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hypoxic ischemic brain injury
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  缺氧缺血性脑损伤
     Objective To investigate the peripheral and central dynamic changes of levels of neuropeptide Y 1 36 and calcitonin gene related peptide after hyperbaric oxygen therapy(HBO) of hypoxic ischemic brain injury(HIBI) in neonatal rats.
     目的 观察高压氧 (HBO)治疗新生大鼠缺氧缺血性脑损伤后血浆和大脑皮层的神经肽Y1 - 36 (NPY)和降钙素基因相关肽 (CGRP)含量的动态变化。
短句来源
     Objective:To explore the mechanisms of dynorphinA 1-13 in hypoxic ischemic brain injury in neonatal rats.
     目的 :探讨强啡肽A1-13 在新生鼠缺氧缺血性脑损伤中的作用机制。
短句来源
     Objective To explore the effects of brain derived neurotrophic factors (BDNF) on concentrations of cerebral endogenous opioid peptides(EOP)in neonatal rats subject to with hypoxic ischemic brain injury (HIBI).
     目的 观察新生大鼠缺氧缺血性脑损伤 (HIBI)后 ,外源性脑源性神经营养因子 (BDNF)对脑内源性阿片肽 (EOP)水平的影响。
短句来源
     DYNAMIC CHANGES OF LEVELS OF VASOACTIVE INTESTINAL PEPTIDE AND SUBSTANCE P IN PLASMA AFTER HYPOXIC ISCHEMIC BRAIN INJURY IN NEONATAL RATS
     新生大鼠缺氧缺血性脑损伤后血浆血管活性肠肽和P物质水平的动态变化
短句来源
     Objective To develop an improved neonatal piglet model of hypoxic ischemic brain injury (HIBI).
     目的 研究新生猪缺氧缺血性脑损伤 (HIBI)模型的制备。
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  低氧缺血性脑损伤
     Objective To explore the role of β endorphin and opioid μ receptor on the experimental treatment of hypoxic ischemic brain injury(HIBI)by intracerebral transplantation of genetically modified myoblasts expressing and secreting brain derived neurotrophic factor(BDNF)in neonatal rats.
     目的 探讨 β 内啡肽及阿片 μ受体在脑内移植脑源性神经营养因子 (BDNF)载体细胞治疗新生大鼠低氧缺血性脑损伤 (HIBI)中的作用。
短句来源
  缺氧缺血脑损伤
     Investigation of A Neonatal Piglet Model of Hypoxic Ischemic Brain Injury
     8%和4%低氧通气状态对新生猪缺氧缺血脑损伤模型制备的影响
短句来源
     Investigation of A Neonatal Piglet Model of Hypoxic Ischemic Brain Injury
     新生猪缺氧缺血脑损伤模型制备的研究
短句来源
     Parenteral solution of rhEPO (10 U/g) and saline at the same volume were injected into rats through intraperitoneal injection immediately after operation. Mixture of oxygen with volume fraction of 0.08 and nitrogen fume with volume fraction of 0.92 was sucked in rats of the two groups 2 hours after operation to establish neonatal rat models with hypoxic ischemic brain injury and models in the treatment of EPO.
     ②促红细胞生成素组和模型组大鼠结扎右颈动脉,手术后即刻分别腹腔内注射重组人红细胞生成素注射液(10U/g)及同体积生理盐水,手术后2h两组大鼠吸入体积分数为0.08氧气和体积分数为0.92氮气的混合气体2h,建立缺氧缺血脑损伤新生鼠模型及促红细胞生成素治疗模型。
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  “hypoxic ischemic brain injury”译为未确定词的双语例句
     Protective effects of the MK801 on the hypoxic ischemic brain injury
     MK801对缺氧缺血性脑损伤的保护作用
短句来源
     Nursing Care of Neonates With Hypoxic Ischemic Brain Injury Accepted Sub-hypothermia Therapy
     亚低温治疗新生儿缺氧缺血性脑损伤的护理
短句来源
     NOS inhibitor L NAME may make microcirculation dysfunction worse and lead to a further hypoxic ischemic brain injury.
     此时抑制内源性 NO的合成 ,可加重脑组织的微循环障碍而导致脑缺氧缺血性损害的进一步加重
短句来源
     Neural stem cells and differentiated cells were identified by immunocytochemistry. Newborn rats were sustained hypoxic ischemic brain injury. One week later, animals received neural stem cells transplants(operated group=16) or PBS transplants(control group=8).
     用出生 7天的SD大鼠的新生鼠制作缺氧缺血性脑损伤的动物模型 ,7天后接受神经干细胞移植 (移植组 ,n =16只 ) ,同时设置对照组 ,只注射磷酸缓冲液 (对照组 ,n=8只 )。
短句来源
     Conclusions HI could induced the changes of the second messengers PKC and IP 3. The continuous PKC down regulation and c fos gene expression may take part in neuron injuries during hypoxic ischemic brain injury.
     结论 HIE诱导第二信使PKC及IP
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  hypoxic ischemic brain injury
Although autophagy generally prevents cell death, our recent study using conditional Atg7-deficient mice in CNS tissue has demonstrated the presence of autophagic neuron death in the hippocampus after neonatal hypoxic/ischemic brain injury.
      
