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Despite the lack of requirement for NOX2 for the development of pressure overload hypertrophy, it was found that NOX2 knockout mice developed less interstitial fibrosis and contractile dysfunction than wild-type littermates [ 41] indicating a dissociation between hypertrophy per se and fibrosis or contractile dysfunction.
Finally, after liver injury, GRK2-deficient mice developed less severe portal hypertension than control mice.
We recently described the accelerated induction of anti-DNA Abs in NZB/NZW mice immunized with Escherichia coli (EC) dsDNA; paradoxically these mice developed less renal disease than unimmunized mice or mice immunized with calf thymus DNA.
Mmp8−/− mice developed less fibrosis than their wildtype counterparts.
When exposed to different renal insults, the latter mice developed less severe forms of kidney disease compared to those with normal meprin levels, suggesting a potential role for meprin in the pathology of acute renal failure [31].
Precisely, while the polyp number in ApcΔ14/+FHL2+/+ could reach more than 40, the great majority of ApcΔ14/+FHL2−/− mice developed less than 9 tumors and none of the animals had more than 19 polyps (Fig. 2C).
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Additionally, HIF-1α knock-out mice develop less clinical signs of sepsis [24].
Two other studies have documented that Tlr4-deficient mice develop less renal fibrosis after UUO [23], [34].
The reduced expression of IL-18 in epididymal WAT is of special interest, since ApoE−/− IL-18−/− mice develop less atherosclerosis than control ApoE−/− mice [21].
Taken together these results show that FcRγ−/− mice develop less IgG1 and C3c deposits in the splenic vessel walls and lower IgG1 titre in the renal mesangium compared to Hg-treated wt mice.
Significantly, intact females had less severe OA than OVX females and although intact male mice showed more severe OA than intact females, orchiectomized mice develop less OA than intact males [ 26].
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