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Because cadmium levels used in experimental models are much higher than exposure in the U.S. general population, the relevance of these mechanisms to human hypertension is uncertain.
Application to preparations of reduced thickness (e.g., tissue slices) may hold interesting potential because these experimental models are more representative of in situ structure and function and are less photosensitive than monolayers or cells.
A few experimental models were brought out in France under the name of Matford.
Two different experimental models were used.
Because the experimental model was set to accelerate unfavorable effects in biocompatibility, a direct comparison to clinical circumstances is not given.
The present experimental model was chosen because it creates reproducible severe global cerebral ischemia.
Moreover, our experimental model was complex, because it combined pre- and postnatal stimuli.
It is difficult to say whether the experimental model was an ideal model because the experimental model has different material properties from those of an actual mandible.
Historically, several of the inflammatory activities of Th17 cells were attributed to Th1 cells because experimental models of autoimmune diseases were inhibited by the use of antibodies against IL-12 p40 or mice deficient in the p40 subunit of IL-12 (reviewed in [ 99]).
Hence, experimental exacerbation models are warranted.
MIRIAM annotation ultimately improves interlinking with experimental datasets because components in models are annotated with the same biological identifiers as the datasets.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com