These neuroimaging findings included acute perinatal focal arterial infarction, hypoxic-ischemic brain injury, and intracranial hemorrhage.
      
It was later determined that plaintiff Mejia had suffered brain damage due to a hypoxic-ischemic brain injury during labor.
      
Excitotoxicity, oxidative stress, and apoptosis comprise the major routes to neuronal death after hypoxic-ischemic brain injury.
      
A major cause of neurologic morbidity is hypoxic-ischemic brain injury.
      


bjective To determine the effect of high risk obstetric factors on neonatal hypoxic-ischemic brain injuries. The obstetric factors were investlgated,including maternal complications during pregnancy and labor,the mcde of delivery. Methods Intensive B-ultrasound brain monitoring in 211 newborns within the first 48 hours of life was carried out.The abnormalities were followed up by B-ultrasound.We assessed the extent of hypo- xic-ischemic brain injuries with two...

bjective To determine the effect of high risk obstetric factors on neonatal hypoxic-ischemic brain injuries. The obstetric factors were investlgated,including maternal complications during pregnancy and labor,the mcde of delivery. Methods Intensive B-ultrasound brain monitoring in 211 newborns within the first 48 hours of life was carried out.The abnormalities were followed up by B-ultrasound.We assessed the extent of hypo- xic-ischemic brain injuries with two kind of types,mild and severe. The mild type included 1-2 degree intracranial hemorrhage and the local hypoxic-ischemic encephalopathy. The severe type included 3-4 degree intracranial hemorrhage and extensive cerebral edema. Results Thirty-nine cases(18. 5%)were diagnosed intracranial hemorrhage and 22 cases(10.4%)vvere diagnosed hypoxic-ischemic encephalopathy(HIE)or cerebral edema. The total positive rate was 28.9%。Of the positive cases,67.2%were mild brain injuries without clinical symptoms. Those cases need no medical treatment and recovered in a natural course. The rates of brain injuries in groups of pregnancy induced hypertension,fetal distress, neonatal asphyxia and premature newborns,were 46.1%,48.9%,66.7%and 71.4%respectively.It suggested that high risk obstetric factors were closely related to neonatal brain injuries. 15.9%of positive cases were from normal mothers with- out any obstetric complications. The brain injuries in those cases were mild.Conclusions The study showed that as a non-invasive procedure,B ultrasound brain examination is necessary for newborns with perinatal high risk factors of brain injuries. The study also suggested that perinatal care and systematic fetal monitoring were key-points for reduction of neonatal brain injuries.

为从母亲孕期、产时合并症及分娩方式等方面探讨引起新生儿缺氧性脑损伤的高危因素,对211例新生儿于出生后48小时内进行颅脑8超检查。结果:新生儿颅内出血39例(18.5%),脑缺氧缺血改变、脑水肿22例(10.4%),总阳性率28.9%。其中轻型脑损伤67.2%,无临床症状,不需处理即可自行恢复。母亲好高征患儿、胎儿宫内窘迫、新生儿窒息及早产儿的颅脑8超阳性率依次为46.1%、48.9%、66.7%和71.4%。围产期无任何合并症的新生儿颅脑B超阳性的仍有15.9%,但脑损伤程度较轻。提示:好高征、胎儿窘迫及早产系缺氧性脑损伤的主要高危因素,脑损伤程度较重。对有围产期高危因素的新生儿行颅脑B超的筛查是必要的。

Dynamic observation in measument of A Ⅱ ET and ALD in 35 cases of neonatal asphyxia and respiratory failure were reported. 20 cases of normal newborns were tested as controlled group. The results showed A Ⅱ value in acute stage was obviously higher than the convalesed stage (546. 80± 334. 52: 286. 44±278.0 ng/L)and also higher than the normal controlled group (384. 99±311. 13 ng/L) (P<0. 01). The increasement of A Ⅱ activity was related to the degree of hypoxia. The value of ET in acute stage was also higher...

