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Schizogony erythrocytic

Bitonti, A. J., McCann, P. P., and Sjoerdsma, A. (1987). Plasmodium falciparum and Plasmodium berghei Effects of ornithine decarboxylase inhibitors on erythrocytic schizogony. Exp. Parasitol. 64, 237-243. [Pg.330]

Thus, the infected erythrocyte has access to host plasma lipids, predominantly from HDL. Further, the HDL, or its lipids, must be transported from the erythrocyte membrane and through the parasitophorous vacuole membrane to the developing parasite (for review see ref. 29). The importance of this for Plasmodium is illustrated by the work of Grellier et al. (30) who showed that HDL alone supports the differentiation and multiplication of the parasite. Very low density lipoproteins (VLDL), low density lipoproteins (LDL) or apolipoproteins do not support complete schizogony and... [Pg.136]

Malaria is caused by protozoan parasites of the genus Plasmodium, four species of which infect humans. P. falciparum, P. vivax, P. malariae, and P. ovale) (48,49). The disease is initiated when infective sporozoites are injected into the human host during feeding by an infected mosquito. The sporozoites enter parenchymal cells of the liver within minutes where they multiply asexually into merozoites. After development for 6-16 days, depending on the species, merozoites are released from the hepatic cells into the peripheral blood where they quickly bind to and invade erythrocytes. This initiates the cycle of erythrocytic schizogony in... [Pg.516]


See other pages where Schizogony erythrocytic is mentioned: [Pg.482]    [Pg.1145]    [Pg.294]    [Pg.559]    [Pg.613]    [Pg.294]    [Pg.50]    [Pg.84]    [Pg.85]    [Pg.148]    [Pg.278]    [Pg.266]    [Pg.267]    [Pg.781]    [Pg.233]    [Pg.234]    [Pg.235]    [Pg.236]    [Pg.267]    [Pg.444]    [Pg.97]    [Pg.225]    [Pg.253]    [Pg.1964]    [Pg.1965]   
See also in sourсe #XX -- [ Pg.55 ]




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Schizogony

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