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tumor necrosis factor super family
相关语句
  肿瘤坏死因子超家族
     Expression of Tumor Necrosis Factor Superfamily Member LIGHT and Its Receptor HVEM in the Peripheral Blood of Patient with Multiple Sclerosis
     多发性硬化患者外周血肿瘤坏死因子超家族成员LIGHT及其受体HVEM的表达
短句来源
     The number of tumor necrosis factor superfamily(TNFSF) and tumor necrosis factor receptor superfamily(TNFRSF) has been extremely expanded since large-scale sequencing of "expressed sequence tags(ESTs)" and Bioinformatics have been used.
     肿瘤坏死因子超家族(tumor necrosis factor superfamily,TNFSF)和肿瘤坏死因子受体超家族(TNFRSF)的成员不断增加,它们不仅广泛参与哺乳动物多种生理功能,而且与许多疾病的发病密切相关。
短句来源
     Gene expression of tumor necrosis factor superfamily in peripheral blood mononuclear cells during chronic heart failure
     肿瘤坏死因子超家族基因在慢性心力衰竭外周血单核细胞的表达
短句来源
     The tumor necrosis factor superfamily (TNFSF) members and their corresponding receptor superfamily (TNFRSF) members are the key inducers and regulators in the cellular responses including cellular apoptosis, differentiation and proliferation etc.
     肿瘤坏死因子超家族(TNFSF)及其相应的受体超家族(TNFRSF)在细胞功能调控方面具有重要地位,其调控作用涉及细胞的多种行为,与机体的生理和病理过程密切相关。
短句来源
  肿瘤坏死因子受体超家族
     The number of tumor necrosis factor superfamily(TNFSF) and tumor necrosis factor receptor superfamily(TNFRSF) has been extremely expanded since large-scale sequencing of "expressed sequence tags(ESTs)" and Bioinformatics have been used.
     肿瘤坏死因子超家族(tumor necrosis factor superfamily,TNFSF)和肿瘤坏死因子受体超家族(TNFRSF)的成员不断增加,它们不仅广泛参与哺乳动物多种生理功能,而且与许多疾病的发病密切相关。
短句来源
     Combination of tumor necrosis factor super family member and corresponding death ligand can activate apoptosis signal pathway. Tumor necrosis factor α can induce the apoptosis of chondrocyte when the other apoptosis factors exist or survival-promoting factors were lacked.
     肿瘤坏死因子受体超家族成员与相应的死亡配体结合能激活凋亡信号通路,当存在其他前凋亡因子或缺乏某些促存活因子时肿瘤坏死因子α能诱导软骨细胞凋亡。
短句来源
  “tumor necrosis factor super family”译为未确定词的双语例句
     Objective Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a new member of the tumor necrosis factor superfamily. TRAIL can bind the necrotic receptor on the surface of the target cell membrane and induce tumor apoptosis selectively while having no significant toxic effect on the normal cell.
     目的:肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor-related apoptosis-inducing ligand,TRAIL)属于肿瘤坏死因子超家族的新成员,能够与细胞表面的死亡受体结合而启动凋亡信号传导。
短句来源
     TRAIL: A New Member of Tumor Necrosis Factor Superfamily.
     肿瘤坏死因子家族新成员——TRAIL
短句来源
     TRAIL, Caspase-3, Survivin is now new-found several genes for promoting/ repressing apoptosis, among them TRAIL is a new member of the tumor necrosis factor super family( TNF), It is a kind of II type transmembrane protein, and can steadily express in almost all normal tissue, primarily and selectively induce the tumor cell apoptosis , but to the normal tissue almost have no any influence;
     TRAIL、Caspase-3、Survivin是目前新发现的一类促进/抑制凋亡基因,其中TRAIL是肿瘤坏死因子(TNF)超家族的新成员,是一种Ⅱ型跨膜蛋白,可稳定地表达于几乎所有正常组织,主要选择性地诱导肿瘤细胞凋亡,而对正常组织几乎没有影响;
短句来源
     TRAIL(tumor necrosis factor related apoptosis inducing ligand), which is also called APO 2L, is a new member of the tumor necrosis factor superfamily and was cloned recent year.
     从人胎盘中提取总RNA ,利用RT PCR技术扩增了可溶性TRAIL(凋亡素配体 2 )基因片段。
短句来源
     B lymphocyte stimulators(Blys)is a new member of tumor necrosis factor superfamily,which produces a marked effect through specific binding with three receptors.
     B细胞刺激因子(Blys)是肿瘤坏死因子(TNF)超家族的新成员,通过与B细胞表面三个受体特异性结合而发挥作用。
短句来源
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Objective: Both ODF (osteoclast differentiation factor, a newly identified member of the tumor necrosis factor super-family) and M-CSF (macrophage colony-stimulating factor) are indispensable for OC (osteoclast) formation. The purpose of this study was to test the possibility that the combination of ODF and M-CSF was sufficient for OC development in primary murine marrow cell culture. Methods: Bone marrow cells were isolated from 5- to 6- week-old mice and incubated...

