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Thus, it appears that CHL1−/− mice manifested an ongoing hyperactive sympathetic nervous system.
Both WT and Cx3cr1 −/− mice manifested an increase in ALT and AST activity 8 weeks after cercariae infection.
Following LI, diabetic mice manifested an altered SP gradient between BM, peripheral blood and limb muscles, accompanied by a depressed recruitment of NK1R-HSPCs to the ischaemic site.
Importantly, Chop −/− mice manifested an 80% reduction for LDH activity as compared with that of WT mice, suggesting that Chop deficiency protected tubular cells undergoing UUO-induced apoptosis, thereby prevented the occurrence of secondary necrosis.
Interestingly, Cx3cr1 −/− mice manifested an opposite phenotype, in which significantly higher levels of Arg-1, a typical marker for Th2 responses, were detected, whereas iNOS expression was significantly suppressed as compared to WT control mice.
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LS- G6pc−/− mice manifested a milder pathological situation in comparison with G6pc−/− mice.
However, these mice manifested a liver phenotype typical of GSD-1a, characterized by hepatomegaly.
By contrast, Cx3cr1 −/− mice manifested a 4.8-fold reduction in iNOS expression as compared to WT mice (Fig. 4D).
Indeed, WT mice manifested a 1.5-fold higher MyD88 expression in the UUO-induced kidneys as compared with that of Chop −/− mice.
However, high levels of tubular apoptosis were characterized in WT mice upon UUO induction, and Chop −/− mice manifested a twofold reduction for tubular apoptosis.
Wild-type mice manifested a continuously increased clinical arthritis score beginning at day 31 until day 41, the last day observed, after primary immunization).
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