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inflammation protein
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  炎性蛋白
     Injection of dexamethasone and ibuprofen 1hr ahead of time could prevent the increase of the vascular permeability Meanwhile,the pulmonary contents of TNFα,interleukin1β(IL1β),macrophage inflammation protein1α(MIP1α) and mRNA increased with increasing doses of endotoxins,their peak values being at 2,6,and 12hr respectively.
     同时观察到肺组织中TNFα、白细胞介素1β(IL1β)、巨噬细胞炎性蛋白1α(MIP1α)及mRNA含量随内毒素剂量增大而增多,峰值在2,6和12小时,地塞米松、布洛芬对肺组织中细胞因子表达具有明显抑制。
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     Objective: To investigate the inhibiting effects and mechanism of recombinant viral macrophage inflammation protein rvMIP against HIV-1SF1 out of the body.
     目的:研究重组病毒巨噬细胞炎性蛋白(rvMIP)体外的抗HIV-1SF1作用效果和机制。
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  “inflammation protein”译为未确定词的双语例句
     In operated group, rats were sacrifice d at 1,3,6,12,24,48 hours respectively after 1 hour of middle cerebral arter y occlusion(MCAO),the brains were taken out, sliced and embedded in paraffin use d to examine nuclear factor kappa B65(NF κB65), intercellular adhesion molec ule 1(ICAM 1),macrophage inflammation protein 1α(MIP 1α)and myeloperoxidas e(MPO) with immunohistochemical method.
     用免疫组化方法检测切片核因子(nuclearfactorkappaB65,NF-κB65)、细胞间黏附因子-1(intercellularad-hesionmolecule-1,ICAM-1)、巨噬细胞炎症蛋白-1(macrophageinflamma-tionprotein-1,MIP-1α)、髓过氧化物酶myeloperoxidase,MPO的着色情()况,并应用计算机图像分析系统进行灰度分析,同时观察病理变化。
短句来源
     Inflammation cell in airway release a large number of cytokine and inflammation protein and interact each other, make the onset of asthma.
     该炎症使易感者对多种激发因子具有气道高反应性。 随着对哮喘气道炎症研究的深入,气道神经源性炎症与哮喘的关系倍受重视。
短句来源
     Results:The results showed that:characteristic of renal pathology dynamic change of 5/6 nephrectomy:glomenrulus mesangial cells hyperplasia,tubule expansion ,tubule-interstitial inflammation,protein tube of tubule,developing glomenrulus fibrosis and glomenrulosclerosis.
     结果 :5 / 6NT大鼠肾脏病理变化的基本特征为肾小球系膜细胞 (glomenrulusmesangialcells,GMC)增生 ,肾小管扩张 ,肾间质炎症反应 ,肾小管蛋白管型形成 ,并逐渐形成肾小球纤维化、硬化。
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  相似匹配句对
     protein.
     protein。
短句来源
     Inflammation
     炎症(1)
短句来源
     The relation between inflammation and C-Reaction Protein(CRP)
     感染与C-反应蛋白的关系
短句来源
     C-reactive protein (CRP) was a sensitive marker of inflammation.
     C 反应蛋白 (C reactiveprotein ,CRP)是反映炎症的敏感指标。
短句来源
     Protein Monolayers
     蛋白质分子膜
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We used the animal model of endotoxemia (endotoxin was used to stimulate the whole blood) The result showed that the concentration of the supernatant blood tumor necrosis factor (TNFα) increased with increasing doses of endotoxins Dexamethasone obviously inhibited the release of TNFα,while ibuprofen had dual efects on TNFα In acute lung injury in rats induced by penitoncal injection of endotoxins, the permeability of the pulmonary capillaries increased with increasing doses of endotoxins. Injection of dexamethasone...

