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Previous theoretical analyses did not identify the stabilization caused by the mutations at positions 1, 46, and 48.
Gene ontology analyses did not identify a single key pathway altered in these cell populations.
Our analyses did not identify SNPs or haplotypes that were segregating with the disease in the overall sample.
Meta-regression analyses did not identify the magnitude of within-study gradients in assigned (or achieved) tidal volumes or airway pressures between treatment groups as important effect modifiers (data not shown).
Despite a significant structural similarity between VLM and cereulide and an organizational similarity between the vlm gene cluster and the ces gene cluster [13] (Figure S1), our analyses did not identify a close relationship between these two gene clusters.
DNA microarray analyses did not identify differential mRNA expression of any gene as a result of E2 at any time (we could not reject the global null that E2 was independent of mRNA expression of all genes represented on the chip).
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However, these analyses do not identify which PKC family member mediates the observed phenotypes.
In terms of other limitations, these analyses do not identify those survivors whose cancer was cured, those in active therapy or those dying from cancer; this information is not available through the Registry.
Our analyses do not identify any strong consensus sequence outside the conserved unique termination codon TGA, although we observe a preference for A in the position two bases upstream of the termination codon, and a T immediately downstream.
For the cases where low impedance was observed at lower echogenicity, sub-analyses did not identify a variable that could account for the lower impedance.
3 Subsequently, two published meta-analyses did not identify any superiority for linezolid over vancomycin for the treatment of pneumonia.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com