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The results of their study suggested that the spontaneous and persistent coughs observed in Ttll1-KO mice were related to the post-nasal drips that probably activated the pharyngeal and/or laryngeal rapidly adapting receptors in these mice.

These findings in MyMRKO mice were related with low macrophage recruitment to vascular wall and lower gene expression in situ of Rantes and Tnfα, compared with litter mate mice [ 93].

Interestingly, many genes that were differentially expressed in MyD88 KO mice were related to apoptosis, which may be due, in part, to the inability to trigger NF-κB (nuclear factor κB) activation, a well known survival signal (Van Antwerp et al., 1996; Li et al., 1999).

To determine if the effects in the Faah−/− mice were related to a correction in the baseline alterations in the proportion of NPCs within the SGZ converting into neurons or astroglia in the GFAP/Gp120//Faah−/− mice, we performed analysis on brain sections double labeled for BrdU and GFAP.

Indeed, the results show that down-regulated genes unique to macrophages derived from resistant mice were related among others to MAPK signaling pathways whereas a set of up-regulated genes were involved in the mTOR signaling pathway, Erbb and Insulin signaling pathways (Additional file 2: Table S2).

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Another possibility is that the skewing of the sexes in Alkbh1−/− mice is related to autosomal sex-ratio distortion.

The cleavage of γ-crystallin in connexin α3 knockout mice is related to the activation of calpain 3 (or Lp82 protease) [17].

The very limited remyelinatin in MOG 35 55 EAE C57BL/6 mice is related to the extensive axonal injury in this specific model.

Here we explore whether the severity of C. burnetii infection in mice is related to differences in male and female gene expression profiles.

To determine if altered number of Tregs in p110δD910A mice is related to their lower expression of CD38, we compared the proportions of Tregs in the thymus and spleen of WT, CD38+/−, CD38−/− and p110δD910A mice (Fig 4A and 4B).

It is possible that changes observed in the leptin-treated mice are related to the overall hormonal changes elicited by the administration of leptin rather than due to the direct effects of leptin on muscle mass.

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