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Healthy mice may also respond differently than critically ill patients, especially in case of injured lungs prior to the start of mechanical ventilation.
These findings suggest that the R26floxneoWnt4 mice may also be useful for Wnt4 misexpression studies in other tissues.
In addition, these mice may also exhibit defects in wound healing that heavily rely on the angionenic processes.
These data suggest that APC from pre-diabetic mice may also start to exhibit a decreased ability to maintain Foxp3 expression in vitro.
Unbiased phenotype-driven approaches in mice may also contribute to identification of genetic loci relevant to the development of the corpus callosum in humans.
The decreased immune response and lung eosinophilia observed in the ICOS+/− mice may also be caused by decreased activation of ICOS+/− T cells.
Therefore, the defect in Th2 differentiation in ICOS+/− mice may also result in decreased chemotaxis of existing Th2 cells to the site of inflammation.
In addition, impaired function of the distended alveolar macrophages in lungs of S1PL−/− mice may also have contributed to the accumulation of proteinaceous alveolar exudates.
Increased lung injury in TLR4lps-d single mutant mice may also account for increased systemic dissemination in these animals relative to lung bacterial burden.
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Getting to the Web over the telephone, rather than using a computer and having to manipulate a mouse, may also help others who are disabled, said Neal Ewers, who is blind and does research and product testing at the Trace Research and Development Center at the University of Wisconsin.
The use of a collagen-sensitive mouse may also affect the response to the graft itself.
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