Sentence examples for rodent model system from inspiring English sources

Because of the poor infectivity of P. berghei sporozoites, we and others [11] moved from the P. berghei to the P. yoelii rodent model system, as the high infectivity of P. yoelii sporozoites in mice is thought to closely resemble the infectivity of P. falciparum and P. vivax in humans and P. knowlesi in rhesus monkeys.

In order to find out how widely is this phenomenon spread among other mammals and also to identify species which would complement the rodent model system for studying this problem, we need to analyze carefully the incidence of this phenomenon in other mammals with longer lifespan using methods allowing for analysis of the whole set of chromosomes, such as CGH.

Such tools have been developed both in Plasmodium falciparum, the main cause of human malaria, and in the rodent model system Plasmodium berghei.

Motives for this criticism are manifold and range from a very general antipathy against the rodent model system to well-founded arguments that highlight physiological variations between species.

Previous work in this laboratory developed a rodent model system that mimicked shrapnel loads seen in wounded personnel from the 1991 Persian Gulf War.

For example, gene knockouts of the conserved PIR orthologs in the more accessible rodent model system may result in important and measurable phenotypes.

Two such vaccines using rodent model systems were constructed – one with Plasmodium chabaudi and the other with P. yoelii.

Because rodent model systems that employ newborn animals to produce lethal infection are generally considered to be farther removed from the human disease being modeled [3], and because of the difficulty of working with newborn mice, we developed a new TCRV mouse infection model based on i.p. challenge of AG129 type I and type II IFN receptor-deficient mice.

Satori has identified a unique class of small molecule gamma-secretase modulators (GSMs) capable of decreasing Aβ42 levels in cellular and rodent model systems.

The main issue with commonly used rodent model systems, such as the mouse, is that the placenta is very different from that of humans, especially with regard to spiral artery modification [51,130].

In the more tractable rodent model systems, there is a strong reliance on the intracellular conversion of testosterone (T) to estradiol (E) during fetal and neonatal androgen signaling that is absent in humans and sheep.