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Chronic stress did not cause any hippocampal damage in doubleridge mice, which instead responded to stress with a dendritic remodelling similar to that observed in normal mice during the recovery phase after stress.
This was not observed to the same extent in adipocytes from HSL null mice, which instead exhibited an even greater size heterogeneity than that observed on the normal diet, with a markedly reduced median cell area compared to wildtype mice (3143±127 µm2) (Figure 4A, panel IV) (Figure 4B).
On the contrary their number was dramatically reduced to 20 cells/mm in IL-10−/− mice, which instead presented a dense peribronchial inflammatory infiltrate containing numerous polymorphonuclear cells.
Similarly, on the genetic background of diabetes-prone NOD mice, diabetes spontaneously developed in +/+, at a lesser incidence in skg/+, but not in skg/skg mice, which instead succumbed to arthritis.
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Therefore, the chymotrypsin-like activity in wild type cells (which contain LMP7) can only be blocked with ONX 0914, whereas in LMP7-deficient mice which incorporate β5c instead of LMP7 into immunoproteasomes, this activity can be inhibited by the β5c-specific inhibitor PR-825.
Analysis on CD4+T cells isolated from CNS revealed drastically decreased amounts of IL-17 producing CD4+T cells in wild-type (WT) EAE mice receiving the Lacto-mix which instead showed a significant upregulation of IL-10 producing CD4+T cells (Fig. 4B and C).
No such effect was obtained by treating both Surf1 −/− and Cox15 −/− mice with the pan-PPAR agonist bezafibrate, which instead showed adverse effects in either model.
Since the function of Ripply3, a gene we found to be both upregulated by Insm1 and enriched in Insm1/ Pdx1-HI cell populations, had not been previously explored in pancreas, we analyzed mouse pancreatic tissues from Ripply3 β-Gal mice, which express β-galactosidase instead of Ripply3 (Okubo et al., 2011).
To clarify these issues, we used SOD1H46R mice, which exhibit a widespread axonal degeneration with slowly progressive motor neuron degeneration in the spinal cord [31] instead of SOD1G93A mice, and generated SOD1H46R mice on an Als2-null background.
They have been tested on mice, which are also vertebrates.
"The study subjects were mice, which are herbivores.
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