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The absence of a resetting phenotype in Prkg1 mutant mice might also be explained by species-specific differences.
Therefore, Pol β Tg mice might also be suitable models for duodenal carcinogenicity following treatment with appropriate carcinogens.
Therefore, the reduced expressions of MBP and MAG in Olig1−/− mice might also contribute to the delayed onset of EAE.
To assess whether p23-ST1 mightmight also have urinary problems in both the frequency and volume of urine produced, the urination frequency and the amount of void urine were evaluated under mild stress (detailed in Materials and Methods).
The relative increase of adiponectin that we detected in Nscl-2 mice might also contribute to improved insulin signalling in non-adipose tissue and to normal serum glucose levels in vivo.
Positive results from the CD treatment study in NPC1 disease led us to hypothesize that Npc2−/− mice might also benefit from treatment, as NPC2 disease is similarly characterized by cholesterol and GSL accumulation and the two NPC proteins may function in the same metabolic pathway [9], [10].
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The discrepancy of DNA methylation profile between human and mouse might also suggest an evolutionary role.
The distinct phenotype of the Enpp1−/− mouse might also directly influence the metabolic parameters observed in the present study.
As found in the human [ 52], the segmental duplication regions in the mouse might also be "hot spots" for the occurrence of non-allelic homologous recombination, leading to genomic mutations such as deletion, duplication, inversion or translocation [ 53- 55].
This raises an intriguing question, i.e. whether the femoral artery enlargement in Hoxc11 −/− mice might conceptually also be viewed as a homeotic transformation, in this case from distal vessel of smaller size towards a larger more proximal vessel; addressing this will be the focus of future studies.
The low neuronal differentiation rates observed in ephrin-B3−/− mice might, however, also be in part due to the limited observation period of 4 weeks with a maximum age of newborn cells of 20 days due to the BrdU-labeling protocol.
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