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The consequences of these different particle states on the coating microstructure are also discussed in this article.
Several different operating modes are considered, going from batch, through semi-batch, to continuous, and the consequences of these different configurations on the overall process are evaluated.
Hence, an explicit comparison of the consequences of these different causes of alteration in growth trajectories could be worthwhile.
We explored the consequences of these different combinations by running the multilocus GFG model at all combinations of both high and low host resistance and parasite virulence costs (cH and cP); the results for all combinations of cost functions are given in the online Supplementary Material (Figs S1, S2, S3, S4, S5, S6), but here we just present the key results.
The consequences of these different β-catenin levels were investigated.
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The photoexcited NPs can de-populate only by radiative emission with rates r0,r1 for m j = 0, m j = ±1, respectively (note that, here, we set these equal; we will consider the consequences of these being different in a future work), spin-lattice relaxation to spin states lower in energy (γ ij ), or thermal excitation to spin states higher in energy by Δ ij (γ ij = γ exp -Δ ij /k T)).
The consequences of these forces have been different for fathers and mothers.
Both SCR and FAMA bind to RBR via an LxCxE motif, yet the consequences of these transcription factor/RBR interactions are different; RBR antagonizes SCR function in asymmetric division in the root stem cell compartment (Cruz-Ramirez et al., 2012, 2013), whereas RBR and FAMA have similar functions promoting differentiation at the terminal stage of stomatal development.
This may be the consequence of the different modifying effects which these polymorphisms have on the balance during the DNA repair process.
Our results suggest a similar mechanism in vernal pools, and it would be interesting to examine the consequences of these interactions on species composition patterns at different spatial and temporal scales.
While it is known that mutations in KRAS, BRAF and PIK3CA may determine the responsiveness to targeted therapies such as EGFR, MEK or mTOR inhibitors [ 53, 57, 58], the consequences of these mutations for neurotensin signalling in the different cell lines are not obvious.
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