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体外对猫骨髓集落形成的选择性抑制归因于具有独特长末端重复序列的分子克隆猫白血病病毒株。

In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat.

作者信息

Nagashima N, Hisasue M, Nishigaki K, Miyazawa T, Kano R, Hasegawa A

机构信息

Department of Pathobiology, Nihon University School of Veterinary Medicine, 1866, Kameino, Fujisawa, Kanagawa 252-8510, Japan.

出版信息

Res Vet Sci. 2005 Apr;78(2):151-4. doi: 10.1016/j.rvsc.2004.07.003.

Abstract

Molecularly cloned feline leukemia virus (FeLV)-clone 33 (C-33), derived from a cat with acute myelocytic leukemia (AML), was examined to assess its relation to the pathogenesis of AML and myelodysplastic syndrome (MDS). To evaluate in vitro pathogenicity of FeLV C-33, bone marrow colony-forming assay was performed on marrow cells infected with FeLV C-33 or an FeLV subgroup A strain (61E, a molecularly cloned strain with minimal pathogenicity). The myeloid colony-forming activity of feline bone marrow mononuclear cells infected with FeLV C-33 was significantly lower than that of cells infected with 61E. This suggests that FeLV C-33 has myeloid lineage-specific pathogenicity for cats, and that FeLV C-33 infection is useful as an experimental model for investigating pathogenesis of MDS and AML.

摘要

对从一只患有急性髓细胞白血病(AML)的猫身上获得的分子克隆猫白血病病毒(FeLV)-克隆33(C-33)进行了检测,以评估其与AML和骨髓增生异常综合征(MDS)发病机制的关系。为了评估FeLV C-33的体外致病性,对感染了FeLV C-33或FeLV A亚群毒株(61E,一种致病性极低的分子克隆毒株)的骨髓细胞进行了骨髓集落形成试验。感染FeLV C-33的猫骨髓单个核细胞的髓系集落形成活性明显低于感染61E的细胞。这表明FeLV C-33对猫具有髓系谱系特异性致病性,并且FeLV C-33感染可作为研究MDS和AML发病机制的实验模型。

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