Sentence examples for rodent models such from inspiring English sources

Despite some differences compared to the human pathophysiology, our knowledge of how T1D develops has benefited significantly from studies in rodent models such as the non-obese diabetic mouse (NOD)[2].

Other applications, which have been used in rodent models, such as sorting parasites by flow cytometry (Fig. 2), in vivo imaging of ookinete behavior (Supplementary Mov. 1) and ex vivo observation of sporozoite motility (Supplementary Mov. 2) traversal and invasion are now possible.

Rodent models such as drug-induced chronic hyperprolactinemia in rats (19), pituitary-transplanted rats (20), or dopamine D2 receptor-deficient mice (21) have not provided sufficient information about the reproductive consequences of these endocrine alterations.

Elevated levels of circulating gonadotropins are clearly associated with stromal tumor development based on studies using genetically engineered rodent models such as the inhibin-α knockout, estrogen receptor-α knockout, and transgenic animals that over-express LH-β.

Transgenic mutation reporter rodent models, such as Muta™Mouse [ 1], enable the detection of spontaneous and induced mutations in vivo (reviewed in ref. [ 2]) and the identification of chemical mutagens.

Furthermore, these results were consistent with the findings of other previous reports on DPP-4 inhibitors in various rodent models such as db/db mice and streptozocin-induced diabetic rats.

In vivo transgenic rodent models incorporating such mechanisms are used to identify mechanisms involved in tumor formation and as selective tests for carcinogens.

However, the currently used rodent tumor models, such as the subcutaneous (ectopic) tumor graft models in nude mice, do not sufficiently represent clinical cancer, particularly with regard to metastasis formation, since the subcutaneous micro-environment for visceral tumors is considerably different from their original environment [1, 2].

It may be important to assess and compare the relevance of the current guinea pig model with that of other rodent CS models such as the mouse.

Given the reduced number of Pfmc-2TM gene family members in rodent malaria parasites compared to P. falciparum and the more tractable rodent model system, such studies should now be feasible.

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].