Power from adolescent THC or vehicle-treated mice were compared using MWU tests (significant P<0.05).
Wild-type (WT) mice were compared with knockout (KO) mice lacking neuronal nitric oxide synthase (nNOS) or endothelial (eNOS).
But their brains were simply not able to detect it.The mice were compared with normal males in tests of masculinity.
Tissue accumulation of PS-MPs, biomarker responses and relative contents of serum metabolites in exposed mice were compared with control ones by one-way ANOVA and post-hoc comparison (Bonferroni) was used to discriminate between mean values.
When adenomas of age-matched, 120 days old ApcMin mice were compared, the Ap4-deficient mice showed a ~5-fold decrease in the number of adenomas, whereas the size of the adenomas was not affected (Fig. 2a-c).
Furthermore, IgE antibodies in the sera of patients with peanut allergy and mice were compared for antibody binding to Ara h 2 isoforms and allergenic epitopes.
Because reelin and prestin genes are located close together on mouse chromosome 5, reelin homozygous mutant mice were compared with littermate controls.
Cerebral [11C]flumazenil concentrations in WT and Mdr1a/1b dKO mice were compared (genetic disruption model).
To compare the kidney-specific differences in the function of these adaptor proteins, NHERF-1 and NHERF-2 null mice were compared with wild-type control mice.
Biopsy and whole gland specimens from acutely infected BALB/c mice and latently infected, immunosuppressed BALB/c mice were compared for active murine CMV infection.
The retinas of wild-type (WT), CX3CR1 null (CX3CR1gfp/gfp, KO), and heterozygous (CX3CR1+/gfp, Het) mice were compared in the presence and absence of streptozotocin (STZ -induced diabeteSTZ -induced
