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The mutant mice also appear to have weaker memories of scary encounters than normal mice do.
DBA mice also appear susceptible to increased body weight when provided a HF diet.
The differences between the immune response in humans and mice also appear to apply to the downstream effectors of IFN-γ, NOS2 and IRG.
The different responses to CWD in Tg mice also appear to recapitulate aspects of CWD pathogenesis in the natural hosts.
The OHCs of P4 Ptprq-CAT-KO homozygous mice also appear to exhibit delayed differentiation, similar to diminuendo heterozygotes but with a greater delay (Fig. 3).
CLOCK-deficient mice also appear to differ, phenotypically, from Clock Δ19/ Δ mutant mice, which have an intronic splice site point mutation in the Clock gene that leads to exclusion of exon 19 from the transcript.
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Interestingly, female mice also appeared to respond better to AV.RSV.MCAT treatment.
Male mice also appeared to die over a greater time span (Figure 3D).
Protected mice also appeared to have increased CD8+ T cells in lung granulomatous regions at day 7 post-secondary challenge (Figure 7E) compared to non-protected mice (Figure 7B).
Hence the deleterious effect of CCBs in Marfan mice also appears to be AT1R-dependent.
The UR-KD mice also appeared healthy throughout the study, but displayed oily fur and stool discoloration (yellowish).
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