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But Dr. Vijg noted that since the drug did not extend the maximum life span of fat mice, it would be surprising if it did so with lean mice.
Although the process might be good enough in mice, it would have limited use in humans, who have much thicker skin.
And presumably, if it's there in mice it would also be present in humans at least it's likely to be, given what researchers have seen in humans consuming sweeteners.
If there was in fact less myelination in these mice, it would be logical to expect that they should be more susceptible to EAE induction.
Therefore, even if there was an alternative acceptor splice site in mice, it would not result in a translated CXCR3-B splice variant similar the one proposed in humans.
Based on these data and on the early expression of endogenous ICAM-1 in the SG of mice, it would be interesting to study sICAM-1/Fc delivery at an earlier age than 8 weeks.
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And even if the mouse made it to a human mouse it would still have a mouse-brain offspring".
The screen is simply too small, and there's no mouse - it would surely drive me mad within hours.
The authors say there is 95% sequence homology between human and mouse, it would be interesting to see how conserved the sequence the antibody was raised against is.
In particular we investigated whether this manipulation of OSVZ progenitors might promote additional cortical folding or rather, similar to mouse, it would only expand cortical surface area without additional gyrification.
Although our studies are undertaken in an adult mouse it would be of interest to examine an older group and extend evaluation beyond 105 days noting that human disease progression is age-dependent [ 3, 4].
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