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retinal
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  视网膜
    Morphology and Distribution of Bullfrog Retinal Müller Cells and Their Expression of γ-aminobutyric Acid Transporters, Glutamate Transporter EAAC1 and Metabotropic Glutamate Receptors
    牛蛙视网膜Müller细胞的形态、分布及γ-氨基丁酸转运体、谷氨酸转运体EAAC1及代谢型谷氨酸受体的表达
短句来源
    A QUANTITATIVE STUDY ON THE RETINAL GANGLION CELL NECROSIS INDUCED BY
    大鼠视网膜缺血/再灌流损伤导致视网膜节细胞坏死的定量研究
短句来源
    THE CULTURE OF HUMAN RETINAL MuLLER CELLS-ULTRASTRUCTURAL OBSERVATION AND IMMUNOCYTOCHEMICAL CHARACTRION
    人视网膜Muller细胞培养及超微结构免疫组织化学观察
短句来源
    PRIMARY CELL CULTURE OF HUMAN RETINAL GLIAL CELLSIN VITRO
    人视网膜神经胶质细胞原代培养
短句来源
    nal Fluid on Stimulation of Human Retinal Glial Cells and the Relationship to PVR
    视网膜下液体对人视网膜神经胶质细胞生长的刺激作用与PVR关系
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  “retinal”译为未确定词的双语例句
    CHARACTERIZATION OF SEROTONERGIC, 5-HT2 RECEPTORS IN CULTURED RAT RETINAL
    培养大鼠视网膜色素上皮细胞5-HT_2受体分析
短句来源
    DIFFERENT RESPONSES OF CHORIOCAPILLARY ENDOTHELIAL CELLS AND RETINAL CAPILLARY ENDOTHELIAL CELLS TO MITOGENIC AND VASOACTIVE FACTORS
    DIFFERENT RESPONSES OF CHORIOCAPILLARY ENDOTHELIAL CELLS AND RETINAL CAPILLARY ENDOTHELIAL CELLS TO MITOGENIC AND VASOACTIVE
短句来源
    Conclusion The EAU model is successfully induced in Wistar mice immuned with bovine retinal S-Ag.
    结论以牛S抗原免疫Wistar大鼠的EAU模型建立成功。
    Apoptosis of activated lymphocytes induced by retinal pigment epithelial cells in vitro
    视网膜色素上皮细胞诱导活化淋巴细胞的凋亡
短句来源
    Effects of cytokines on collagen synthesis in human retinal pigment epithelial cells
    细胞因子对培养的人视网膜色素上皮细胞胶原合成的影响
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  retinal
Best-corrected visual acuity, intraocular pressure, retinal thickness and FFA were observed.
      
At the early stages of retina development, the neuroepithelial cells divide synchronously, thus leading to the accumulation of a certain number of the retinal rudiment cells.
      
Synchronous divisions precede the asynchronous ones, when the differentiation of the retinal cells is initiated.
      
The multipotent cells of the retinal ciliary-terminal zone and cells of the pigment epithelium in the eye periphery provide for the growth of amphibian and fish eyes during the entire life of these animals.
      
The main event of retinal regeneration in newts is the transdifferentiation of the pigment epithelium cells.
      
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After the HRP had been embedded into the bilateral superior colliculi of the rats, a double reaction of the cytochrome oxidase and the retrograde HRP tracing of the retinal ganglion cells were successfully studied by means of cobalt chloride cytochrome oxidase technic. The results showed that the pure high cytochrome oxidase activity the HRP-labeled and the double reaction ganglion cells were revealed even in the same microscopic field. As a pure high cytochrome oxidase activity ganglion cell, the blue-grey...

After the HRP had been embedded into the bilateral superior colliculi of the rats, a double reaction of the cytochrome oxidase and the retrograde HRP tracing of the retinal ganglion cells were successfully studied by means of cobalt chloride cytochrome oxidase technic. The results showed that the pure high cytochrome oxidase activity the HRP-labeled and the double reaction ganglion cells were revealed even in the same microscopic field. As a pure high cytochrome oxidase activity ganglion cell, the blue-grey colour product of the enzyme appeared within its perikaryon and processes. No visible cytochrome oxidase product, except the brown HRP grains could be found in the perikaryon and processes of the HRP labeled ganglion cells. The double reaction ganglion cells were demonstrated by the HRP grains emerged the from background of cytochrome oxidase product within its perikaryon and processes. Hydrogen peroxide was cancelled in this techenic.

大鼠经双上丘辣根过氧化物酶埋藏后,用氯化钴细胞色素氧化酶反应法处理视网膜,观察到节细胞分别呈高细胞色素氧化酶活性反应、辣根过氧化物酶标记和细胞色素氧化酶/辣根过氧化物酶联合反应,说明此法可作联合反应法使用。本实验中辣根过氧化物酶标记是在不使用过氧化氢的条件下作出的。

The changes of cytochrome oxidase activity of retinal ganglion cell (RGC) caused by the artificial high intraocular pressure (HIOP) was presented in this paper. Normal saline was injected into the anterior chamber of the right eye of 36 rats. that resulted in an intraocular pressure up to 60 mmHg for 3 hours. The experimental rats were divided into 0-, 3- and 7-day groups according to their survival time. Both retinae of each rat were whole mounted on the same slide, the left one being used as control....

