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Using mouse models, studies also showed that nicotine stimulated angiogenesis in the settings of inflammation, ischemia, atherosclerosis and tumor growth [9] [11].
Using both zebrafish and mouse models, studies have shown that mutation alone is not sufficient to confer stability to the protein in the absence of stress.
In support of this hypothesis, mouse models studies have repeatedly suggested that GBM can originate from transformed neural stem/precursor cells [ 2- 4].
Despite that, we were able to prove positive association between H. pylori and colorectal polyps consistent with the colon cancer mouse models studies [ 58].
There was a suggestion that the combination of aspirin and statin was associated with a lower incidence of CRC, and in vitro cell line and mouse models studies would support a beneficial interaction between statins and cyclo-oxygenase inhibitors [ 14, 40- 43].
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In the mouse models studied here, we found that the majority of bacilli were indeed intracellular within macrophages through most of the infection.
Here we report that all circadian gene-mutant mouse models studied are cancer-prone and that hyperplastic growth of Per-mutant somatic cells is dependent upon extracellular mitogens.
For instance, several mouse models studying Lactobacillus species of probiotics have demonstrated dampening of allergic lung responses [29], [30], [31], [32].
Although these are two artificial mouse models, studying their phenotype enhanced our understanding of the biology of IGF1 in tissues.
In particular, of the mouse models studied, the expression signature of the C3(1)Tag GEM model appears to most closely correlate to the human basal-like subtype [ 8].
Thus, despite the apparent lack of gross FA symptoms in mouse models, studying them has allowed us to learn a great deal about the pathology of FA.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com