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It lays the foundation for using the power of mouse molecular genetics to discover the X genes that cause KS phenotypes and the Y genes that make XYY mice different from XY.
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However, unlike wild mice, different individuals from the same strain express the same protein pattern, an artifact of many generations of inbreeding.
Taken together, none of the MG abnormalities observed in MMTV-cortactin mice were different from WT FVB/N mice.
The behavioral outcomes shown in A30 mice were different from those of S30 mice, despite equivalent sweetness of the aspartame solution to that of the sucrose solution.
Taken together, the underlying mechanism for TRI-induced hepatomegaly in Pparα-null and h PPARα mice was different from that in m PPARα mice.
Moreover, the types of tumor developed in TAp73-/ mice are different from those displayed by p53-/ knockout mice.
Limitations Despite important similarities, mice are different from humans in anatomy, genetics and physiology, and thus mouse models cannot fully recapitulate human systems.
At 72 hours, the increase in inflammatory cells seen histologically in the airways of Nlrc4−/− mice is different from the bronchoalveolar lavage data that has no difference.
Interestingly, the TREome landscapes of C3H/HeJ (toll-like receptor-4 [TLR4] mutant) inbred mice were different from its control C3H/HeOuJ (TLR4 wild-type) strain.
The pattern of induction of NQO1 in the SCD mice was different from that observed for HO-1.
The kinetics of serum CK levels in mdx mice were different from that of the MYOM3 fragments during the first weeks of age.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com