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These naturally-occurring variants were all shown to result from CD8+ T cell mediated immune pressure in prior studies[2], [3], [6], [7].
However, as the SVA-SS, SVE-SS and AVA-SS variants were all activated against TO it seems that any interaction between Ser552 and Ser554 (Ser563 and Ser565 in rat HSL) only has relevance in vivo.
DNA variants were all weighted equally.
The novel nonsynonymous variants were all in heterozygote state and mostly predicted to be benign.
ORs conferred by these variants were all modest (Table 1 and Supplementary Material, Table S2).
These variants were all inserted into the same genomic locus to minimize position effects on levels of transcription.
Similar(41)
As discussed, benign tumours, vascular diseases, connective tissue disorders, traumatic injuries, and anatomic variants are all potentially discovered on imaging.
We assume that functional variants are all causative.
We show that the short variants are all up-regulated after BDNF treatment in the rat hippocampus, and that they are expressed in the adult human brain (mostly in cortices and hippocampus).
Notably, somatic variants are all heterozygous, while some polymorphic variants are homozygous.
The families with the p.S1655F and p.R1699W variants are all predicted above the cutoff point.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com