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In contrast, elevated MMP-9 levels in mesangial cells from Alport mice were linked to ERK pathway activation.
Furthermore, we found that the beneficial effects of H2 on brain injury in septic mice were linked to the decreased levels of inflammatory cytokines and oxidative products and the increased activities of antioxidant enzymes in serum and hippocampus.
To determine if the phenotypes in β8 −/− mice were linked to integrin control of Nrp1 protein expression, control and β8 −/− brain sections were immunolabeled with anti-Nrp1 antibodies.
To test whether metabolic phenotypes in HFD-fed mice were linked to a specific gut microbial signature, 100 4-week-old C57Bl/6 male mice were fed a diabetogenic/non-obesogenic carbohydrate-free (<1%) HFD for 3 months (figure 1A).
Elevated levels of MMP2, MMP9 and TNFα in these mice were linked to increased production of collagen types I and III by CFBs in a TGFβ-dependent manner, leading to myocardial fibrosis [ 130].
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Next, we examined the parasite load to determine if worse histopathology in CD40−/− mice was linked to inability to control the parasite.
Secondly, the present investigation further showed that olfactory preferences in humans and mice are linked to the physicochemical structure of odorants.
The 4-1BB-mediated IFN-γ inhibition selectively in spleen cells of DNA-primed and protein-boosted mice was linked to the induction of 4-1BB exclusively on CD8+ T cells of these mice upon Ag85B stimulation.
To determine if enhanced metastasis observed in the genistein-treated mice was linked to altered phosphorylation patterns, Western blot analysis was performed on tumor-derived protein lysates using an anti-phosphotyrosine antibody.
Recently, a very similar premature thymic degeneration phenotype observed in postnatal mice was linked to the dose of Foxn1 expressed by TECs resulting from expression of an altered Foxn1 allele [79].
To this effect, it was recently reported that differences in susceptibility to chronic viral-induced myocarditis between a C57Bl/6 and A.BY/SnJ mice was linked with reduced production of TNF-α and CCL5 following coxsackievirus B3 infection in a potentially TLR3-dependent manner [49].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com