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Family members of patients showing a rare coding variant were tested for that variant by direct Sanger sequencing.
The lead candidate antibody and its affinity maturated variant were tested in experimental mouse models of endotoxic shock and Escherichia coli peritonitis sepsis.
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Each variant was tested for association with T2D in the sequenced individuals, and, to increase power, most were tested in larger numbers of individuals (>80% of low-frequency coding variants in ~82 K Europeans via the exome chip, and ~90% of low-frequency non-coding variants in ~44 K Europeans via genotype imputation).
Both a boron-containing and boron-free variant are tested in tension at 750 °C, with further in-situ tests carried out using scanning electron microscopy (SEM), to clarify the mechanism of ductility improvement.
This allowed them to identify which genes were responsible for making the 1918 virus so virulent, as each new variant was tested on mice, chicken embryos and human lung cells.
The PDHX variant was tested by Sanger sequencing, and the mutation was shown to be co-segregating within the family.
Each risk variant was tested for an interaction with these groups of birth weight in the prediction of adult BMI.
Published GWAS studies typically used a single-locus test (SLT), in which each variant is tested individually for association with a specific phenotype.
Independent of which variant was tested, antibodies with specificity for Rosetta gami-produced DBL5ε VAR2CSA were seen only in plasma from P. falciparum-exposed pregnant women living either in Benin (Ben) or in Senegal (Sen) (Figure 6A).
When IGV supported a structural variant call, the variant was tested with PCR.
In addition, the frequency of p.Arg1129Leu variant was tested between in arSTGD patients and controls.
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