Summary
In this study we have modified a micro Plasmodium falciparum in vitro growth inhibition assay to allow dissection of growth inhibition induced by test sera into two categories: inhibition of intracellular schizont growth and inhibition of uptake of merozoites into a second cohort of erythrocytes. This was achieved using morphology‐controlled synchronised cultures with incubation times restricted to cover either ring to schizont development or schizont to ring development. Sera tested were obtained from a large prospective study of healthy residents of Madang, Papua New Guinea, who were carefully documented with respect to presence of malarial parasites in the blood, spleen size, age, sex and history of fever. In the ring to schizont assay sera from all the children tested inhibited parasitic growth by at least 20%, compared to only 10 of 39 adults tested (P < 0.0005). In the schizont to ring assay 20 of 39 adult sera tested inhibited the uptake of 14C‐isoleucine into P. falciparum protein compared to 3 of the 15 children's sera tested (P < 0.01). These results are interpreted as reflecting a switch from non‐specific mechanisms of resistance with increasing age.
Culture adapted isolates of P. falciparum had different growth patterns (P less than 0.01) when cultured in the presence of sera obtained from 31 healthy Papua New Guinea residents. Both enhancement and suppression of growth was observed. Less variation was observed using an indirect immunofluorescent antibody method directed against schizont antigens, and no correlation between the two assays was found. This bioassay is assessed as a basis for serotyping P. falciparum strains.
Summary. P. falciparum malaria was cullured in vitro in the presence of sera from patients wiili cerebral malaria, nieningiiis and also after choloroqiiinc administration. inira-erythrcKytic parasite damage was seen by lighi and eleciron mitroscopy. The signiricance of the results is discussed wiih relevance to non-specific immune mechanisms, and ihe damage itiduced by these mechanisms compared wiih that from chloroquine.
Experiments were conducted to determine the sensitivity of Quackenbush strain (QS) mice to the foetotoxic effects of single subcutaneous injections of CdClz (2, 4 and 8 mg of cadmium per kilogram body weight) on days 1, 2, 4 or 8 of pregnancy. Autopsies performed on day 16 of pregnancy revealed that cadmium was teratogenic and increased the incidence of malformed forelimbs and exencephaly and decreased foetal weight. The metal caused foetal weight changes and exencephaly only when it was administered on day 8 of pregnancy indicating that the post-implantation stage presents the QS mouse with a period of increased sensitivity to the foetotoxic effects of cadmium.Although injections of cadmium (8 mg per kilogram body weight) during early pseudopregnancy did not prevent the uterus from undergoing a decidual reaction in response to a peanut oil stimulus, they did in some cases prevent alkaline phosphatase from reaching maximal activity levels in decidualized uterine horns. Thus, inhibition of alkaline phosphatase occurred only in response to the metal injected on day 4 of pseudopregnancy and the enzyme was not affected when cadmium was administered on days 1,2, 3, 5 or 6 of pseudopregnancy.The results suggested that changes in either progesterone and oestrogen production by the ovary or the alkaline phosphatase activity of the uterus are unlikely to be responsible to any great extent for the teratogenic effects of single subcutaneous injections of cadmium in the QS mouse during early pregnancy.
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