We used the animal model of endotoxemia (endotoxin was used to stimulate the whole blood) The result showed that the concentration of the supernatant blood tumor necrosis factor (TNFα) increased with increasing doses of endotoxins Dexamethasone obviously inhibited the release of TNFα,while ibuprofen had dual efects on TNFα In acute lung injury in rats induced by penitoncal injection of endotoxins, the permeability of the pulmonary capillaries increased with increasing doses of endotoxins. Injection of dexamethasone and ibuprofen 1hr ahead of time could prevent the increase of the vascular permeability Meanwhile,the pulmonary contents of TNFα,interleukin1β(IL1β),macrophage inflammation protein1α(MIP1α) and mRNA increased with increasing doses of endotoxins,their peak values being at 2,6,and 12hr respectively. Dexamethasone and ibuprofen markedly inhibited the expression of the cellular factor in the pulmonary tissues It is suggested that TNFα,IL1β and MIP1α play an important role in pulmonary injury induced by endotoxins,and dexamethasone and ibuprofen can protect the acutely injured lungs by inhibiting the eapression of the cellular factor.

首先用全血内毒素血症动物模型,以内毒素刺激全血,显示动物上清液肿瘤坏死因子(TNFα)浓度随内毒素剂量增加而增加,地塞米松明显抑制其释放,布洛芬对αTNFα释放为双向效应。腹腔注射内毒素复制大鼠急性肺损伤模型,显示肺毛细血管通透性随内毒素剂量增大而增加,提前1小时注射地塞米松、布洛芬能防止血管通透性增加;同时观察到肺组织中TNFα、白细胞介素1β(IL1β)、巨噬细胞炎性蛋白1α(MIP1α)及mRNA含量随内毒素剂量增大而增多,峰值在2,6和12小时,地塞米松、布洛芬对肺组织中细胞因子表达具有明显抑制。说明TNFα、IL1β、MIP1α在内毒素诱发的肺损伤中起重要作用,地塞米松、布洛芬通过抑制细胞因子表达,对急性肺损伤起保护作用

Objective: To investigate the pathological course in the intracranial aneurysms. Methods: One case normal intracranial artery (from cortex fistulization), 11 cases ruptured aneurysms, two cases unruptured aneurysms were obtained from neurosurgical excision. Routine HE stain was used to observe histological characteristics, immunohistochemistry was used to observe the expression of monocyte chemoattractant protein-1 (MCP-1) and macrocyte inflammation protein-1α (MIP-1α) in the walls of the normal artery...

Objective: To investigate the pathological course in the intracranial aneurysms. Methods: One case normal intracranial artery (from cortex fistulization), 11 cases ruptured aneurysms, two cases unruptured aneurysms were obtained from neurosurgical excision. Routine HE stain was used to observe histological characteristics, immunohistochemistry was used to observe the expression of monocyte chemoattractant protein-1 (MCP-1) and macrocyte inflammation protein-1α (MIP-1α) in the walls of the normal artery and aneurysms (unruptured and ruptured). Result: By the HE strain the wall of the ruptured aneurysms (10 cases) and unruptured ones (2 cases) consisted of incrassated intima and connectivum extima. The fibroblast in the intima was arrayed in the disorder. Monocyte-like cells could be seen in the whole aneurysm wall. In one case of aneurysm wall(ruptured) glass-like fiber structure was left over, and few cells could be seen. Nine cases of mural thrombus could be found. The thrombus represented with organization. Immunohistochemistry: MCP-1 and MIP-1α were not detectable in the normal artery; the immunohistochemistry signal of MCP-1 and MIP-1α could be observed upregulated in the ruptured aneurysms (10 cases) and unruptured ones (2 cases), often in the intima. MCP-1 and MIP-1α appeared to be expressed by Fibroblast cell in its cytoplasm. Monocyte-like cells had little cytoplasm, the signal was seldom seen. The immunohistochemistry signal was discontinuous in the intima, MCP-1 and MIP-1α expressed where fibroblast and monocyte-like cells assembled. One case of ruptured aneurysms had no signal because there were no cells, only glass-like fiber. Mural thrombus had upregulated signal of MCP-1 and MIP-1α in the cytoplasm of fibroblasts and endotheliocytes of its micrangium. Conclusion: the pathological representation of the ruptured and unruptured aneurysms and the upregulated expression of MCP-1 and MIP-α in the aneurysm wall suggest that the development of the aneurysm may be a course of the chronic inflammation whose main inflammatory cells are monocyte-like cells.

