Ganglioside was injected intraperitoneally into neonatal rats before and after CHI(10 mg/kg). An improved Green was used to measure NO contents in serum, the numerical density of NOS positive neurons and the number of cell apoptosis were determined by sterological method .Result The NO contents in plasma in CHI neonatal rats were significantly higher than those in the control group, and NO contents in plasma in GM 1 group were significantly lower than those in the CHI group(P<0.01) . The numerical density of NOS positive neurons and the number of cell apoptosis in CHI neonatal rats were significantly higher than those in the control group, and the numerical density of NOS positive neurons and the ratio of cell apoptosis in GM 1 group were much lower than those in the CHI group(P<0.01 ).Conclusion These preliminary results suggest that the CHI of neonatal rat might relate to the increase of NO, which might take part in the pathological process and mechanisms of CHI in new born rats. Ganglioside has the protection and curing effect on CHI, whose mechanism of the effect is correlated with blocking production of NO, and reducing the ratio of apoptosis of neuron.

目的 研究新生大鼠缺氧缺血性脑损伤 (CHI)时一氧化氮 (NO)和神经细胞凋亡情况 ,探讨神经节苷脂(GM1)治疗新生大鼠CHI的作用和可能机制。方法 选 6dSprague Dawley新生鼠 36只 ,随机分为假手术对照组、CHI组和GM1治疗组。采用结扎右侧颈总动脉并吸入低氧的混合气体制作的新生大鼠CHI动物模型 ,用镀铜镉还原法测定血清NO水平、NADPH d法检测一氧化氮合酶 (NOS)阳性神经元和原位末端标记法检测细胞凋亡 ,并作定量分析。结果 假手术对照组、CHI组和GM1治疗组新生大鼠血浆NO-2 /NO-3 含量分别为 (4 3.8± 9.2 )、(6 1.4± 15 .2 )和 (4 8.9± 11.6 )μmol/L ;NOS神经元数密度分别为 (30 .3± 4.8)、(71.3±8.7)和 (34 .7± 5 .9)个 /mm3 ;平均灰度分别为 16 1.0± 10 .0、12 1.0± 8.0和 15 6 .0± 9.0 ;细胞凋亡比例分别为 15 .1%±3.6 %、39.6 %± 4.1%和 17.6 %± 5 .6 %。CHI组上述指标显著高于对照组 ,差异有显著性 (P...

目的 研究新生大鼠缺氧缺血性脑损伤 (CHI)时一氧化氮 (NO)和神经细胞凋亡情况 ,探讨神经节苷脂(GM1)治疗新生大鼠CHI的作用和可能机制。方法 选 6dSprague Dawley新生鼠 36只 ,随机分为假手术对照组、CHI组和GM1治疗组。采用结扎右侧颈总动脉并吸入低氧的混合气体制作的新生大鼠CHI动物模型 ,用镀铜镉还原法测定血清NO水平、NADPH d法检测一氧化氮合酶 (NOS)阳性神经元和原位末端标记法检测细胞凋亡 ,并作定量分析。结果 假手术对照组、CHI组和GM1治疗组新生大鼠血浆NO-2 /NO-3 含量分别为 (4 3.8± 9.2 )、(6 1.4± 15 .2 )和 (4 8.9± 11.6 )μmol/L ;NOS神经元数密度分别为 (30 .3± 4.8)、(71.3±8.7)和 (34 .7± 5 .9)个 /mm3 ;平均灰度分别为 16 1.0± 10 .0、12 1.0± 8.0和 15 6 .0± 9.0 ;细胞凋亡比例分别为 15 .1%±3.6 %、39.6 %± 4.1%和 17.6 %± 5 .6 %。CHI组上述指标显著高于对照组 ,差异有显著性 (P <0 .0 1) ,GM1治疗组上述指标明显低于CHI组 ,差异有显著性 (P<0 .0 1)。结论 新生大鼠CHI后NO增加 ,它可能参与新生大鼠CHI的病理过程 ,与CHI的发生发展有密切关系 ,神经节苷脂GM1可抑制CHI后NO的生成和有保护神经元的作用 ,在CHI的防治方面可能具有一定的作用

 
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