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nimodipine group
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  尼莫地平组
    Methods 65 patients with AD were randomly divided into two groups:Nimodipine group (n=32), treated with Nimodipine injection;
    方法将65例AD患者随机分成两组,尼莫地平治疗组(尼莫地平组,32例):尼莫地平注射液治疗;
短句来源
    The scores of MMSE increased significantly(all P<0.01), P300 latencies reduced and amplitudes increased significantly(Nimodipine group P<0.01, Piracetam group P<0.05)in both two groups 14 d and 30 d after treatment.
    治疗14d、30d时,两组MMSE评分显著提高(均P<0.01),P300潜伏期均有缩短,波幅均有提高(尼莫地平组P<0.01,吡拉西坦组P<0.05);
短句来源
    The score of MMSE increased significantly,P300 latencies reduced and amplitudes increased significantly(all P<0.01) only in the Nimodipine group 90 d after treatment.
    治疗90d时,尼莫地平组MMSE评分显著提高、P300潜伏期显著缩短、波幅显著提高(均P<0.01)。
短句来源
    The intellectual amelioration was significant in the Nimodipine group than that of in the Piracetam group (76.67%,70%)(P<0.05).
    治疗后14d时认知功能改善尼莫地平组明显优于吡拉西坦组(总有效率分别为76.67%,70%)(P<0.05)。
短句来源
    Nimodipine group rats orally took Nimodipine 0.5 mg/kg while control group and AD model group orally took normal saline. This process lasted for 60 days, twice per day, each time 2 ml.
    尼莫地平组给予尼莫地平 0 .5mg/kg ,空白对照组和AD模型组以生理盐水代替尼莫地平 ,连续灌胃 6 0d ,每d 2次 ,每次 2ml。
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  “nimodipine group”译为未确定词的双语例句
    The nimodipine group of 35 patients (M 18, F 17; age 62 a± s 12 a) was teated with nimodipine 30 mg, po, tid for 8 wk.
    分别给尼莫地平 30mg ,丁咯地尔15 0mg ,po ,tid ,8wk为一个疗程。
短句来源
    Compared with the model group in the immunohistochemistry results, the expressions of Glu Calpain II , Caspase -3 , Bax are lower in the Rg2 groups and the nimodipine group.
    在免疫组化结果中,Glu、CalpainⅡ、Caspase-3、Bax表达均增高。
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  nimodipine group
Six months after injury 93 (53%) of the nimodipine group and 86 (49%) of the control group had a favourable outcome (moderate/good recovery).
      
The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates.
      
The underlying cause of death was major bleeding in 6 of 9 deaths, 5 in the nimodipine group and 1 in the placebo group.
      


Aim: To determine the effects of nimodipine on brain nitric oxide (NO) and nitric oxide synthase (NOS) levels and behavioral science in Alzheimer disease (AD) rats. Methods: A total of 30 rats were allocated into control group, AD model group and nimodipine group (10 in each group). By the technique of solid-location and microinjection, in AD model group and nimodipine group, IBO 1 μl(5 μg)was injected into bilateral basal nuclei of Meynert (nbM)of rats to set up AD animal model. In...

Aim: To determine the effects of nimodipine on brain nitric oxide (NO) and nitric oxide synthase (NOS) levels and behavioral science in Alzheimer disease (AD) rats. Methods: A total of 30 rats were allocated into control group, AD model group and nimodipine group (10 in each group). By the technique of solid-location and microinjection, in AD model group and nimodipine group, IBO 1 μl(5 μg)was injected into bilateral basal nuclei of Meynert (nbM)of rats to set up AD animal model. In control group IBO was replaced by 0.1 mol/L PB (pH 7.4). Nimodipine group rats orally took Nimodipine 0.5 mg/kg while control group and AD model group orally took normal saline. This process lasted for 60 days, twice per day, each time 2 ml.Then learning and remembering abilities were tested by maze experiment and jumping table experiment. Then all rats were decapitated, and hippocampus and cerebral cortex were dissected respectively to examine the concentrations of NO and NOS. Results: Compared with control group, in AD model group rats, the learning and remembering abilities decreased significantly, and the contents of NO and NOS increased significantly; compared with AD model group, in nimodipine group the learning and remembering abilities increased and the contents of NO and NOS decreased significantly. Conclusion: Ruining bilateral nbM of rats by IBO can set up ideal AD animal model. Nimodipine could significantly improve the learning and remembering abilities and reduce the contents of NO and NOS in hippocampus and cerebral cortex of AD model rats.

