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Gapa相关的网络例句
与 Gapa 相关的网络例句 [注:此内容来源于网络,仅供参考]

Methods On the basis of bilirubin-induced encephalopathy model in guinea-pig, 10 μg/g of GAPA was injected intraperitoneal.

在制作胆红素脑病动物模型基础上予GAPA干预,观察对照组、模型组、模型干预组新生豚鼠(每组10只)干预后4、8 h脑组织超微结构、脑组织ATP含量与含水量。

The GC contents of the entire region of the GapA cDNA (64.2%) were similar to the average GC content (65.2%) which was obtained by Porphyra EST analysis.

条斑紫菜GapA的cDNA序列中GC含量很高(64.2%),与紫菜EST分析中得到的结果(65.2%)近似。

Results The brain ATP production in bilirubin induced neurotoxicity guinea-pig decreased within 4 hours after exposure to bilirubin, and secondary brain edema could be found 8 hours later; GAPA could prevent the secondary brain edema effectively ,but could not prevent the ATP decreasing significantly.

沉积于脑组织胆红素可抑制神经元能量代谢,致脑细胞水肿;兴奋性氨基酸受体拮抗剂GAPA可减轻脑水肿,但不影响能量代谢变化,其作用环节介于能量代谢变化与脑水肿之间。

Methods On the basis of bilirubin induction and NMDA receptor an-tagonist GAPA administration in guinea pigs. The brain extracellular EAA neurotransmitter was ex-tracted with microdialysis and analysed with HPLC; then, brain tissue ATP was measured by fluores-cence assay and intracellular Ca2 + was measured by fluorescence imaging analysis.

制作胆红素脑病动物模型基础上,在体脑内微透析提取兴奋性氨基酸神经递质,HPLC检测天冬氨酸、谷氨酸、甘氨酸,并给予模型动物NMDA受体拮抗剂GAPA干预,电镜检测脑组织超微结构,荧光检测脑组织ATP与细胞内Ca2+含量。

Results ATP andEAA Neurotransmitter Gly were greatly increased in the bilirubin induced neurotoxicity brain; neuralcytosolic Ca2 + in the bilirubin precipitated brain tissue was significantly more than that in the controlgroup; NMDA receptor antagonist GAPA could significantly decrease the cytosolic Ca2+ overload.

结果 胆红素毒性脑组织ATP含量显著降低,细胞外Gly与细胞内Ca2+显著升高;GAPA不影响胆红素毒性脑组织ATP含量,但可显著降低细胞内Ca2+,减轻胆红素毒性脑水肿。

EAA neurotransmitter Gly increased the sensitivity of the ligand Asp and Glu to theNMDA receptor, thus increased the NMDA receptor activity and cytosolic Ca2 + in the bilirubin precipi-tated brain tissue. NMDA receptor antagonist GAPA could prevent the cytosolic Ca2 + overload, and re-lieve brain edema.

NMDA受体过度活化致细胞内Ca2+超载参与介导胆红素神经毒性,NMDA受体拮抗剂可望成为胆红素神经毒性防治的重要途径。

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