为探讨脑动脉瘤发生发展的病理过程 ,对 2例未破裂动脉瘤和 1 1例破裂的动脉瘤壁进行常规HE染色观察 ,并应用免疫组化方法观察单核细胞趋化蛋白 1 (MCP 1 )和巨噬细胞炎性蛋白 1α(MIP 1α)在颅内动脉瘤壁内的表达及位置。 2例正常脑动脉做对照比较。结果 :2例未破裂和 1 0例破裂动脉瘤HE染色 ,瘤壁由增厚的内膜和结缔组织外膜组成 ;纤维增厚的内膜有长梭形的成纤维细胞不规则排列 ;瘤壁全层有单核性细胞浸润。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞成分 ;9例有附壁血栓 ,血栓呈机化表现。免疫组化 :正常动脉未见MCP 1和MIP 1α表达。 2例未破裂和 1 0例破裂动脉瘤壁内有MCP 1和MIP 1α的高表达 ,表达细胞多为成纤维细胞 ,颗粒沉积于胞质。阳性细胞呈局灶聚集 ,分布于动脉瘤内膜 ,多在排列紊乱的成纤维细胞、淋巴细胞聚集处。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞 ,未见表达信号。动脉瘤附壁血栓内有MCP 1和MIP 1α的表达 ,表达细胞有成纤维细胞、微血管的内皮细胞 ,表达部位在胞质。未破裂的和破裂动脉瘤的病理表现和MCP 1、MIP 1α在动脉...

为探讨脑动脉瘤发生发展的病理过程 ,对 2例未破裂动脉瘤和 1 1例破裂的动脉瘤壁进行常规HE染色观察 ,并应用免疫组化方法观察单核细胞趋化蛋白 1 (MCP 1 )和巨噬细胞炎性蛋白 1α(MIP 1α)在颅内动脉瘤壁内的表达及位置。 2例正常脑动脉做对照比较。结果 :2例未破裂和 1 0例破裂动脉瘤HE染色 ,瘤壁由增厚的内膜和结缔组织外膜组成 ;纤维增厚的内膜有长梭形的成纤维细胞不规则排列 ;瘤壁全层有单核性细胞浸润。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞成分 ;9例有附壁血栓 ,血栓呈机化表现。免疫组化 :正常动脉未见MCP 1和MIP 1α表达。 2例未破裂和 1 0例破裂动脉瘤壁内有MCP 1和MIP 1α的高表达 ,表达细胞多为成纤维细胞 ,颗粒沉积于胞质。阳性细胞呈局灶聚集 ,分布于动脉瘤内膜 ,多在排列紊乱的成纤维细胞、淋巴细胞聚集处。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞 ,未见表达信号。动脉瘤附壁血栓内有MCP 1和MIP 1α的表达 ,表达细胞有成纤维细胞、微血管的内皮细胞 ,表达部位在胞质。未破裂的和破裂动脉瘤的病理表现和MCP 1、MIP 1α在动脉瘤壁内的局灶性的高表达 ,提示脑动脉瘤的发展是单核性细胞的不断聚集加强的慢性炎性过程

AIM:To study the effect of buflomedil on polymorphonuclear leukocytes(PMNs) in filtration after cerebral ischemia reperfusion injury on rats. METHODS:The experiment was completed in the Cerebrovascular Laboratory,the Dep artment of Neurology,the First Affiliated Hospital of Zhengzhou University.Total ly 144 healthy male SD rats were divided into sham operated group,operated grou p,physiological saline treatment group and buflomedil chlorhydrate treatment gro up at random,36 rats in each group.Rat transient...

