Sentence examples for mice demonstrated normal from inspiring English sources
Rtn4r-deficient mice demonstrated normal neurological signs and normal pain threshold levels using the hot plate assay (data not shown).
In addition, compound Pkd1+/Δ Kif3a+/Δ heterozygous mice demonstrated normal expression of the osteoblastic, adipocytic and osteoclastic transcripts in whole bone (Table 1).
In the sociability test, both SCR mice and WT mice demonstrated normal sociability [Table S2; time spent around cage, with stranger vs. empty; WT: p = 0.315, SCR : p = 0.497, paired t-test].
However, assessment of urinary GC metabolites in LKO mice demonstrated normal values.
Wild-type mice demonstrated normal intramembranous and endochondral ossification with mineral deposition in the secondary palate (Fig. 4A).
For the three JQ1-treated males that had not yet sired offspring, these mice demonstrated normal mating behavior as evident by the presence of copulation plugs.
In contrast, wild-type mice demonstrate normal limb posture when suspended by their tails.
It has been consistently shown that PI3 kinase is necessary for insulin-stimulated but not for contraction-stimulated glucose uptake, 24– 27 while Akt2 knockout mice demonstrate normal basal and contraction-stimulated glucose uptake.
We generated mice in which the two Atm phosphorylation sites in the Smc1 protein are mutated; cells from these mice demonstrate normal ATM activation, normal phosphorylation of both Nbs1 and Brca1 after IR, and normal migration of these proteins to DNA breaks [ 3].
Although NMDAR function was disrupted in virtually all DA neurons in our NR1DATCre transgenic mice, these animals demonstrated normal sensitization to repeated cocaine treatments in both, the home cage and a novel environment.
Although T cells from PI3Kγ-deficient mice have been reported to be defective in proliferation and cytokine production 8– 10, other studies with independently generated PI3Kγ-deficient mice demonstrated a normal T-cell proliferative response 11, 12.
