Sentence examples for mice which exhibited from inspiring English sources

Escalating morphine doses (10 40 mg/kg) administered over a 4-day period selectively induced a twofold decrease (p < 0.00005) in adenosine abundance in the brainstem of C57BL/6 mice, which exhibited symptoms of narcotic drug dependence; but did not decrease adenosine abundance in 129Sv1 mice, which do not exhibit symptoms of dependence.

Importantly, we show direct evidence from MCP-1 knockout mice, which exhibited reduced clearance of P. aeruginosa and increased pathological alterations in the lungs.

No deficits in avoidance learning were evidenced in Gpr3−/− mice, which exhibited similar performance than wild-type mice in the active avoidance paradigm.

The RVG-9r peptide elicited no adverse inflammatory or other immune response in treated mice, which exhibited no adverse side effects and appeared to tolerate the treatment very well.

A custom microarray identified a subset of miRNAs that were differentially down-regulated in livers of SHP−/− mice, which exhibited a 2-fold or greater decrease in expression (Figure 1a).

The first indication of miRNA involvement in Treg differentiation came from findings in Dicer-deficient mice, which exhibited reduced numbers of Treg cells and immune pathology such as colitis, and lung and liver inflammation [10].

Using gene microarrays, we compared gene expression patterns in the somatosensory cortex of wild type and ephrinA5 deficient mice, which exhibit subtle, but highly reproducible alterations of thalamocortical projections and intrinsic cortical circuits.

To investigate this, opiate-induced brain metabolomic responses were profiled using a semi-targeted method in C57BL/6 and 129Sv1 mice, which exhibit extreme differences in their tendency to become opiate dependent.

BDNF overexpressing mice, which exhibit a precocious development of intracortical inhibition, also show an accelerated development of visual acuity [29].

This phenotype is reminiscent of male androgen receptor knockout (ARKO) mice, which exhibits severe developmental defects and spermatogenesis arrest [42].

Further evidence for this hypothesis was recently demonstrated in AKAP12 knockout mice, which exhibit prostatic hyperplasia and focal dysplasia [26].