Giuliana Giribaldi

TL;DR: In this article, a systematic analysis was conducted on five different strains of P falciparum (FCR-3, KI, C10, HB3B, and T9/96) and found that there was no significant difference in either invasion or maturation when the parasites were grown in either normal or G6PD-deficient (Mediterranean variant) E.

TL;DR: The present results may offer a mechanistic explanation for depression of cellular immunity in malaria and iron released from ingested pigment is responsible for the intoxication of monocytes.

TL;DR: The data demonstrate that estrogen deficiency enhances the production of the pro-osteoclastogenetic cytokines TNFalpha and RANKL and increases the number of circulating OC precursors, and it is shown that T cells and monocytes from women with osteoporosis exhibit a higher production of TNF alpha than those from the other two groups.

TL;DR: Interestingly, a number of hereditary haemolytic disorders, known to exert a protective effect on malaria, tend to exacerbate this phenomenon leading to a more precocious and effective opsonization of diseased RBC infected by malaria parasites.

TL;DR: Changes in parasitized RBC membranes and induction of phagocytosis were similar to oxidatively damaged, senescent or thalassaemic RBC, indicating that parasite‐induced oxidative modifications of Bd3 were per se sufficient to induce and enhance phagcytosis of malaria‐parasitized R BC.