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No expression of erbB2 or erbB4 was detected in mouse skin (data not shown).
There were no significant differences in collagen content between unwounded DDR2-/ and DDR2+/+ mouse skin (data not shown).
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Tumor induction data in the mouse skin initiation-promotion system were found to be consistent with a quadratic function where the coefficient of the linear term depended on the dose of the promoter.
Mouse S100A7/psoriasin was however first identified in an expression library constructed from normal mouse skin (Genbank Acc AA792680 and AY465109) and our data have confirmed mouse S100A7/psoriasin RNA expression in normal mouse skin (see Figure 2A).
Our current data from a model of mouse skin inflammation is also consistent with such a role, since a significant upregulation in mouse S100A7/psoriasin expression occurs simultaneously with the acute phase of skin inflammation after application of croton oil to the mouse tail skin.
Various response measures and statistical methods appropriate for the analysis of data collected in the SENCAR mouse skin assay are examined.
In our latest study, using hairless mice, which we irradiated with UVB light, we confirm that adiponectin level in serum and gene expression level of HAS2 of mouse skin were increased by AVGP intake (Saitou M, unpublished data, 2015).
These data indicate that there are some limitations in using mouse skin initiation/promotion experiments as the sole basis for identifying substances with carcinogenic activity.
Data in Fig. 1 clearly demonstrated that pretreatment of mouse skin with microneedles significantly increased the permeability of 5-FU through the skin.
Our data are the first in vivo evidence that EMT occurs during mouse skin development.
Collectively, the data in Fig. 7 indicate that P2X7 receptor expression levels in mouse skin cancer tissues are four-five folowerwer than in mouse normal skin tissues.
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