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To conclude, clustering of data is a logical consequence of multicenter designs [ 26, 27].
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No samples were flagged as outliers, and we concluded that clustering present in PCA plots represents real biological variation.
We conclude that clustering based on gene expression alone is insufficient for classifying leukemia types.
Despite problems with inconsistent nomenclature, we conclude that clustering pathways by the Jaccard Index uncovers core signal transduction cascades shared between differing pathways.
According to expression profile of transcripts in each cluster, it was possible to conclude that clusters contain transcripts preferentially expressed in some of the transcriptomic units defined previously but not in all.
It would have been possible to conclude that phosphosites clustering is a mere result of the fact that phosphosite generally reside in limited regions.
To conclude, this cluster can be viewed as a combination of the green, yellow and part of the blue homeostatic clusters and is formed as a result of increased SM transport and degradation during neurodegeneration.
We therefore conclude that clusters of vanadia species on the surface of the catalysts are responsible for the de-NOx activity rather than isolated vanadia surface molecules.
Therefore, Carrington et al. (2005) conclude that cluster analysis is to form the most connected nodes into one group, and remove nodes with little connection outside the subgroup.
We conclude that cluster N1a does not affect reactive oxygen species production by the complex I flavin; it is probably required for enzyme assembly or stability.
Even so, the first three pieces of evidence described above are sufficient to conclude that cluster I variants originated from an intrasubtype recombinant virus (established epidemiologically important founder strains).
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