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This model suffers from strong multipath fading and shadowing.
Unfortunately, this model suffers from two major limitations.
Below it will be shown that this model suffers from a bias towards regulation of genes with a large part of their upstream sequence evolutionarily conserved, simply because it is more likely to predict a binding site within a longer sequence stretch than within a short one.
However, this model suffers from an issue typical of gene network inference models, which is that the number of genes is greater than the number of experimental observations.
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This model suffered from being only two-dimensional.
Standard MH for the model suffers from critical slowdown, while IMH is free from critical slowdown.
Moreover, the model suffers from the absence of detailed algorithmic specifications on how RL can be implemented in this three layered learning architecture.
However, considering the importance of external validation and reproducibility, the model suffers somewhat as evidenced by the CV measures.
We examined the variance inflation factors to check whether the model suffered from multicollinearity.
This latter model suffered from the lack of evidence that could explain the spatial paradox of this direct inhibition: under normal circumstances, Bax is in the cytosol, whereas Bcl-2 is on the surface of mitochondria.
This model however suffers from the same limitations as Model 1.
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Since I tried Ludwig back in 2017, I have been constantly using it in both editing and translation. Ever since, I suggest it to my translators at ProSciEditing.

Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com