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[伯氏疟原虫感染小鼠病程的进一步观察]

[Further observations of the course of Plasmodium berghei infection in the mouse].

作者信息

Büngener W

出版信息

Tropenmed Parasitol. 1979 Mar;30(1):24-34.

PMID:375509
Abstract

Invasion of immature and mature erythrocytes by merozoites of Plasmodium berghei seems to obey the following rules: Merozoites prefer unparasitized immature erythrocytes. Multiple infections of immature erythrocytes occur in conditions of high merozoite production and low concentration of unparasitized immature erythrocytes, when frequently repeated contacts between merozoites and unparasitized or freshly parasitized immature erythrocytes become increasingly probable. Mature erythrocytes are invaded when the relative density of unparasitized immature erythrocytes drops below 0.2--0.5%, in other words, when merozoites do not meet unparasitized immature erythrocytes in 200--500 erythrocytes. Failure to invade mature erythrocytes is obviously not due to inability of the merozoites to penetrate the erythrocyte membranes.--Merozoites of Plasmodium vinckei, on the other hand, show random invasion of parasitized and unparasitized mature erythrocytes, leading to frequencies of unparasitized and singly or multiply parasitized erythrocytes approaching a Poisson distribution.--The Plasmodium berghei infection regularly leads to a lowered density of polychromatophilic erythrocytes in the peripheral blood. This depression of polychromatophilic erythrocytes uses to be of very different duration, form and intensity. The relative density of immature erythrocytes may show pronounced fluctuations in this phase. As has been seen in one animal, even monocytes and polymorphonuclear leucocytes may, alongside with the immature erythrocytes, for some time totally disappear from the peripheral blood. The depression of polychromatophilic erythrocytes evidently goes along with pronounced alterations of the erythropoesis in spleen and bone marrow. Leucocytes in the peripheral blood generally show rather uncharacteristic alterations of their concentration, they may form very high concentration peaks.

摘要

伯氏疟原虫裂殖子侵入未成熟和成熟红细胞似乎遵循以下规律

裂殖子优先侵入未被寄生的未成熟红细胞。在裂殖子产生量大且未被寄生的未成熟红细胞浓度低的情况下,未成熟红细胞会发生多重感染,此时裂殖子与未被寄生或刚被寄生的未成熟红细胞之间频繁反复接触的可能性越来越大。当未被寄生的未成熟红细胞的相对密度降至0.2% - 0.5%以下时,即裂殖子在200 - 500个红细胞中遇不到未被寄生的未成熟红细胞时,成熟红细胞会被侵入。未能侵入成熟红细胞显然不是由于裂殖子无法穿透红细胞膜。另一方面,文氏疟原虫裂殖子对被寄生和未被寄生的成熟红细胞表现出随机侵入,导致未被寄生以及单个或多个被寄生红细胞的频率接近泊松分布。伯氏疟原虫感染通常会导致外周血中嗜多色性红细胞密度降低。嗜多色性红细胞的这种减少在持续时间、形式和强度上差异很大。在此阶段,未成熟红细胞的相对密度可能会出现明显波动。正如在一只动物身上所观察到的,甚至单核细胞和多形核白细胞可能会与未成熟红细胞一起在外周血中完全消失一段时间。嗜多色性红细胞的减少显然与脾脏和骨髓中红细胞生成的明显改变同时发生。外周血中的白细胞通常表现出其浓度相当无特征性的变化,它们可能形成非常高的浓度峰值。

相似文献

1
[Further observations of the course of Plasmodium berghei infection in the mouse].[伯氏疟原虫感染小鼠病程的进一步观察]
Tropenmed Parasitol. 1979 Mar;30(1):24-34.
2
[Malaria plasmodia in the mouse. Parasitization of mature and immature erythrocytes by Plasmodium berghei, Plasmodium yoelii and Plasmodium chabaudi (author's transl)].[小鼠体内的疟原虫。伯氏疟原虫、约氏疟原虫和查巴迪疟原虫对成熟和未成熟红细胞的寄生作用(作者译)]
Tropenmed Parasitol. 1979 Jun;30(2):198-205.
3
[Experimental production of variants with lowered preference for polychromatophilic erythrocytes in Plasmodium yoelii (author's transl)].
Tropenmed Parasitol. 1980 Jun;31(2):209-12.
4
Virulence of plasmodium yoelii line YM is caused by altered preference for parasitized and unparasitized immature and mature erythrocytes.
Trop Med Parasitol. 1985 Mar;36(1):43-5.
5
Hematopoietic tissue in malaria: facilitation of erythrocytic recycling by bone marrow in Plasmodium berghei-infected mice.疟疾中的造血组织:伯氏疟原虫感染小鼠的骨髓对红细胞再循环的促进作用
J Parasitol. 1983 Apr;69(2):307-18.
6
Monoclonal antibodies to a 140,000-m.w. protein on Plasmodium knowlesi merozoites inhibit their invasion of rhesus erythrocytes.针对诺氏疟原虫裂殖子上一种分子量为140,000的蛋白质的单克隆抗体可抑制其对恒河猴红细胞的侵袭。
J Immunol. 1984 Jan;132(1):438-42.
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Chloroquine resistance in malaria: variations of substrate-stimulated chloroquine accumulation.疟疾中的氯喹耐药性:底物刺激的氯喹蓄积变化
J Pharmacol Exp Ther. 1975 Dec;195(3):389-96.
8
The role of free radicals and antioxidative enzymes in erythrocytes and liver cells in the course of Plasmodium berghei and Plasmodium vinckei infection of mice.伯氏疟原虫和文氏疟原虫感染小鼠过程中自由基和抗氧化酶在红细胞及肝细胞中的作用
Acta Microbiol Immunol Hung. 1994;41(2):153-61.
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Characterization of a subpopulation of mouse red blood cells as preferential target for malarial invasion.将小鼠红细胞亚群鉴定为疟疾侵袭的优先靶点。
Electrophoresis. 1998 Jun;19(7):1215-9. doi: 10.1002/elps.1150190724.
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Iron deficiency influences the course of malaria in Plasmodium berghei infected mice.缺铁会影响感染伯氏疟原虫的小鼠的疟疾病程。
Biochem Biophys Res Commun. 2007 Jun 8;357(3):608-14. doi: 10.1016/j.bbrc.2007.03.175. Epub 2007 Apr 9.

引用本文的文献

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Rodent and nonrodent malaria parasites differ in their phospholipid metabolic pathways.啮齿类和非啮齿类疟原虫在其磷脂代谢途径上存在差异。
J Lipid Res. 2010 Jan;51(1):81-96. doi: 10.1194/jlr.M900166-JLR200.
2
Natural cytotoxicity for Plasmodium berghei in vitro by spleen cells from susceptible and resistant rats.来自易感和抗性大鼠的脾细胞对体外伯氏疟原虫的天然细胞毒性。
Immunology. 1986 Oct;59(2):277-81.
3
Pathophysiology of hypoxia in mice infected with Plasmodium berghei.感染伯氏疟原虫的小鼠低氧血症的病理生理学
Parasitol Res. 1987;73(4):298-302. doi: 10.1007/BF00531081.