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Fibrin-based 3D mitral valve constructs can be produced using primary cell cultures derived from canine mitral valves, and show a phenotype reminiscent of diseased valves.
As we have previously isolated RAD-seq markers that flank the supergene (Richards et al. 2013), we could use those markers to confirm or refute individuals that show a phenotype that might have arisen due to recombination within the supergene.
Therefore T cells induced by latency-associated antigens show a phenotype of multifunctional T cells, which have been shown to protect against TB in the mouse model [23].
Diseased brains show a phenotype of iron deficiency in the presence of increased brain iron, suggesting sequestration of iron in biologically unavailable complexes [32].
There are a number of mouse and rat strains that show a phenotype similar to the LEW/Ztm-ci2 rat such as the shaker-2 mouse (STOCK Myo15sh2/J), which incidentally carries a mutation in the Myo15 gene [3].
Finally, low dose C. burnetii infection causes death in SCID and T cell deficient mice, but does not show a phenotype in B cell deficient mice, suggesting that T cells are essential for host resistance to C. burnetii infection [11].
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We designed a screen using the fission yeast Squizossaccharomyces pombe, to isolate strains showing a phenotype of chromosome mis-segregation and higher sensitivity to the antitumoral drug Bleomycin.
Moreover, the double mutant D4-D9 showed a phenotype and an expression profile similar to D4.
Absence of Shb shows a phenotype that is clearly distinct from PTEN deficiency, but two similarities are apparent.
In our assays (Fig. 2 and 3), the ORF4.STOP mutant showed a phenotype very similar to the phenotype of the ORF4−Tet+ mutant.
∼4% of individuals still showed a phenotype.
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