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In our unbiased screen for potential dopamine-independent actions of putative TAAR1 ligands on the movement control in DDD mice, we failed to detect significant effects of trace amines and major metabolites of monoamines ([12]; Table 1).
Next to the fact that we observed increased levels of this cytokine in diseased mice we failed to observe statistically significant differences across genotypes (Supplementary Figure 2C).
Finally, we would also like to stress that part of the novelty of the present paper arises from the fact that in a large cohort of 3xTg-AD mice, we failed to observe the beneficial effects of exenatide.
Interestingly, even though IL-12p70 levels were elevated in ConA-stimulated splenocytes cultures from the PPC- and DHEAS-treated mice, we failed to detect a significant enhancement of IFNγ in these cultures.
Looking at the endogenous anti-tumor responses in elderly mice, we failed to observe these effects in older 18-month-old mice (Fig. 2), suggesting these responses wane with age regardless of the CR dietary intervention.
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To explore the possibility of pituitary dysfunction as an explanation for the strain differences in hormone responsiveness, we evaluated serum levels of prolactin in control and progestin-treated mice, but we failed to observe any difference between C57BL/6 and BALB/c mice.
Metastasis was found in lung tissue collected from telomerase-proficient MMT mice, whereas we failed to detect tumor metastasis in the sections of lungs from telomerase-deficient MMT mice [ 21], suggesting that distant metastasis in MMT mice requires telomerase activity.
However, our preliminary results do not support any induction or impairment of this process either in the TPP-1-deficient cells or in the brain from 120-days-old CLN2 −/− mice, since we failed to observe any conversion of LC3-I into LC3-II, a frequently used marker of macroautophagy (results not shown).
Unlike the LPS-induced response in THP-1 cells and mouse macrophages, we failed to observe up-regulation of miRNA-146 or -155 [ 38, 39].
Thus, as expected from a known anxiogenic effect of PTX treatment [46], this tendency indicates that our PTX-treatment regimen may enhance anxiety levels in nonTg mice even though we failed to find a statistical difference between PTX- and saline- treated groups.
Though previous study examined that a high fat diet significantly accelerate atherosclerosis lesion formation in ApoE−/− mice [ 26], we failed to detect a significant increase in the number of adherent leukocytes at 6 weeks after a high-fat diet.
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