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In another mouse study, in which the AT1b coding exon was replaced with the reporter gene lacZ, there was no detectable lacZ expression in kidneys and heart [ 28].
In a mouse study in which T1D is induced by streptozotocin, a Dicer deficiency in pancreatic islet cells enhanced disease severity, indicating that miRNAs expressed in islet beta cells play protective roles during T1D [ 67].
This was suggested by the mouse study, in comparison with Illumina, and the rat kidney comparison with qRT-PCR data, although fold changes of gene expression in the rat datasets were comparable with those from Illumina and Operon arrays.
Together, this wild-type mouse study in combination with the Tg2576 model and rat data, demonstrate the ability of SPI-1865 to lower both Aβ38 and Aβ42 in vivo.
There were no differences between the CK expression in the human and mouse study in the combined groups (p = 0.51), the group of very likely endogenous (p = 0.34) or the group of uncertain endogenous (p = 0.72).
Following the in vivo mouse study, in vitro studies were carried out to determine the mechanism by which AT2 receptor expression in stromal cells modifies the growth of pancreatic carcinoma cells.
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We eventually plan to merge both human and mouse studies in humanized, gnotobiotic animals that are colonized with human microbiota, taking advantage of the newly established gnotobiotic facility at Yale.
Thus, to mimic the mouse studies in humans, you may need to run a 5 – 8 year study in thousands of patients and measure clinical outcomes.
IARC had to cherry-pick the results from two mouse studies in order to make its tortured case that the animal evidence supported a conclusion of carcinogenicity.
Again, this is in line with mouse studies in which remethylation occurs in male germ cells during late gestation [ 5].
This dichotomy may overemphasize the role of IL-6 (from mouse studies) in human Th17-mediated osteoclast formation.
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