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Given that B. burgdorferi numbers are lower in the Nod2 deficient mice, this did not seem like a likely explanation for the results in our model.
While levels of p40 and p19 tended to be lower in pDCs from naïve C3H mice compared to those from A/J mice, this did not reach statistical significance (Figure S3).
Although there was a trend towards decreased memory at 1-day in these mice, this did not reach statistical significance (p = 0.1 with n = 13 wild-type; n = 11 mutant).
Although TNFα stimulation increased leukocyte rolling in wild-type mice, this did not reach significance.
As in mice, this did not result from the decreased fitness of V-073-resistant virus.
Although the correlations eventually reached stable CT levels in KO mice, this did not occur until the next day.
Similar(47)
Similar to Cav1.3 deficiency in mice, this does not cause unwanted central nervous system side effects in treated individuals.
Furthermore, the mechanical ventilation-induced increase in pulmonary IL-1β levels was less pronounced in anti-KC-treated mice compared with untreated mice, although this did not reach statistical significance (Figure 3).
The infarct volume in bmf-deficient mice was 27.9±1.8% compared with 35.9±5.2% in WT mice; however, this did not reach the level of statistical significance.
The production of IL-13 was also consistently increased in treated mice, although this did not reach statistical significance.
Thus, hAFSC do stimulate a modest tissue reaction by nu/nu mice, but this did not cause any measurable perturbation of kidney function.
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