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To counter this criticism, Tyl (2009) presented a table (her Table 2) of mouse prostate weights from other laboratories.
Mean control mouse prostate weights by lobe and age in our studies are presented in Table 1.
Adult control prostate weights in our reproductive toxicity studies with E2 (Tyl et al. 2008a, 2008b) and BPA (Tyl et al. 2008c) (Table 1) are well within the weight range of other published studies (Table 2), and, as expected, our mouse prostate weights increased with increasing age.
We found no BPA effects on mouse prostate weights at any dietary dose, from 3 μg/kg/day to 600 mg/kg/day, whereas vom Saal and colleagues reported increased prostate weights at 2 and 20 μg/kg/day BPA, administered on gestational days 11 17 (Nagel et al. 1997).
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Possible reasons for the non-reproducibility of vom Saal's study are the small numbers of only seven mice per dose groups and the lack of control of the confounding effect of dominant versus subservient mice on prostate weights during group housing (Table 2, criticism 2).
Table 2 shows mean mouse whole-prostate weights of mice of various ages reported by others.
The ability of high ω-3 diet to slow promotion of tumorigenesis in our mouse model was also observed as less GU and prostate weights in mice that consumed high ω-3 diet.
vom Saal's CF-1 mice did not exhibit increased prostate weights with age, likely because of his postwean caging regimen.
In contrast to prostate weights of older mice (2m and 4 5m), prostate weights of young PSA-Cre Pten-loxP/loxP mice (4–5w) were not different from control littermates (Figure 2A).
Furthermore, we found G-1 to have little or no effects (weight and histology) on mouse prostate and on growth-quiescent immortalized benign prostatic epithelial cells in cultures.
However, prostate weights in castrated mice treated with testosterone plus DFMO were significantly lower than those of intact controls.
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