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The task of how to model this response therefore arises.
Conventional modeling approaches consider only beam and column flexibility using concentrated plasticity or springs to model this response.
To model this response it was assumed the serotonin release occurred instantaneously, had a long decay and was directly proportional to the amount of activity in the circular muscle.
The potential for rapid information transmission by latencies warrants special efforts to model this response feature.
Unless there are strong reasons to make prior assumptions about the form of the response of the series to the intervention, simple transfer functions should be used to model this response.
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As with other osteoblast models, this response was enhanced when IL-1β and dexamethasone were added together.
In animal models, this response can be somewhat blunted by early debridement, but such early intervention is not usually feasible in most clinical settings.
Interestingly, in culture and in vivo, some tumor cells retain the ability to senesce and do so in response to DNA damaging chemotherapy; in mouse models, this response is associated with arrested tumor progression and eventual regression [ 11– 13].
However, unlike the LIF model, this transient response, although rapid, is not instantaneous.
47 In the Foxn1 nu mouse model, this neutrophil response must remain intact to prevent tumor relapse.
In our experimental model, this adaptive response may represent a feedback mechanism of ATP supply to maintain cellular ion homeostasis.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com