Sentence examples for mice were due from inspiring English sources

with EPI showed that the above stimulatory effects of this amine in both the PNMT-inhibited and home-caged mice were due to activation of α1-receptors.

To determine whether the autophagic phenotype and lethality in Spink3 mice were due to lack of pancreatic trypsin inhibitor, we conducted breeding studies with Spink3 heterozygous mice and TgN(Psti1) mice.

Given the fact that RNF13 is significantly induced in the macrophages of damaged muscles after injury, we hypothesized that the increased levels of IL-4 and IL-6 in such macrophages from RNF13-/ mice were due to the loss of RNF13 function in these macrophages.

These results suggest that the differences between transgenic (WTTg and KOTg) and non-transgenic (WT and KO) mice were due to locomotion defects rather than defects in anxiety or exploratory behavior.

This again suggests that the long-term GFP-labeled cells from the TET-GFP mice were due to a leaky background expression from the H2B-GFP strain and not the appropriate tetracycline-regulated response.

All errors made during this session were associated with responses triggered by S-, suggesthat thet the mistakes made by irradiated mice were due to an impaired memory of odors, but not of the go/no-go task procedure.

Lastly, we conducted the adoptive transfer experiment to examine whether the increased TFH cells in Cic mutant mice was due to derepression of ETV5.

This ruled out the possibility that a stronger anti-tumor effect of IR in CCR2−/− mice was due to poor tumor vasculature.

Impaired apoptosis of BMDN from iNOS KO mice was due to reduced caspase-8 activity which subsequently prevented caspase-3 and -9 activation.

Deficient mineralization of intramembranous bone in vitamin D-24-hydroxylase-ablated mice is due to elevated 1,25-dihydroxyvitamin D and not to the absence of 24,25-dihydroxyvitamin 24,25-dihydroxyvitamin

These experiments also clarified whether the enhanced efficacy of radiation on tumor regression in CCR2−/− mice was due to a congenic intrinsic development defect in trafficking and maturation of myeloid-derived cells in the knockout mouse.