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In control DEREG/Krt76+/+ mice, the increase in lymph node Tregs following DT treatment was not statistically significant (Fig. 8d).
The basicity of the 2′-amine was found to be well correlated to acute toxicity data in mice: the increase in the basicity is associated with the toxicity increase.
In WT mice, the increase in viscosity elicited a vasodilation of ∼20% in the absence of NO- and cyclooxygenase inhibitors (Fig. 5A).
Given the trend of more fat accumulation in our Fto knockout mice, the increase in the energy expenditure seemed overwhelmed by the increase in food intake.
Of note, in this group of mice, the increase in tau phosphorylation at AT8 was again greater than that observed at PHF-1 and CP13.
In TLR2/4-/ mice, the increase in the E. coli numbers was also strongly alleviated, if compared to wt mice (P<0.001), and these mice displayed only an approximately 10-fold rise in E. coli after colitis induction (Figure 5A).
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In tg mice, the increased activity was dramatically extended, especially following the extensive stress.
In β3-null mice the increased Rac1-1 activity likely results in changes in downstream signaling that confer the enhanced angiogenic responses.
Notably, in Cln1 −/− mice the increased serpina1‐mRNA levels were appreciable as early as 1 month of age.
This conclusion is confirmed by the fact that in the obese WT mice, the increased superoxide generation is abolished by the eNOS inhibitor L-NAME.
Even though this resulted in a comparable ratio of β/ α-MHC between the WT and OPN−/−-mice, the increase in metabolic turnover in OPN−/−-mice may represent an additional burden under ischemic stress.
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