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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].
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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.
Our in vitro system models this inflammatory response by replicating the interface between the parenchyma and shunt using an astrocyte-seeded 3D alginate scaffold surrounding a portion of the shunt's ventricular catheter.
In this model, the response at a given covariate value is subject to random right censoring by two independent censoring times.
In this model, the response to a startle-eliciting stimulus, such as a loud tone, is attenuated if the stimulus is preceded within a few hundred milliseconds by a lower-intensity stimulus, or pre-pulse [43], [44].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com