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Lesions from the diabetic ApoE−/− mice showed complex plaque anatomy with cholesterol clefts whereas lesions from age-matched non-diabetic ApoE−/− mice were at an earlier (fatty streak) stage.
In our experience such mice were at most 24 h from death, and time to death of these animals was estimated on this premise.
For the 5 or 15 U/kg/wk doses, serum anti-GCase IgG signals toward either Vela- or Imig-injected mice were at background or very low levels from each bleed (not shown).
Maximum H2O2 production was verified 8 days following infection, when the levels in the lung and spleen of immunized mice were at least 3- and 4-fold higher, respectively, than those detected in the organs of control animals.
Levels of WldS protein in the brains of old WldS mice were at least as high as those found in young (2 month old) WldS mice (data not shown) [33].
The IgA levels found in the immunized mice were at least 5-fold higher than those verified in the feces of control mice during the whole 42-day period that followed the second immunization (Fig. 1A), thus indicating that a strong and persistent mucosal response production was triggered by immunization with S. enterica Typhimurium expressing VapA.
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After CsA administration, the peak brain uptake in mice was at 1.5 min and at 1.2 min in rats.
The first detected TCR expression in Rec-HY mice was at the DN4 stage of development.
The onset of Golgi fragmentation in G1del mice is at about 14 15 weeks of age [ 29].
The indicated age of mice is at the day of the terminal optical imaging experiment.
IL-12-deficient mice are at high risk of Mtb infection.
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