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Our initial interpretation of these results was that this could originate from the differential organoleptic properties between -PPO and WT tubers arising from metabolic dissimilarities and/or due to the reduced browning in -PPO tubers, allowing a slower deterioration and making them palatable for longer periods of time than WT tubers [10].
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This emission could originate from inverse-Compton scattering of solar photons by tens MeV electrons.
This difference could originate from the different fluorination processes used for the multi-layers (direct fluorination with F2 gas at high temperature to produce graphite fluorides) and for the monolayers (FGIC synthesised at lower temperatures), see Section 6.
In particular, the calculated β, observed at λ ~ 1000 nm (the period of the NP array), is very deep and narrow, indicating that this dip could originate from the Wood anomaly [17].
Our data demonstrate that this chemokine could originate from sources in the hippocampus as well as the transplant population.
While some of this deletion could originate from the mothers of CKO male mice, it appears likely that at least some of these cases originate from partial Tek-Cre expression in the male germ line.
We hypothesize that this variation could originate from the differences in the epigenetic context that the fusion protein encounters and that minor baseline epigenetic changes may have a relevant bearing on SYT-SSX function.
The driving force for this flow could originate in parenchymal capillaries that act as a source of fluid production.
This discrepancy could originate from differences in BPA doses, treatment duration, the in vitro culture system, animal species, or the levels of cellular purity and differentiation.
For example, this adenosine could originate from PAP and/or TNAP, as these enzymes are located in the same region and can also hydrolyze ADP to adenosine.
This variability could originate from incomplete deletion of both Brg1 alleles, compensation via Brm/Smarca2 and/or via other mechanisms such as prolonged stability of the Brg1 proteins.
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