Dynamic observation in measument of A Ⅱ ET and ALD in 35 cases of neonatal asphyxia and respiratory failure were reported. 20 cases of normal newborns were tested as controlled group. The results showed A Ⅱ value in acute stage was obviously higher than the convalesed stage (546. 80± 334. 52: 286. 44±278.0 ng/L)and also higher than the normal controlled group (384. 99±311. 13 ng/L) (P<0. 01). The increasement of A Ⅱ activity was related to the degree of hypoxia. The value of ET in acute stage was also higher that the convalesed stage and the normal controlled group. The value of ALD in acute stage was the highest htan all other group. Thus, For increasement of cerebral blood flow to improve hypoxic-ischemic brain injury to use vasodilatation durgs, early derection of A Ⅱ ET and ALD was suggested during asphyxia and respiratory failure.

本文报告了新生儿窒息呼吸衰竭35例血浆血管紧张素Ⅱ(AⅡ)、内皮素(ET)及醛固酮(ALD)的动态变化,20例正常新生儿作为对照组。结果显示:AⅡ急性期值明显高于缓解期(546.80±334.52:286.44±278.0ng/L)也高于正常新生儿对照组(384.99±311.13ng/L),P<0.01。随着缺氧程度加重AⅡ活性增高,ET急性期值也高于缓解期和正常对照组,而且急性期ALD明显高于其它组。因此,我们建议在窒息和呼吸衰竭时早期检测AⅡ、ET及ALD为使用血管扩张药以增加脑血流改善缺氧缺血脑损害提供依据。

AIM To explore the role of nitric oxide (NO) and endothelin (ET) in the early phase of hypoxic brain injuries by examing the effect of N ω nitro L arginine methyl ester (L NAME), an inhibitor of nitric oxide synthase (NOS), on brain NO production and serum ET level in newborn rats with hypoxic brain injuries. METHODS The rats were divided into normal control group, hypoxia group and L NAME+ hypoxia group. The ET level in serum, NO production, NOS activity,...

AIM To explore the role of nitric oxide (NO) and endothelin (ET) in the early phase of hypoxic brain injuries by examing the effect of N ω nitro L arginine methyl ester (L NAME), an inhibitor of nitric oxide synthase (NOS), on brain NO production and serum ET level in newborn rats with hypoxic brain injuries. METHODS The rats were divided into normal control group, hypoxia group and L NAME+ hypoxia group. The ET level in serum, NO production, NOS activity, pathology and capillary perfusion in brain were investigated in 3 groups. RESULTS The serum ET level of hypoxia group was significantly higher than that of controls ( P <0.01), but NO production and NOS activity were not significantly different between 2 groups ( P >0.05), and the brain capillary perfusion was more serious in hypoxia group that that in controls. Compared with the hypoxia group, the serum ET level of L NAME+ hypoxia group was increased significantly ( P <0.05), NO production and NOS activity in brain was decreased significantly ( P <0.01), and brain capillary perfusion was serious significantly ( P < 0.05 ). CONCLUSION Abnormal increase of serum ET in early phase of acute hypoxia is the main factor of brain injury; NOS inhibitor L NAME may make microcirculation dysfunction worse and lead to a further hypoxic ischemic brain injury.

目的 用新生大鼠急性缺氧模型 ,探讨 NO合成酶抑制剂 L-硝基 -精氨酸甲酯 (L- NAME)在缺氧后脑损伤中的作用 ,进而探讨一氧化氮 (NO)和内皮素 (ET)在早期缺氧性脑损伤中的作用地位 .方法 检测正常对照组、缺氧组和缺氧前应用 L- NAME预处理的新生大鼠血浆 ET及脑组织匀浆 NO含量及 NOS的活性 ,并观察各组大鼠脑组织病理改变及毛细血管充盈不良程度 .结果 缺氧组血浆 ET水平较正常对照组显著升高 (P<0 .0 1) ,而脑 NO水平及 NOS活性无显著变化 (P>0 .0 5 ) ,脑毛细血管充盈不良程度与正常对照组相比明显加重 (P<0 .0 5 ) ;L- NAME组血浆 ET水平较缺氧组显著升高 (P<0 .0 5 ) ,脑 NO含量及 NOS活性较缺氧组显著下降 (P<0 .0 1) ,脑毛细血管充盈不良程度与缺氧组相比明显加重 (P<0 .0 5 ) .结论 急性缺氧早期 ,ET异常增高是脑损伤的主要因素 ;此时抑制内源性 NO的合成 ,可加重脑组织的微循环障碍而导致脑缺氧缺血性损害的进一步加重

 
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