Objective: Both ODF (osteoclast differentiation factor, a newly identified member of the tumor necrosis factor super-family) and M-CSF (macrophage colony-stimulating factor) are indispensable for OC (osteoclast) formation. The purpose of this study was to test the possibility that the combination of ODF and M-CSF was sufficient for OC development in primary murine marrow cell culture. Methods: Bone marrow cells were isolated from 5- to 6- week-old mice and incubated in M-CSF (10 ng/ml). After 24 hours, non-adherent cells were harvested and resuspended in a-MEM /BCS. The suspension was added to the wells of 24-well plates with different concentration of ODF and/or M-CSF. TRAP (tartrate-resistant acid phosphatase) staining was used to identify OC. The bone resorption pits on slices of bovine cortical bone were examined with inverted phase contrast microscope, and the changes of Ca2+ concentration in the medium during whole culture period were measured by atomic absorption spectrophotometer. Results: When bone marrow cells were cultured for up to 11 days either in the presence of M-CSF (10 ng/ml) or ODF (50 ng/ml) , no cells expressing TRAP and bone obvious resorption was found. But in the presence of ODF and M-CSF, many TRAP-positive mono- and multi-nucleated cells were formed after 7 days. The number of TRAP-positive miJti-nucleated cells and the change of Ca2+ in the culture medium increased dose-dependently with ODF concentration. Conclusion: The combination of ODF and M-CSF can induce OC formation and bone resorption in murine marrow cell culture, and it can be employed to investigate the direct effects of factors on OC differentiation and activation.

目的:探讨破骨细胞分化因子(ODF)和巨噬细胞集落刺激因子(M-CSF)联合应用进行体外诱导小鼠骨髓细胞形成破骨细胞(OC)的能力。方法:收集5~6周小鼠骨髓细胞,在含M-CSF(10 ng/ml)的α-MEM全培养液中培养24h,然后将悬浮生长的细胞接种到24孔培养板,并加入不同浓度的ODF和M-CSF。,通过观察抗酒石酸盐酸性磷酸酶(TRAP)染色的阳性细胞和能否在骨磨片上形成吸收陷窝来鉴定OC形成情况。结果:在只加入ODF或M-CSF一种细胞因子时,未见有TRAP阳性或CTR阳性细胞形成,同时加入ODF和M-CSF,可形成典型的OC。TRAP阳性多核细胞的数目和培养液中钙离子浓度的增加与ODF的浓度呈正相关。结论:小鼠骨髓来源的单核细胞在ODF和M-CSF共同作用下可形成具有骨吸收功能的OC,为体外研究OC的分化发育和功能调节提供了一种新的方法。

AIM: There are many results about on the incidence and developmental mechanism of osteoarthritis. Study on apoptosis factor of chondrocyte has new meaning. DATA SOURCES: Literatures about cellular apoptosis of chondrocyte in osteoarthritis from January 1985 to December 2004 were computer-searched in Medline, with the of "osteoarthritis, chondrocyte, and apoptosis" and the language was limited to English.STUDY SELECTION: Abstracts of the materials were selected by the primary trial .The literatures includes those...

AIM: There are many results about on the incidence and developmental mechanism of osteoarthritis. Study on apoptosis factor of chondrocyte has new meaning. DATA SOURCES: Literatures about cellular apoptosis of chondrocyte in osteoarthritis from January 1985 to December 2004 were computer-searched in Medline, with the of "osteoarthritis, chondrocyte, and apoptosis" and the language was limited to English.STUDY SELECTION: Abstracts of the materials were selected by the primary trial .The literatures includes those in the experimental group and control group, and the whole paper was searched. Inclusion criteria: ① Randomly controlled trial. ② Control group was included. Exclusion criteria: ① Literatures in the control group were not set. ② Reviewed literatures, Meta analysis, repeated study.DATA EXTRACTION: Totally 111 tests on apoptosis factors of chondrocyte in osteoarthritis were collected, but only 35 literatures met the inclusion criteria. Altogether 28 literatures were excluded due to reviewed papers and 48 due to repeated study. The 35 literatures were mostly about tests of chondrocyte cultured in vivro, and the apoptosis factors were evaluated separately. DATA SYNTHESIS: Among the chondrocytes of patients with osteoarthritis and aging people, inflammatory reaction of chondrocyte appeared due to degredation of extracellular matrix or normal extracellular matrix was destroyed through glycosylated and tyrosine nitroso mordification and promotes its death. Various mechanical stimulations are the important regulation factors of the function of chondrocyte. Acceleration of mechanical stress pressured determines the injury of chondrocyte and type and degree of death of chondrocyte . Normal chondrocyte affected by some cytokines and chondrocyte cultured separately produce high level of NO, which can induce the death of chondrocyte. Combination of tumor necrosis factor super family member and corresponding death ligand can activate apoptosis signal pathway. Tumor necrosis factor α can induce the apoptosis of chondrocyte when the other apoptosis factors exist or survival-promoting factors were lacked. Damage of energy metabolism can make the other death-promoting factors much sensitive. In the process of osteoarthritis related development, the exact mechanism deserves to clarify although p53 participants in the cellular death. And also no enough and direct proof to indicate c-myc can influence the survival and death of chondrocyte.CONCLUSION: There are many cellular apoptosis-influencing factors in osteoarthritis with complex mechanism. Pathway of apoptosis of chondrocyte induced by many factors deserves to further study.

