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Our results revealed that C58/J mice display elevated activity levels by postnatal day 6, which persist into adulthood.
Cells derived from mice lacking telomerase RNA component (mTERC−/− mice) display elevated telomere-mediated chromosome instability.
Therefore, FcγRIIB−/− mice display elevated Ig levels and enhanced immune complex-mediated tissue injury in response to Ag challenge [33].
Recently it was shown that miR-375 knockout mice display elevated plasma glucose levels due to a small reduction in beta cell mass with a concomitant increase in the number of alpha cells per islet as well as increased circulating glucagon [12].
RenTg mice display elevated systolic blood pressure as early as 2 month old (146±8 compared to 110±4 mm Hg for age matched wild type, p<0.01); at the age of 3 month they show slightly increased albuminuria (18.3±3.5 vs 1.5±0.1 g/mol creat, p<0.01).
NET knockout mice display elevated cardiac NE, hypertension and tachycardia [ 44].
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The citalopram-treated male mice displayed elevated anxiety-like behavior in an open field test and lower locomotor activity in their home cage during the subjective night.
Since Cdk5 KO mice displayed elevated neuronal excitability and susceptibility to seizures, we examined the levels of p25 in Cdk5 KO mice.
Both KO→KO and WT→KO mice displayed elevated G-CSF serum levels, most likely due to the fact that their LECs were capable of producing large amounts of this cytokine (Figures 7A and 7B).
Indeed, as expected iNOS+/+ LPS treated mice displayed elevated basal glycemia (Figure 2C) and a reduced glucose infusion rate compared to saline treated controls (Figure 2D and E) during the hyperinsulinemic-euglycemic clamp (HIEC).
In addition, young Lepr db/db mice displayed elevated fasting glucose and impaired glucose tolerance.
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