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brain after hypoxic ischemic
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  缺氧缺血性
     Objective To assess the expression of Bcl 2 and Bax proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship with apoptosis in the neonate.
     目的 研究Bc1-2蛋白和Bax 蛋白在新生儿缺氧缺血性脑损伤(HIBD)中的表达,以及与细胞凋亡的关系。
短句来源
     Objective To study the changes and roles of glutamate(Glu) content and cyclic nucleotide levels in neonatal rat brain after hypoxic ischemic brain damage(HIBD).
     目的 研究新生大鼠缺氧缺血性脑损伤 (HIBD)时谷氨酸 (Glu)和环核苷酸 (cAMP和cGMP)的代谢改变及意义。
短句来源
     Objective To assess the expression of Bcl 2 and Fas ligand (FasL) proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods The HIBD model was produced with 7 old day Wistar rats. The expression of Bcl 2 and Bax proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were determined by immunohistochem and terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining.
     为研究 Bcl- 2和 Fas配体 (Fas L )基因蛋白在新生儿缺氧缺血性脑损伤 (HIBD)中的表达及与细胞凋亡的关系 ,将新生 7日龄 Wistar大鼠制成 HIBD模型 ,应用免疫组织化学 - SP法及原位缺口末端标记 (TUNEL )研究 Bcl- 2和 Fas L蛋白在新生大鼠及缺氧缺血 (HI)后脑中表达及与凋亡的关系。
短句来源
     Nestin expression protein in neonatal rat brain after hypoxic ischemic brain damage
     新生大鼠缺氧缺血性脑损伤后神经干细胞巢蛋白表达的变化
短句来源
     Objective To assess the expression of Caspase-3 protein in brain after hypoxic ischemic(HI)and investigate the protective effect of extract of ginkgo biloba(EGb)on hypoxic ischemic brain damage(HIBD)in neonatal rats.
     目的探讨缺氧缺血(H I)后C aspase-3的变化及银杏叶提取物(EG b)对新生大鼠缺氧缺血性脑损伤(H IBD)的保护作用。
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  “brain after hypoxic ischemic”译为未确定词的双语例句
     ALM To study the effects of ginkgo biloba extract (GbE) on expressions of neuron specific enolase (NSE) and S 100 protein(S 100) mRNA in newborn rat brain after hypoxic ischemic brain damage (HIBD) and the mechanism of GbE against HIBD.
     目的 研究银杏叶提取物 (GbE)对新生鼠缺血缺氧性脑损伤 (HIBD)后脑组织神经元特异性烯醇化酶 (NSE)、S 10 0蛋白 (S 10 0 )mRNA表达的影响 ,以探讨GbE抗脑缺血缺氧的药理作用机制。
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  相似匹配句对
     Brain hypoxic and ischemic proconditioning
     脑缺血缺氧预处理
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     Expression of caspase-1 after hypoxic-ischemic brain damage
     缺氧缺血性脑损伤鼠半胱氨酸天冬氨酸蛋白酶-1的表达及其意义
短句来源
     Erythropoietinand Hypoxic-ischemic Brain Damage
     促红细胞生成素与缺氧缺血性脑损伤
短句来源
     Caspase and hypoxic ischemic brain damage
     半胱天冬酶与缺氧缺血性脑损伤
短句来源
     The expression and effect of IL-18 after hypoxic-ischemic brain damage
     白细胞介素-18在缺氧缺血性脑损伤后的表达及其检测意义
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Department of Pedictrics, The First University Hospital, China Medical University,shenyang, 110001. \;Objective To assess the expression of Bcl 2 and Fas ligand (FasL) proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods The HIBD model was produced with 7 old day Wistar rats. The expression of Bcl 2 and Bax proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were...

Department of Pedictrics, The First University Hospital, China Medical University,shenyang, 110001. \;Objective To assess the expression of Bcl 2 and Fas ligand (FasL) proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods The HIBD model was produced with 7 old day Wistar rats. The expression of Bcl 2 and Bax proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were determined by immunohistochem and terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining. Results Apoptosis coexisted with necrosis after HIBD by TUNEL, but apoptosis was a major form of cell death. Bcl 2 immunostaining ranged from weak to intense (++~++++) in the brain of normal neonatal rat. After hypoxia ischemia (HI), a decrease or absence in immunoreactivity for Bcl 2 in apoptotic and necrotic neurons was observed. No or weak FasL immunoreactive protein was detected in the brain of nomal neonatal rat. After HI, strong FasL immunoreactive was found in a few scattered apoptotic cells in the infarcted areas. Conclusion A shift in the ratio of Bcl-2 to FasL may contribute to neuronal apoptosis after HI. (Original article on page 257)

