Sentence examples for mice led us from inspiring English sources

The uncertain homology of teeth between WT and mutant mice led us to adopt a nomenclature using Tx and Tx where T and x respectively symbolize the tooth and its rank within the row (e.g. T1 for the first upper cheek tooth, T1 for the first lower cheek tooth).

Studies of TrkB mutant mice led us to hypothesize that signaling through a specific phospholipase (PLC), PLCγ1, promoted development of kindling.To test this hypothesis, we examined the development of kindling in PLCγ1 heterozygous mice.

The decreased tumor weight observed in diclofenac treated mice led us to examine proliferation and apoptosis of tumor cells.

The unexpected result of abnormal mammary gland morphology and increased neovascularization in Hpse-KO mice led us to search for a possible explanation for this phenotype.

Attenuation of bone density in TH mice led us to examine the expression levels of osteoblast- and osteoclast-mediated gene markers in bone marrow cells.

The change in color of WAT towards a more brownish appearance together with the increase in size of mitochondria from HFD-fed HSL null mice, led us to hypothesize that WAT of HSL null mice had attained BAT characteristics.

The results of our in vitro experiments with HBMECs, as well as in vivo findings in mice lead us to conclude that InhA invades the endothelial cells, degrades the TJ protein ZO-1, and thus contributes to hemorrhage in the CNS.

Our experience in the mating of the LRP1 loxp mice to APPswe/PS1dE9 mice leads us to believe that there may be some more complex interaction between PS1dE9 and RAP/LRP1 that reduces viability.

The prominent degenerative changes in the inferior retina of some Crb1 rd8/rd8 mice lead us to further investigate an association between photoreceptor death and Müller and microglia activation (Fig.  5).

Our unexpected discovery of a vascular phenotype in the CUL3WT/Δ403 459 mice leads us to speculate that their hypertension may not be driven by salt retention in the DCT alone.

The finding that a proportion of mice developed neurological deficits following oral infection with S. Typhimurium and that these mice had a significantly greater bacterial load in the brain compared to non-affected mice lead us to test whether mice developed meningitis following infection.