目的 :探讨尼莫地平对阿尔茨海默病 (AD)大鼠脑组织一氧化氮 (NO)、一氧化氮合酶 (NOS)浓度及行为学改变的影响。方法 :SD大鼠 30只 ,随机分为空白对照组 ,AD模型组和尼莫地平组 ,采用大鼠脑组织立体定位微量注射技术 ,尼莫地平组和AD模型组用鹅膏蕈氨酸 (IBO) 1μl(5 μg)损毁大鼠双侧迈内特基底核 (nbM )建立AD动物模型 ,空白对照组以 0 .1mol/LpH7.4PB液代替IBO。尼莫地平组给予尼莫地平 0 .5mg/kg ,空白对照组和AD模型组以生理盐水代替尼莫地平 ,连续灌胃 6 0d ,每d 2次 ,每次 2ml。做迷宫试验及跳台试验测学习记忆能力 ,然后将大鼠断头处死 ,分离海马及大脑皮质 ,分别检测NO、NOS含量。结果 :AD模型组较空白对照组学习记忆能力显著降低 ,海马及大脑皮质NO、NOS含量显著升高 ;尼莫地平组较AD模型组学习记忆能力显著升高 ,海马及大脑皮质NO、NOS含量显著降低。结论 :用IBO损毁大鼠双侧nbM可建立AD动物模型 ,尼莫地平可显著改变AD模型大鼠的学习记忆能力 ,降低海马及大脑皮质NO、NOS含量。

AIM: To compare the efficacies of buflomedil and nimodipine in the treatment of vascular dementia. METHODS: Using double blind radomized comparative method, 70 patients with vascular dementia were randomly divided into two groups. The nimodipine group of 35 patients (M 18, F 17; age 62 a± s 12 a) was teated with nimodipine 30 mg, po, tid for 8 wk. The buflomedil group of 35 patients (M 20, F 15; age 64 a±7 a) was treated with buflomedil 150 mg, po, tid for 8 wk. Then their MMSE,...

AIM: To compare the efficacies of buflomedil and nimodipine in the treatment of vascular dementia. METHODS: Using double blind radomized comparative method, 70 patients with vascular dementia were randomly divided into two groups. The nimodipine group of 35 patients (M 18, F 17; age 62 a± s 12 a) was teated with nimodipine 30 mg, po, tid for 8 wk. The buflomedil group of 35 patients (M 20, F 15; age 64 a±7 a) was treated with buflomedil 150 mg, po, tid for 8 wk. Then their MMSE, HDS, ADL, WMS, CGI, EI and adverse reaction were compared. RESULTS: In nimodipine group the scores of WMS, MMSE, ADL, CGI, EI were 59±22, 20±6, 30±12, 3.0±0.7, 1.9±0.7, as that were 70±18, 22±4, 26±9, 2.2± 0.9 , 2.5±0.8 in buflomedil group. There were significant differences between the two groups ( P <0.05, P <0.01). The rates of adverse reaction were equal. CONCLUSION: With equal safety, buflomedil is more effect than nimodipine in treating vascular dementia.

目的 :比较丁咯地尔与尼莫地平治疗血管性痴呆的临床疗效。方法 :70例血管性痴呆病人 ,以双盲随机对照研究方法分为尼莫地平组 35例 ,丁咯地尔组 35例。分别给尼莫地平 30mg ,丁咯地尔15 0mg ,po ,tid ,8wk为一个疗程。治疗后评价MMSE ,HDS ,ADL ,WMS ,CGI ,EI及不良反应。结果 :治疗后WMS ,MMSE ,ADL ,CGI ,EI评分尼莫地平组为 (5 9± 2 2 ,2 0± 6 ,30± 12 ,3.0± 0 .7,1.9±0 .7)分 ;丁咯地尔组为 (70± 18,2 2± 4 ,2 6± 9,2 .2±0 .9,2 .5± 0 .8)分 ,2组比较P <0 .0 5或P <0 .0 1,2组不良反应比较P >0 .0 5。结论 :丁咯地尔治疗血管性痴呆疗效较尼莫地平显著

Objective Comparative the curative effect and security of nimodipine and fluoxetine.Methods 67 patients with depression after cerebral infarction were randomly divided into treating group with nimodipine and controlled group with fluoxetine.Clinical progress was monitored with HAMD and neural function defect score.Results The over effective rate of nimodipine group and fluoxetine group were 90.3% and 88.8%,respectively.The results have no remarkable differences in the two groups(P>0.05).The...

Objective Comparative the curative effect and security of nimodipine and fluoxetine.Methods 67 patients with depression after cerebral infarction were randomly divided into treating group with nimodipine and controlled group with fluoxetine.Clinical progress was monitored with HAMD and neural function defect score.Results The over effective rate of nimodipine group and fluoxetine group were 90.3% and 88.8%,respectively.The results have no remarkable differences in the two groups(P>0.05).The neural function defect score of nimodipine group was lower remarkably than that of fluoxetine group during the 3rd and 6th week of treatment.The difference was not significant in the side effect between two groups.Conclusion In the treatment of depression after cerebral infarction,nimodipine has higher effective rate,wild side effect,neural function was improved significantly.It is worthly to be popularized.

目的 比较尼莫地平和氟西汀治疗脑梗死所致抑郁症状的疗效和安全性。方法 将 6 7例脑梗死所致抑郁症状的患者分为尼莫地平组和氟西丁组 ,于疗前、治疗第 3周、6周进行HAMD量表和神经功能缺损评分。结果 尼莫地平组和氟西汀组总有效率分别为 90 .3%、88.8%,二者无显著性差异 (P >0 .0 5 ) ;尼莫地平组神经功能缺损评分在治疗第 3周、6周时均显著低于氟西汀组 ;两组副反应发生率无显著性差异 (P >0 .0 5 )。结论 尼莫地平对脑梗死的抑郁症状有良好疗效 ,且副作用轻微 ,并能明显改善患者的神经功能 ,值得推荐于临床。

 
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