AIM:To study the effect of buflomedil on polymorphonuclear leukocytes(PMNs) in filtration after cerebral ischemia reperfusion injury on rats. METHODS:The experiment was completed in the Cerebrovascular Laboratory,the Dep artment of Neurology,the First Affiliated Hospital of Zhengzhou University.Total ly 144 healthy male SD rats were divided into sham operated group,operated grou p,physiological saline treatment group and buflomedil chlorhydrate treatment gro up at random,36 rats in each group.Rat transient cerebral ischemic injury model was established with suture emboli method.In operated group, rats were sacrifice d at 1,3,6,12,24,48 hours respectively after 1 hour of middle cerebral arter y occlusion(MCAO),the brains were taken out, sliced and embedded in paraffin use d to examine nuclear factor kappa B65(NF κB65), intercellular adhesion molec ule 1(ICAM 1),macrophage inflammation protein 1α(MIP 1α)and myeloperoxidas e(MPO) with immunohistochemical method.Then computer image analysis system was u sed to analyze the gray values of NF κB65,ICAM 1,MIP 1αand MPO,and the path ological observation was performed. RESULTS: Activated NF κB65,ICAM 1,MIP 1αand MPO immunoreactive cells wer e observed at each time point in the operated group,physiological saline treatme nt group and buflomedil chlorhydrate treatment group but not in sham operated g roup.There were no significant differences in the gray values of NF κB65,ICAM 1,MIP 1αand MPO between the operated group and physiological saline treatmen t group(P >0.05).The gray values of NF κB65,ICAM 1,MIP 1αand MPO were highe r in the buflomedil chlorhydrate treatment groups than in the operated groups an d physiological saline treatment group operated groups,except for the 1 hour re perfusion group(NF κb65:100.13±3.31;ICAM 1:153.90±3.82;MIP 1α:187.72±3.4 1 )(P< 0.05). CONCLUSION:The cerebral protection of buflomedil chlorhydrate can carry out by reducing PMN infiltration against inflammation.

目的:观察丁咯地尔对大鼠脑缺血再灌注后多形核白细胞浸润的影响,研究丁咯地尔的脑保护作用机制。方法:实验在郑州大学第一附属医院神经内科脑血管病实验室完成。选择健康雄性SD大鼠144只,随机分为假手术组、手术组、生理盐水治疗组、丁咯地尔治疗组,每组各36只,各组又分再灌注1,3,6,12,24,48h6个时间点。建立大鼠脑缺血再灌注损伤模型,缺血时间为1h,在相应时间点处死大鼠后,取脑,制成蜡块。用免疫组化方法检测切片核因子(nuclearfactorkappaB65,NF-κB65)、细胞间黏附因子-1(intercellularad-hesionmolecule-1,ICAM-1)、巨噬细胞炎症蛋白-1(macrophageinflamma-tionprotein-1,MIP-1α)、髓过氧化物酶myeloperoxidase,MPO的着色情()况,并应用计算机图像分析系统进行灰度分析,同时观察病理变化。结果:假手术组在各时间点均无NF-ΚB65,ICAM-1,MIP-1α和MPO免疫组化阳性细胞表达,手术组、生理盐水治疗组和丁咯地尔治疗组均出现NF-κB65,ICAM-1,MIP-1α和MPO免疫阳性细胞,...

目的:观察丁咯地尔对大鼠脑缺血再灌注后多形核白细胞浸润的影响,研究丁咯地尔的脑保护作用机制。方法:实验在郑州大学第一附属医院神经内科脑血管病实验室完成。选择健康雄性SD大鼠144只,随机分为假手术组、手术组、生理盐水治疗组、丁咯地尔治疗组,每组各36只,各组又分再灌注1,3,6,12,24,48h6个时间点。建立大鼠脑缺血再灌注损伤模型,缺血时间为1h,在相应时间点处死大鼠后,取脑,制成蜡块。用免疫组化方法检测切片核因子(nuclearfactorkappaB65,NF-κB65)、细胞间黏附因子-1(intercellularad-hesionmolecule-1,ICAM-1)、巨噬细胞炎症蛋白-1(macrophageinflamma-tionprotein-1,MIP-1α)、髓过氧化物酶myeloperoxidase,MPO的着色情()况,并应用计算机图像分析系统进行灰度分析,同时观察病理变化。结果:假手术组在各时间点均无NF-ΚB65,ICAM-1,MIP-1α和MPO免疫组化阳性细胞表达,手术组、生理盐水治疗组和丁咯地尔治疗组均出现NF-κB65,ICAM-1,MIP-1α和MPO免疫阳性细胞,手术组和生理盐水治疗组各时间点比较灰度值差异无显著性意义(P>0.05);丁咯地尔治疗组除再灌注1h犤NF-κB65:100.13±3.31;ICAM-1:153.90±3.82;MIP-1α:187.72±3.41犦,其余各时间点灰度值均高于手术组和生理盐水治疗组(P<0.05)。结论:丁

 
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