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关于“脂质病毒”的本质

On the nature of the "lipovirus".

作者信息

Chang R S, Pan I H, Rosenau B J

出版信息

J Exp Med. 1966 Dec 1;124(6):1153-66. doi: 10.1084/jem.124.6.1153.

Abstract

Experiments designed to elucidate the nature of the "lipovirus" are described. The development of characteristic nuclear lesions in human cells in vitro depended on the presence of an ameboid cell in the inoculum. The spatial separation of the ameboid cells from the human cells by a membrane filter 150 micro in thickness was sufficient to prevent the development of nuclear lesions. Nuclear lesions appeared to be the primary change of the affected human cells. This development of nuclear lesions was partially suppressed by FUDR and the suppression was reversed by thymidine. Time-lapse microcinematography showed that a 30 min intermittent contact between an ameboid cell and a human cell resulted in the retraction of both progenies of the human cell after a lapse of about 36 hr. Other human cells not in contact with the ameboid cell remained polygonal and continued to divide. Radioautography of the ameboid cell revealed the presence in the cytoplasm of thymidine-containing DNAse-sensitive materials. The development of antigens related to the ameboid cell within the cytoplasm of the human cell is described in the accompanying report (4).

摘要

本文描述了旨在阐明“脂病毒”本质的实验。体外培养的人细胞中特征性核损伤的出现取决于接种物中变形细胞的存在。通过厚度为150微米的膜过滤器将变形细胞与人细胞在空间上分隔开,足以防止核损伤的出现。核损伤似乎是受影响人细胞的主要变化。这种核损伤的发展部分受到氟脱氧尿苷(FUDR)的抑制,而胸腺嘧啶核苷可逆转这种抑制作用。延时显微电影摄影显示,变形细胞与人细胞之间30分钟的间歇性接触会导致人细胞的两个子代在大约36小时后回缩。其他未与变形细胞接触的人细胞仍保持多边形并继续分裂。对变形细胞的放射自显影显示,其细胞质中存在含胸腺嘧啶核苷的对DNA酶敏感的物质。随附报告(4)中描述了人细胞细胞质内与变形细胞相关抗原的发展情况。

相似文献

1
On the nature of the "lipovirus".关于“脂质病毒”的本质
J Exp Med. 1966 Dec 1;124(6):1153-66. doi: 10.1084/jem.124.6.1153.
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DNA synthesis in the ooplasm of Drosophila melanogaster.黑腹果蝇卵质中的DNA合成。
J Cell Biol. 1966 Feb;28(2):199-208. doi: 10.1083/jcb.28.2.199.

本文引用的文献

1
Radiation Resistance in Lipovirus-Altered Human Cells.脂病毒改造的人类细胞中的辐射抗性。
Science. 1965 Jun 25;148(3678):1746-7. doi: 10.1126/science.148.3678.1746.

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