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The mathematical analysis of these models is non-trivial.
Appropriate choice and analysis of these models is essential.
The development and analysis of these models is described in the present paper.
The mathematical analysis of these models is sophisticated due to degeneracies of the associated Fokker-Planck equations.
To evaluate the generality of these conclusions, we extended the analysis of these models to finite populations.
The analysis of these models unveiled analogies and differences among the different members of the Rpf protein family.
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Bootstrap confidence intervals and sensitivity analysis of these model parameters are presented.
Principal component analysis of these model input parameters is then carried out to identify which defect behaviors are strongly correlated with changes in damage accumulation metrics when varying many parameters at once.
This is mimicked in our models by the role of Yfh1 in Section I of Figure 2. The analysis of these mathematical models shows that, if Yfh1 had such a function, Δyfh1 cells would have impaired ISC dependent protein activity.
A thorough analysis of these three models shed new light onto the dynamical constraints of SC regulation in the SAM: none of the models was able to correctly predict CLV3 and WUS over-expression phenotypes and SC homeostasis under changing growth conditions at the same time.
Through the analysis of these TPNs models, wrong information and missing information in scenarios can be detected.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com