目的:近年来国外对骨关节炎的发生及发展机制有许多研究成果,骨关节炎中软骨细胞凋亡影响因素的研究颇具新意。资料来源:应用计算机检索Medline1985-01/2004-12与骨关节炎中软骨细胞凋亡相关的文献,检索词“osteoarthritis,chondrocyte,apoptosis”并限定文献语种为English。资料选择:对资料的摘要进行阅读初审,选取包括试验组和对照组的文献,开始查找全文。纳入标准:①随机对照试验。②试验包括对照组。排除标准:①没有设立对照组的文献。②综述类文献、Meta分析、重复研究。资料提炼:共收集到111篇关于骨关节炎中软骨细胞凋亡影响因素的试验,纳入符合标准的文献35篇。排除的文献为综述类文献28篇和重复研究48篇。35篇文献多为软骨细胞体外培养有关的试验,分别对各种凋亡影响因素进行评价。资料综合:在骨关节炎患者和老年人的软骨中,由于细胞外基质成分降解或通过高级糖基化、酪氨酸亚硝基化等修饰作用破坏了正常的细胞外基质从而使软骨细胞发生炎症反应并促进其死亡。各种机械性刺激是软骨细胞功能的重要调节因素,施加机械压力的加速率也决定软骨损伤和软骨细胞死亡的类型与程度。经某些细胞因子作用...

目的:近年来国外对骨关节炎的发生及发展机制有许多研究成果,骨关节炎中软骨细胞凋亡影响因素的研究颇具新意。资料来源:应用计算机检索Medline1985-01/2004-12与骨关节炎中软骨细胞凋亡相关的文献,检索词“osteoarthritis,chondrocyte,apoptosis”并限定文献语种为English。资料选择:对资料的摘要进行阅读初审,选取包括试验组和对照组的文献,开始查找全文。纳入标准:①随机对照试验。②试验包括对照组。排除标准:①没有设立对照组的文献。②综述类文献、Meta分析、重复研究。资料提炼:共收集到111篇关于骨关节炎中软骨细胞凋亡影响因素的试验,纳入符合标准的文献35篇。排除的文献为综述类文献28篇和重复研究48篇。35篇文献多为软骨细胞体外培养有关的试验,分别对各种凋亡影响因素进行评价。资料综合:在骨关节炎患者和老年人的软骨中,由于细胞外基质成分降解或通过高级糖基化、酪氨酸亚硝基化等修饰作用破坏了正常的细胞外基质从而使软骨细胞发生炎症反应并促进其死亡。各种机械性刺激是软骨细胞功能的重要调节因素,施加机械压力的加速率也决定软骨损伤和软骨细胞死亡的类型与程度。经某些细胞因子作用的正常软骨和分离培养的软骨细胞产生高水平的NO,而NO产物又能诱导软骨细胞死亡。肿瘤坏死因子受体超家族成员与相应的死亡配体结合能激活凋亡信号通路,当存在其他前凋亡因子或缺乏某些促存活因子时肿瘤坏死因子α能诱导软骨细胞凋亡。正是由于能量代谢受损使软骨细胞对其他的致死因子变得更加敏感。在发育和骨关节疾病相关过程中,软骨细胞的死亡虽然有p53的参与,但其精确的机制有待阐明,同时没有足够的直接证据表明c-myc能够影响软骨细胞的存活或死亡。结论:骨关节炎中影响软骨细胞凋亡的因素很多,机制复杂,许多因素导致软骨细胞凋亡的通路有待进一步阐明。

 
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