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As the middle section was repeatedly the most inflamed section in all mice we only analyzed this portion in later experiments and data is shown only for this section.

Interestingly, as was suggested by the measurement of variance in gene expression levels in high and low freezing mice, we only saw significant changes in the separation of log-normal gene expression distributions in the hippocampus and not in the amygdala.

In young mice, we only observed a mild increase in red cell distribution width (RDW), also called anisocytosis, which might indicate alterations in RBC production or turnover (Table  1).

Because HR and HRV were highly variable between sleeping and awake states in mice, we only analyzed ECG data from the resting state for baseline activity in a 1 min base.

Fourth, given that there were no significant changes in ERα in aged wild-type mice, we only examined the correlation of tau phosphorylation with ERβ and did not observe similar positive correlation of ERβ with Tau1 (Fig. S1d).

Similar(55)

For both ER and GR mapping in mouse, we only considered transcripts with σ>0.15 (median within-strain σ for ER mapping and between-strain σ for GR mapping), since probes with little or no variability across all samples are unlikely to show large differences in variability between subsets of samples.

When examining imprinted gene expression in each species separately (human and mouse), we only used genes that had a confirmed imprinting status (i.e., those that are marked with a tick in an additional table [see Additional file 1]) that were present on the respective expression array (that is, GNF1M for mouse and HG-U133A for human).

Although we find differentiation of proximal epithelium is also affected in lungs of Creb1−/− mice, we detected only sparse activation of Creb1 in these cells.

As an important target of ASA was removed in these mice we can only speculate that the "off target" effects of ASA we have observed are those that mediate the mortality in response to infection.

Conversely, in LSK-EVAi transplanted mice we observed only a partial reappearance of 3-D thymic architecture and modest keratin redistribution (Fig. 4B), with a few lymphocytes repopulating thymus (Fig. 4A).

Although forebrain weight data are now available for both the original "Taylor" BXD mice and the "Williams" BXD mice, we focus only on the "Taylor" BXD mice.

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