The changes of cytochrome oxidase activity of retinal ganglion cell (RGC) caused by the artificial high intraocular pressure (HIOP) was presented in this paper. Normal saline was injected into the anterior chamber of the right eye of 36 rats. that resulted in an intraocular pressure up to 60 mmHg for 3 hours. The experimental rats were divided into 0-, 3- and 7-day groups according to their survival time. Both retinae of each rat were whole mounted on the same slide, the left one being used as control. Thirty-six pairs of retina were treated with the modified cytochrome oxidase (CCO) histochemical technique under similar conditions. The high CCO activity of RGC were counted. The extinction of the cytoplasm of RGC, which indicates the degree of CCO activity, was measured with microphotometer. As compared with the normal eyes, the high CCO activity RGC of experimental eyes were reduced significantly. It was found that the high CCO activity of RGC in the temporal side of retina has been reduced much more than that of the nasal side. However, the high CCO activity of RGC in 3- and 7-day groups were more than that of 0-day group, the extinction of CCO activity of RGC in 7-day group was lower than that of the 3-day group. These facts showed that the CCO activity might restore in various degrees followed by a longer survival time. This experiment emphasized the fact that the HIOP led to metabolic changes of RGC, which may be of value to the study of glaucoma.

本文以生理盐水加压注入大鼠眼前房,二道生理记录仪监测眼内压,制成大鼠急性高眼压模型。采用改良的细胞色素氧化酶(CCO)组织化学法,研究高眼压对视网膜节细胞代谢的影响。实验动物依存活期分为0、3、7天3组,根据视网膜节细胞酶活性强度和结构变化,把CCO反应的节细胞分为3级,Ⅲ级及Ⅲ级以上的节细胞为高CCO活性细胞,作高CCO活性节细胞计数,并对各级CCO活性节细胞以显微光度计测定透光率。经自身配对t检验,表明各实验组高CCO活性节细胞数目下降;经方差分析还证明,3、7天组节细胞的酶活性有恢复趋势。对视网膜不同象限结果的比较表明,高眼压所致节细胞损害在视网膜颞侧较鼻侧更显著。

The biochemical basis of pericyte loss in early diabetic retinopathy is still an open question. In studies on the mechanism by which retinal peri-cytes degenerate, we first established a bovine retinal capillary pericyte (BRCP) cell line. Subcultured BRCP grown in high (10-40mmol/L) glucose media were used as an experimental model. We found that high concentrations of glucose suppress the mitotic rate and cell birth rate of cultured BRCP. High concentrations of glucose inhibit myo-inositol transport...

The biochemical basis of pericyte loss in early diabetic retinopathy is still an open question. In studies on the mechanism by which retinal peri-cytes degenerate, we first established a bovine retinal capillary pericyte (BRCP) cell line. Subcultured BRCP grown in high (10-40mmol/L) glucose media were used as an experimental model. We found that high concentrations of glucose suppress the mitotic rate and cell birth rate of cultured BRCP. High concentrations of glucose inhibit myo-inositol transport and result in decreased intracellular myo-inositol content. This inhibition can be partially reversed by sorbinil, an aldose reductase inhibitor (ARI). Myo-inositol is a precursor of inositol phospholipids (IPLs), whose metabolism is responsible for a number of signal transduction processes. Phosphoinositidase (Plase) cleaves the phos-phodiester bond of phosphotidylinositol 4,5 diphosphate (PIP2) to produce two second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG). Further experiments showed that IP3 and DG synergistically activate BRCP proliferation in vitro. High concentrations of glucose altered the formation of both IPLs and inositol phosphate esters (IPEs) in an organ culture of retinal micro-vessels. This alteration can be reversed by adding either high concentrations of myo-inositol or ARI to the medium. Plase activity was attenuated to 82% or 55% when glucose in the growth medium was increased from 5 to 15 or 30 mmol/L, respectively. When IPLs from BRCP were analyzed by HPLC and TLC, we observed the reduction of three IPLs, including the substrate of Plase, PIP2. The reduced levels of IPLs were restored by adding either free myo-inositol or ARI to the high-glucose medium. These findings suggest that the alteration in IPL metabolism in BRCP may be related to insufficient myo-inositol or to an activated sorbitol pathway under high glucose conditions. The supplementation of either inositol or ARIs may be used as in vitro therapy for the treatment of "diabetic pericytes".

在高浓度葡萄糖条件下(模拟糖尿病条件)培养视网膜毛细血管周细胞,由于调控细胞增殖的第二信使——肌醇磷脂代谢产物减少,使周细胞增殖活力降低。在高葡萄糖条件下,周细胞内肌醇水平下降、山梨醇通路被激活;外加肌醇或阻断山梨醇通路则可使异常的肌醇磷脂代谢得到不同程度的纠正,周细胞增殖活力亦随之回升。提示外加肌醇和阻断山梨醇通路是防止糖尿病周细胞衰亡的有效体外治疗。

 
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