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Other mutations are harder to trace because individuals with these mutations may develop very different signs and symptoms, or not develop clinical abnormalities at all.
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But such inherited mutations are hard to find, because they're usually eliminated during evolution, he explains.
Clones initiated by the mDEL1 mutation are harder to explain.
So is vemurafenib, a new drug against malignant melanoma.The problem is that identifying the relevant mutations is hard.
The accumulation of so many contributory mutations is hard to explain solely by the frequency of multiple independent mutation events.
The exact range of the possible biological functions of such somatic mutations is hard to grasp.
The contacts that are broken or newly formed by the conformational change during the mutation are hard to define quantitatively.
For example, in most cases, the influence of a novel fetal mutation is hard to predict.
It is impossible to recognize all the possible regulatory elements, and absolutely confident results on mutation rates are hard to obtain.
However, mutation descriptions are hard to be compared and integrated due to various reference sequences and annotation tools adopted in different articles as well as the nomenclature of diseases/traits.
Prediction of the extremes may appear to be a trivial problem, but this is not always the case -- some damaging mutations are very hard to predict.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com