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双螺旋丝
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  paired helical filaments
     With the monoclonal antibody of phosphorylated neurofilaments (PNF) (molecular weight 160-200KD) and paired helical filaments (PHF) respectively, a competitive enzyme-linked immunosorbent assay (ELISA) has been established for PNF and PHF immunoreac-tivities in the cerebrospinal fluid (CSF).
     应用160~200KD磷酸化神经丝(PNF)和双螺旋丝(PHF)单克隆抗体建立竞争抑制ELISA。
短句来源
     Using monoclonal antibody (mAb) as probes, with purified phosphorylated neurofilaments(PNF) and paired helical filaments(PHF) as coated antigens (Ag) respectively, a competitive enzyme linked immunosorbent assay (ELISA) has been established for PNF and PHF immunoreactivities in the cerebrospinal fluid (CSF).
     目的 建立测定脑脊液 (CSF)中磷酸化神经丝 (PNF)和双螺旋丝 (PHF)免疫活性的检测方法 ,并探讨Alzheimer病 (AD)患者CSF中PNF和PHF免疫活性的变化及其临床意义。
短句来源
  “双螺旋丝”译为未确定词的双语例句
     Detection of Phosphorylated Neurofilament and Paired Helical Filament Immunoreactivities in Alzheimer Cerebrospinal Fluid by ELISA
     ELISA测定Alzheimer病脑脊液磷酸化神经丝和双螺旋丝抗原活性
短句来源
     Results Protein phosphatases 2A and 2B dephosphorylated tau in type II paired helical filament (PHFII tau) at ser 199/ser 202, partially dephosphorylated it at ser 396/ser 404. In addition, PP 2A and PP 2B dephosphorylated PHIFII tau at ser 46 and ser 235, respectively.
     结果蛋白磷酸酯酶(PP)2A和PP2B可使AD神经原纤维缠结中的I型双螺旋丝(PHFItau)在Ser199/Ser202去磷酸化,Ser396/Ser404部分去磷酸化; 此外,PP2A和PP2B可分别使PHFIItau的Ser46和Ser235去磷酸化;
短句来源
     Dephosphorylation of neurofibrillary tangles in Alzheimer brain
     阿尔茨海默病患者脑中双螺旋丝的体外去磷酸化作用
短句来源
     The immunoreactivities of phosphorylated neurofilament and paired helical filament in CSF of
     阿尔茨海默病脑脊液磷酸化神经丝及双螺旋丝免疫活性
短句来源
     Alzheimer's disease:phosphorylated neurofilament and paired helical filament immunoreactivities in CSF
     Alzheimer病脑脊液磷酸化神经丝及双螺旋丝免疫活性(英文)
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  相似匹配句对
     Dual Lenses
     透镜
短句来源
     The immunoreactivities of phosphorylated neurofilament and paired helical filament in CSF of
     阿尔茨海默病脑脊液磷酸化神经丝及螺旋丝免疫活性
短句来源
     Alzheimer's disease:phosphorylated neurofilament and paired helical filament immunoreactivities in CSF
     Alzheimer病脑脊液磷酸化神经丝及螺旋丝免疫活性(英文)
短句来源
     adopting the double cantilevers;
     采用腕臂;
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  paired helical filaments
Electron microscopy of NFTs reveals structures known as paired helical filaments (PHFs).
      
Electron microscopy of material eluted from the stacking gel showed fibers of approximately 7-10 nm diameter, with some twisting; properties consistent with paired helical filaments or amyloid.
      
Abnormally hyperphosphorylated tau which is the major protein subunit of paired helical filaments (PHF)/neurofibrillary tangles is the pivotal lesion in Alzheimer disease (AD) and related tauopathies.
      
The pathological diagnosis of Alzheimer's disease (AD) depends on the presence of plaques consisting of the β-amyloid peptide as well as neurofibrillary tangles consisting of paired helical filaments (PHFs) of the tau (τ) protein.
      
The microtubule-associated protein (MAP) tau is abnormally hyperphosphorylated in the brain of patients with AD, and in this form it is the major protein subunit of paired helical filaments/neurofibrillary tangles (PHF/NFT).
      
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With the monoclonal antibody of phosphorylated neurofilaments (PNF) (molecular weight 160-200KD) and paired helical filaments (PHF) respectively, a competitive enzyme-linked immunosorbent assay (ELISA) has been established for PNF and PHF immunoreac-tivities in the cerebrospinal fluid (CSF). Using the assay, we measured PNF and PHF im-munoreactivities in CSF from 21 patients with Alzheimer's disease (AD), 17 with multi-in-farct dementia, 33 with other neurological diseases control, 33 patients with Schizophrenia,...

With the monoclonal antibody of phosphorylated neurofilaments (PNF) (molecular weight 160-200KD) and paired helical filaments (PHF) respectively, a competitive enzyme-linked immunosorbent assay (ELISA) has been established for PNF and PHF immunoreac-tivities in the cerebrospinal fluid (CSF). Using the assay, we measured PNF and PHF im-munoreactivities in CSF from 21 patients with Alzheimer's disease (AD), 17 with multi-in-farct dementia, 33 with other neurological diseases control, 33 patients with Schizophrenia, and 40 normal control. It was found that the levels of PHF immunoreactivity measured in CSF were significantly higher in AD than in control groups (P<0. 05). The values of PNF/ PHF ratio in CSF were significantly lower in the AD than in the control groups (P<0. 001). These findings demonstrate that this assay is specific and sensitive, and might be developed to be significant by the means of clinical diagnosis of the AD.

