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However, further analysis of the data indicated that there was not a relationship between deer mouse body mass (a proxy for age) and species diversity, thus, differential survival seems less likely than differential dispersal (LMM, estimate = 0.88, Z = 1.09, P = 0.27).
Also, we performed a whole-genome scan analysis on mouse body mass index (BMI) aiming at revealing potential consequences when existing imprinting effects are ignored in genetic analysis.
There was a small increase in casted and SKF 81297 treated wild type mouse body mass compared to uncasted and casted vehicle treated wild type mice.
Hence, mouse body mass index (BMI, defined as body weight divided by the square of tailless body length), considered to be a good indicator of obesity status, was chosen as the target trait in this analysis.
There was a small increase in casted and SKF 81297 treated wild type mouse body mass compared to casted vehicle treated wild type mice with casted vehicle treated wild type mice having a small decrease in body mass compared to uncasted vehicle treated wild type mice.
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This greater O3-induced AHR was not the result of greater obesity in the Cpe fat/ TNFR2 –/– mice: Body mass was the same in the two groups.
Figure 8b shows that mice body masses did not change during the experiment, suggesting that the treatments did not produce any apparent toxicity.
69 As observed in ob/ob mice, lean body mass was increased in TNP-470-treated mice compared to control mice as a result of a decrease in total body fat.
Exposure to an HFD resulted in WT and BACE1 −/− mice gaining body mass, although the BACE1 −/− mice remained leaner throughout the HFD period.
No apparent form of toxicity in vivo, such as mice death, body mass changes, or other apparent toxicity-related features, was observed in mice treated with GEM+SR1.
In WT mice, increased body mass resulted in increased (+ 33%) vertebral cancellous bone volume/tissue volume.
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