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Specifically, the mice appear generally healthy up to ∼7 month of age, at 9 10 month about 60% of the colony is symptomatic and at 12 15 month of age 100% of mice are sick (for a detailed description of this mouse model, see [31]).
When we compared the TH-MYCN mouse tumor microarray expression data to the human NB patient data (A+ quality data only as described above) classified by disease stage and restricted to MYCN amplified patients, we found high similarity between stages 3 and 4 of human disease and the mouse model (see Table 1).
Let- 7 transcript levels were not changed in either mouse model (see Additional file 8: Figure S7).
In addition, in a MNGIE mouse model (see below), mitochondrial dNTP content can be modulated by systemic administration of dCtd or THU (Cámara et al, 2014).
Selective neutralization of IL-23p19 in a humanized mouse model (see above) prevented the development of psoriasis (Tonel et al., 2010), further implicating IL-23 in the development of psoriasis lesions.
It was interesting to note a similar increase in hepatic p-CREB in P2 Smn +/−;SMN2 and P21 Smn 2B/− mice, an intermediate SMA mouse model (see Supplementary Material, Fig. S1).
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This was, in turn, reminiscent of mouse models (see Discussion).
(for the principal structure of PNs in the used mouse models see Figures 1b e).
For a pair-wise comparison between all modules identified in all mouse models, see Additional file 5: Figure S1.
APC's tumor-suppressor role has been confirmed by various mouse models (see Mouse Genome Informatics at http://www.informatics.jax.org).org
This led to the hypothesis that NCAM promotes EOC invasion, an issue that we have investigated at the cellular level as well as in mouse models (see below).
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