Sentence examples for model of dose from inspiring English sources

A simple model of dose density distribution is developed and compared with the measured results to account for dependence of line widths on dose, focus and astigmatism.

In panel A, we sketch the linear model of dose response, whereas panel B shows that this model fits well to the trial data.

One uses a specific model of dose response (response [probability, percentage]) = f [exposure or dose]) developed from theoretical and empirical evidence, applies a policy risk level (response is measured by probabilities), and solves for its corresponding tolerable dose.

A linear model of dose response provides a good fit to the data and a simple characterization of the optimal dose, provided that interpretation is limited to the tested range of doses.

Another important question raised is how to determine the optimal biologic dose of combination targeted therapy regimens, since the MTD identified by the standard model of dose escalation may not be equivalent to the optimal biologic dose for every drug or combination (Parulekar and Eisenhauer, 2004; Sleijfer and Wiemer, 2008; Postel-Vinay et al, 2011).

Traditionally, the potency of these substances relative to TCDD has been expressed as a consensus toxic equivalency factor (TEF), allowing the translation of analytically determined single concentrations of chemicals in a sample into a biological activity measure the TCDD equivalent concentration (TEQ)—assuming a model of dose additivity (Safe 1990; van den Berg et al. 2000).

We assume that the Hill-Slope model of dose-response: y = 1/(1+(x/IC50)∧slope); y is the response corresponding to the dose x (Text S1).

Results show that inhibition curves did not fulfill the theoretical model of dose-dependent hetero-tetramer formation.

The aim of this study is the assessment of the Geant4 capabilities in accurately modeling of dose distribution in a heterogeneous water phantom.

It may be that alternative models of dose intensification, using combinations of more active agents, over short time intervals, may be more effective and we have shown one such strategy to be possible.

TP models are unlikely to contribute quantitatively to risk assessments for several reasons, including that the statistical variability inherent in such complex models severely limits their usefulness in estimating small changes in response, and that such models will likely continue to involve empirical modeling of dose responses.