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Over supply and high partial pressure of oxygen can bring about toxicity effect on neurons.

在过高的氧压下,高压氧作为一种神经毒性因子发挥作用,可导致惊厥。

METHODS: SC lasting for 30 minutes or 3 hours was induced by intraperitoneal injection of lithium chloride and pilocarpine.

采用氯化锂-匹罗卡品法诱发幼年Wistar大鼠SC发作,分别制备惊厥持续发作30 min和3 h的SC模型。

Result: 1、Ethology result:50 rats were injecting convulsive dose kainic acid, showing prodrome such as gaze, wet dog shake in the 0-30 minutes; 1-5 degree epileptic attack in the 30-60minutes; 4-5 degree repteately spontaneous epileptic attack in 60-90 minutes; then status epilepticus,SE-epileptic attack endurance became longer and interval became shorter with bulk salivas and various kinds psychomotor symptoms.

结果:1、行为学结果:SD大鼠(n=50)在注射惊厥剂量(10mg/kg)KA后,0-30min内动物出现凝视,湿狗样抖动(wet dog shake,WDS)等前驱症状;30-60min内动物出现1-5级癫痫发作;60-90min内动物反复自发出现4-5级癫痫发作;其后动物癫痫发作持续时间延长,间隔变短伴有大量唾液分泌,出现各种精神运动症状,呈现SE,SE后10天,用阈下剂量(5mg/kg)KA检测动物对癫痫刺激的敏感性。

Objective To explore the effect of Znic Protoporphyrin and its mechanism on the hemeoxygenase -1 (HO-1) mRNA expression in brain tissue of developing rat with febrile convulsion.

目的 探讨锌原卟啉对高热惊厥发育期大鼠血红素氧合酶-1 mRNA表达的影响及作用机制。

Objective To find out the changes of synaptic density in the periaqueductalgray of the naive and kindled audiogenic seizures-prone rats.

目的 分析正常及点燃后听源性惊厥易感大鼠中脑导水管周围灰质内突触密度的变化情况。

Methods The neuronalstaining method and the immunocytochemical method were used to identify the Fos-postive neurons in the PAG of the audiogenic seizures-prone rats(P77PMC) after audiogenic seizures.

用神经细胞染色和免疫细胞化学技术,观察听源性惊厥发作后易感大鼠(P77PMC)PAG内即早基因c-fos的表达情况。

Objective To explore the changes and clinical significance of neuropeptide Y and neuron-specific enolase levels in children with convulsibility diseases.

目的 探讨神经肽Y和神经元特异性烯醇化酶在小儿惊厥性疾病中的水平变化及其临床意义。

These circumstances are believed to cause metabolic disturbances in neurons in the hippocampus, which may disappear and be subsequently replaced by gliosis.

MTS被认为与婴幼儿其的发热性惊厥和持续癫痫状态相关,这些事件被认为引起了海马区神经元代谢异常,这些神经元丢失并被神经胶质所取代。

Results By univariate analysis 11 risk factors were explored: family poverty, low culture level of mother, history of family on MR or epilepsy in parents, abnormal maternal menstrual cycle before pregnancy, febrile illess during gestation, bleeding in gestation period, chronic disease in gestation period, premature birth, assisted first crying after birth, neonatal febrile illness, convulsion and asphyxiation.

结果单因素分析儿童MR的危险因素有:家庭贫困、母亲文化程度低、父母亲智力低下或癫痫家族史、母亲妊娠前月经周期异常、母孕期发热、母孕期出血、母孕期患有慢性病、早产、出生后第一声啼哭是否需辅助、新生儿发热、惊厥、窒息。

Take the blood specimen to measure the hepatic and renal function and the tissue biopsy after the active and motive abnormities called toxical manifestation such as posture changes, abnormal sound, uneasiness, quiet, thrill, ataxia, convulsion and so on with toxic dose. Measure the tissue biopsy after death with lethiferous dose. If no toxicity or death occur after the experiment of 12 weeks, measure the hepatic and renal function and the tissue biopsy. There was no rat which had the toxical manifestation such as active or motive abnormities and 3 rats died because of environment or others after the experiment of 12 weeks.

实验中分别测定治疗剂量组小鼠在用药4周,8周,12周后的肝肾功能,并进行组织病理检查;中毒剂量组小鼠在出现行为、动作异常,如改变姿势、叫声异常、不安、安静、震颤、运动失调、惊厥等中毒表现时,取血液标本测定肝肾功能,并进行组织病理检查;致死剂量组小鼠发生死亡后进行组织病理检查;若12周实验结束时无小鼠出现中毒表现或死亡,则取血液标本测定肝肾功能,并进行组织病理检查。12周实验结束时,无小鼠出现动作、行为异常等中毒表现,有3只小鼠因为环境或其它原因发生死亡,病理检查结果正常。

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