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Maternal Microchimerism Predicts Increased Infection but Decreased Disease due to Plasmodium falciparum During Early Childhood.

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TLDR
The acquisition of M Mc may result in increased malaria infection but protection from malaria disease, and future studies should be directed at the cellular component of MMc, with attention to its ability to directly or indirectly coordinate anti-malarial immune responses in the offspring.
Abstract
Background A mother's infection with placental malaria (PM) can affect her child's susceptibility to malaria, although the mechanism remains unclear The fetus acquires a small amount of maternal cells and DNA known as maternal microchimerism (MMc), and we hypothesized that PM increases MMc and that MMc alters risk of Plasmodium falciparum malaria during infancy Methods In a nested cohort from Muheza, Tanzania, we evaluated the presence and level of cord blood MMc in offspring of women with and without PM A maternal-specific polymorphism was identified for each maternal-infant pair, and MMc was assayed by quantitative polymerase chain reaction The ability of MMc to predict malaria outcomes during early childhood was evaluated in longitudinal models Results Inflammatory PM increased the detection rate of MMc among offspring of primigravidae and secundigravidae, and both noninflammatory and inflammatory PM increased the level of MMc Detectable MMc predicted increased risk of positive blood smear but, interestingly, decreased risk of symptomatic malaria and malaria hospitalization Conclusions The acquisition of MMc may result in increased malaria infection but protection from malaria disease Future studies should be directed at the cellular component of MMc, with attention to its ability to directly or indirectly coordinate anti-malarial immune responses in the offspring

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References
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Journal ArticleDOI

Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
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Akaike's Information Criterion in Generalized Estimating Equations

TL;DR: This work proposes a modification to AIC, where the likelihood is replaced by the quasi-likelihood and a proper adjustment is made for the penalty term.
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Adherence of Plasmodium falciparum to Chondroitin Sulfate A in the Human Placenta

TL;DR: Placental IRBCs adhered to sections of fresh-frozen human placenta with an anatomic distribution similar to that of naturally infected placentas, and adhesion to CSA appears to select for a subpopulation of parasites that causes maternal malaria.
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Maternal Alloantigens Promote the Development of Tolerogenic Fetal Regulatory T Cells in Utero

TL;DR: It is found that substantial numbers of maternal cells cross the placenta to reside in fetal lymph nodes, inducing the development of regulatory T cells (Tregs) that suppress fetal antimaternal immunity and persist at least until early adulthood.
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Pyrimethamine and Proguanil Resistance-Conferring Mutations in Plasmodium falciparum Dihydrofolate Reductase: Polymerase Chain Reaction Methods for Surveillance in Africa

TL;DR: Methods for collecting fingerstick blood onto filter paper strips that are air-dried, then stored and transported at room temperature and a nested PCR technique that has improved sensitivity and specificity are reported.
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