应用160~200KD磷酸化神经丝(PNF)和双螺旋丝(PHF)单克隆抗体建立竞争抑制ELISA。并检测了21例Alzheimer病(AD)、17例多发梗塞性痴呆、33例其他神经疾病、33例精神分裂症及40例正常人的CSF中PNF和PHF抗原活性。结果AD组CSF中PHF抗原活性明显高于其他各组;而其PNF/PHF比值明显低于其他各组。本法有可能成为诊断AD的实验室方法。

The negative stain electron microscopy revealed a dissociation of the neurofibrillary tangles af-ter incubation of PHF Ⅱ-tau with PP-2A or PP-2B at 37 C for 45 min. The PHF tangles were dissociated in-to individual PHF, and the twists in PHF started becoming less defined. Further dissociation of the PHF and the tangles was seen by 3h dephosphorylation either by PP-2A or by PP-2B. An increasing dissociation of the tangles into individual PHF and dissociation of PHF into straight subfilaments/protofiiaments were...

The negative stain electron microscopy revealed a dissociation of the neurofibrillary tangles af-ter incubation of PHF Ⅱ-tau with PP-2A or PP-2B at 37 C for 45 min. The PHF tangles were dissociated in-to individual PHF, and the twists in PHF started becoming less defined. Further dissociation of the PHF and the tangles was seen by 3h dephosphorylation either by PP-2A or by PP-2B. An increasing dissociation of the tangles into individual PHF and dissociation of PHF into straight subfilaments/protofiiaments were frequently seen in the 3 h dephosphorylated samples. Quantitation by radioimmuno-dot blots revealed a net release of approximately 25% of total tau from PHF following dephosphorylation by PP-2A. Dephosphorylation of PHF II -tau both by PP-2A and PP-2B restored differentially the biological activity of tau in promoting the in vitro assembly of microtubules. These observations demonstrate that PHF Ⅱ -tau is accessible to dephosphory-lation, which makes it dissociable and biologically active. Therefore, dephosphorylation might inhibit and re-verse the neurofibrillary degeneration in Alzheimer brain.

探讨去磷酸化作用对Alzheimer神经原纤维缠结结构和功能的影响。结果发现,将蛋白磷酸酯酶—2A或—2B型与Alzheimer神经原纤维缠结在37℃保温45min可使缠结结构松解,神经原纤维缠结的基本单位双螺旋丝的螺旋性趋于消失;延长去磷酸化反应时间至3h可使缠结结构进一步松解,产生大量单个螺旋丝原纤维,并释放大量游离双螺旋丝片段和比对照组高约25%的游离tau蛋白;去磷酸化作用可不同程度恢复神经原纤维缠结中tau蛋白促微管组装的生物学功能。这从结构和功能双重角度证明了Alzbeimer病脑病理损伤的可逆转性,为Alzheimer病治疗的可能性提供了实验依据。

Objective To explore the pssibility and the way to reverse Alzheimer neurofibrillary degeneration. Methods The methods of dephosphorylation and Western blot were utilized. Results Protein phosphatases 2A and 2B dephosphorylated tau in type II paired helical filament (PHFII tau) at ser 199/ser 202, partially dephosphorylated it at ser 396/ser 404. In addition, PP 2A and PP 2B dephosphorylated PHIFII tau at ser 46 and ser 235, respectively. Dephosphorylation increased the relative electrophoretic...

Objective To explore the pssibility and the way to reverse Alzheimer neurofibrillary degeneration. Methods The methods of dephosphorylation and Western blot were utilized. Results Protein phosphatases 2A and 2B dephosphorylated tau in type II paired helical filament (PHFII tau) at ser 199/ser 202, partially dephosphorylated it at ser 396/ser 404. In addition, PP 2A and PP 2B dephosphorylated PHIFII tau at ser 46 and ser 235, respectively. Dephosphorylation increased the relative electrophoretic mobility of tau. The divalent cations, Mn 2+ and Mg 2+ , stimulated the phosphatase activity in dephosphorylating of PHFII tau. This activity further increased with the increasing of phosphatase concentration. Conclusion The data indicated that tau in the Alzheimer neurofibrillary tangles was still able to be dephosphorylated in vitro by protein phosphatases. Since the abnormal phosphorylation of tau was considered to be the primary lesion in Alzheimer neurofibrillary degeneration, it was postulated that this pathological lesion was reversible in vitro.

目的探讨阿尔茨海默病(AD)脑损伤逆转的可能性及其途径。方法用去磷酸化和免疫印迹法研究AD脑损伤可逆性。结果蛋白磷酸酯酶(PP)2A和PP2B可使AD神经原纤维缠结中的I型双螺旋丝(PHFItau)在Ser199/Ser202去磷酸化,Ser396/Ser404部分去磷酸化;此外,PP2A和PP2B可分别使PHFIItau的Ser46和Ser235去磷酸化;去磷酸化后PHFIItau的相对电泳迁移率加快。Mn2+和Mg2+可增加上述酶对PHFIItau的去磷酸化作用。酶的去磷酸化作用具有浓度依赖性,随着酶浓度的增加,去磷酸化作用增强。结论因为tau蛋白异常过度磷酸化并形成PHF被认为是AD神经原纤维退化的基础,PHF可在体外被蛋白磷酸酯酶去磷酸化的结果提示,AD脑损伤可能是可逆的。

 
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