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We operationally use the term 'anxiety' to describe the increase in percent time spent in a dark closed arm of the EPM, although the actual mood state of the mouse cannot be directly determined.

However, since adipocytes in the mouse cannot be detected histologically until after birth, their appearance coinciding with the onset of nursing underscores the fact that the development of adipose tissue in each animal occurs at the onset of a dynamically variable nutritional environment for each individual.

This is illustrated by a recent study reporting that for approximately 13% of human RefSeq annotated genes, an equivalent splicing isoform in mouse cannot be identified (Zambelli et al. 2010).

Since all experimental mice had similar levels of serum VP6-specific IgG and IgA (data not shown) before the challenge, the failure in protection of the particular mouse cannot be explained with the pre-existing antibody levels.

The importance of this mouse cannot be emphasized enough, because it was the first genetically induced mouse model that faithfully recapitulated neuropathological and biochemical aspects of nGD, paving the way for investigation of basic pathogenic mechanisms and potential treatments.

The relative delay of GH signalling in the mouse makes it a useful model in which to study GH and IGF signalling independently, because any growth effects observed in late gestation and early post-natal development in the mouse cannot be a consequence of an impaired GH pathway.

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The gene-altering approach used on the mice cannot be tried in people, but now that senescent cells appear to be harmful, researchers can devise ways of targeting them.

However, these mice cannot be used to study adaptive immune responses and therefore a more relevant animal model is needed to assist in vaccine development.

However, our experiments with the H1-receptor antagonist d-chlorpheniramine and the H2-receptor antagonist famotidine indicate that the lessening of sepsis-induced organ injury observed in HDC−/− mice cannot be solely attributed to alterations in proinflammatory and chemotactic cytokine production.

Although results from mice cannot be extrapolated directly to humans, says Jerry Shay of the University of Texas Southwestern Medical Center in Dallas, the mice "really do show that telomere erosion can lead to things we see in [elderly] humans".

Nevertheless, although mice cannot be considered as perfect surrogates for humans, they can be used to test hypotheses in a relatively simple controlled system [6], [15], [16].

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