Sentence examples for mouse malaria models from inspiring English sources

Immunization with genetically engineered, attenuated malaria parasites (GAP) that arrest during liver infection confers sterile protection in mouse malaria models.

Mouse malaria models have clear advantages for the study of PAM pathology due to the relative short gestational period that allows a reasonable experimental time frame and to the availability of a wide variety of immunological and genetic tools.

We have previously reported the new formulation of polyethylimine (PEI) with gamma polyglutamic acid (γ-PGA) nanoparticle (NP) to have provided Plasmodium yoelii merozoite surface protein-1 (PyMSP-1) plasmid DNA vaccine with enhanced protective cellular and humoral immunity in the lethal mouse malaria model.

Recently, uric acid derived from hypoxanthine accumulated by the parasite was described as a source of inflammation in Plasmodium yoelii, a mouse malaria model [7].

Whole-blood CQ levels, at least in mice malaria models, could be affected by differences in hematocrit and parasitemia, both of which can vary significantly depending on parasite species, initial inoculum load and day postinfection.

To study the feasibility of this strategy, mice malaria models were used to demonstrate that high doses of CQ also triggered DV permeabilization in vivo and reduced reinvasion efficiency.

With a good model of mouse malaria (one that has been derived from, calibrated and validated with data) we can replicate this experiment in silico with the aim of predicting what kinds of malaria parasites (e.g. those that undergo rapid antigen switching, replicate at higher rates or infect RBCs at faster rates) have an advantage in immunized hosts.

To test the possibility of using murine malaria models, P. berghei and P. yoelii susceptibility to DV permeabilization was assayed using infected blood from hyperparasitemic mice (above 20% parasitemia).

In the causal prophylactic rodent malaria model, mice are intravenously infected with P. berghei sporozoites that target the liver.

Direct experimental evidence of crowding cannot be ethically obtained from human infections, but in the rodent malaria model Plasmodium chabaudi in laboratory mice, we and others have experimentally demonstrated that strong crowding effects occur.

Recently, a series of elegant experiments based on mice made tolerant to the CSP of P. yoelii, another rodent malaria model [25] led to deduce an immunodominant protective role for CSP, an interpretation that contradicts the conclusions reported here.