为研究 Bcl- 2和 Fas配体 (Fas L )基因蛋白在新生儿缺氧缺血性脑损伤 (HIBD)中的表达及与细胞凋亡的关系 ,将新生 7日龄 Wistar大鼠制成 HIBD模型 ,应用免疫组织化学 - SP法及原位缺口末端标记 (TUNEL )研究 Bcl- 2和 Fas L蛋白在新生大鼠及缺氧缺血 (HI)后脑中表达及与凋亡的关系。结果示新生大鼠 HIBD时凋亡与坏死并存 ,以凋亡为主。Bcl- 2免疫蛋白在正常新生大鼠脑内广泛表达 (+~ + + + + ) ;HI后脑病变处 Bcl- 2免疫强度明显下降 (-~ + ) ;Fas L蛋白在正常新生大鼠脑内呈不表达或弱表达 (-~ + + ) ,HI后病变部位散在分布阳性凋亡细胞。由此可见 HI后 Bcl- 2与 Fas L的比例下降有助于 HI后脑细胞的凋亡

Objective To assess the expression of Bcl 2 and Bax proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship with apoptosis in the neonate. Methods The HIBD model was produced with 7 day old wistar rats. The expression of Bcl 2 and Bax proteins as well as the relationship with apoptosis after HIBD in the neonatal rats were determined by immunohistochem and terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling...

Objective To assess the expression of Bcl 2 and Bax proteins in brain after hypoxic ischemic brain damage (HIBD) as well as the relationship with apoptosis in the neonate. Methods The HIBD model was produced with 7 day old wistar rats. The expression of Bcl 2 and Bax proteins as well as the relationship with apoptosis after HIBD in the neonatal rats were determined by immunohistochem and terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining. Results Apoptosis coexisted with necrosis after HIBD by TUNEL, but apoptosis was a major form of cell death. Bcl 2 and Bax immunostaining ranged from weak to intense(+~) in the brain of normal neonatal rat. After hypoxia ischemia(HI),a decrease or absence in immunoreactivity for Bcl 2 in apoptotic and necrotic neurons was observed, and a decrease in immunostaining for Bax was observed in the infarcted areas Among them, there were a few scattered strong positive apoptotic cells. Conclusion Overexpression of Bcl 2 protects cell from apoptosis, but Bax may function as a cell death effector protein.

目的 研究Bc1-2蛋白和Bax 蛋白在新生儿缺氧缺血性脑损伤(HIBD)中的表达,以及与细胞凋亡的关系。 方法 将新生7日龄Wistar大鼠制成HIBD模型,应用免疫组织化学——SP法及原位缺口末端标记(TUNEL)。 结果 新生大鼠HIBD时细胞凋亡与坏死并存,但以凋亡为主。Bcl-2和Bax 在正常新生大鼠脑内广泛表达(+ ~);缺氧缺血(HI)后脑病变处Bcl-2免疫强度明显下降(- ~+ );Bax 的免疫强度也减弱,其中可见散在分布的阳性凋亡细胞;HI后Bcl-2与Bax 的比例下降。 结论 Bcl-2可能抑制细胞凋亡,Bax 可能诱发细胞凋亡

Aim: To assess the expresion of Bcl-2 and P53 proteins in brain after hypoxic-ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods: The HIBD model was established with 7-old-day Wistar rats. The expression of Bcl-2 and P53 proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were deter- mined by immunohistochemistry and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling (TUNEL)...

Aim: To assess the expresion of Bcl-2 and P53 proteins in brain after hypoxic-ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods: The HIBD model was established with 7-old-day Wistar rats. The expression of Bcl-2 and P53 proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were deter- mined by immunohistochemistry and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling (TUNEL) staining. Results: Apoptosis coexisted with necrosis after HIBD by TUNEL, but apoptosis was a major form of cell death. Bcl-2 immunostaining ranged from week to intense (+ + - + + + ) in the brain of normal neonatal rat. After hy- poxia ischemia (HI), a decrease or absence in immunoreactivity for Dcl-2 in apoptotic and necrotic neurons was observed. The expression of P53 immunoreactive protein was not detected in the brain of normal neonatal rat, but strong P53-immunoreac- tive was found in apoptotic and necrotic cells. Conclusion: The expression of Bcl-2 decreased. while P53-immunoreative in- creased. Overexpression of Bcl-2 protects cell from apoptosis, but Bax may be function as a cell death effector protein.

目的:研究Bcl-2的P53蛋白在新生儿缺氧缺血性脑损伤(HIBD)中的表达及与细胞凋亡的关系。方法:将新生7日龄Wistar大鼠制成HIBD模型,应用免疫组织化学-SP法及原位缺口末端标记(TUNEL)研究Bcl-2和P53蛋白在新生大鼠及缺氧缺血(HI)后脑中表达及与凋亡的关系。结果:新生大鼠HIBD时凋亡与坏死并存,以凋亡为主。Bel-2免疫蛋白在正常新生大鼠脑内广泛表达(+~++++);HI后脑病变处Bcl-2免疫强度明显下降(-~+);P53蛋白在正常新生大鼠脑内基本无表达;HI后病变部位散在分布阳性凋亡细胞。结论:HI后Bcl-2免疫表达减弱,P53的免疫表达增强,提示Bcl-2可抑制凋亡,P53可能促进凋亡。

 
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