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In contrast, the mean bone volume of CIA mice increased only 13.5%.
In contrast, during the same period the mean bone density of femurs in CIA mice increased only 15.8%.
In contrast, the mean bone density of the humerus bones in the CIA mice increased only 20.9% between weeks 0 and 9; however significant difference was observed only at week 7. Finally, the mean bone density of tibia bones from control mice increased by 25.1%.
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Three hours after re-feeding, the insulin levels of normal animals rose by nearly 30 times whereas the rise in SirT1-null mice was increased only 10 fold (Figure 3D).
The current study clearly demonstrates that leukocyte adhesion per se is not responsible for the observed permeability increase, since despite equal number of adherent cells in the wild-type and Mac-1 deficient mice, permeability increased only in the wild-type group at early time points (30 min after MIP-2 addition to the superfusate, Figure 1C).
Pdss2 kd/kd mice significantly increased only the kidney total CoQ9 content.
Conversely, anti-MUC1 IgG titers in MUC1Kras mice significantly increased only after 32 weeks, when IgM titers decreased, reflecting an IgM-to-IgG isotype switch (see figure 6 in Budiu et al., 2009).
In wt mice, capillary density increased only in the infiltrated area, whereas it remained similar to non ischemic tissue in the preserved area and decreased in the necrotic non-infiltrated area (fig. 4E).
Finally, picnotic cells in EAE mice were significantly increased only at 20 dpi (1.12 ± 0.5%), compared with HC (0.3 ± 0.06%, P ≤ 0.05) (Fig. 2G).
Furthermore, when muscle fibre CSA was analyzed from days 10 21 post injury we observed that captopril treatment significantly impaired muscle growth as control animals demonstrated an 81% increase in CSA while captopril treated mice increased by only 27% (Figure 1C).
The expression of cyclin E in skin of mice treated with vehicle increased only at day 6.
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