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The total covalency of the compounds was quantified using covalent bond density (CBD), defined by the number of bonds and the bond overlap populations computed in this study.
The cell viability of these compounds was quantified by MTT assay.
The ferric reducing antioxidant power of the compounds was quantified by the method described by [36] with slight modifications.
The structural similarity between compounds was quantified with five similarity measures ((ST^{{ST{text -}opt}}), (ComboT^{{ST{text -}opt}}), (CT^{{CT{text -}opt}}), (ComboT^{{CT{text -}opt}}), and the 2-D Tanimoto), as defined in the "Methods" section, and the clustering thresholds (d thresh in Table 2) were derived from the summary statistics of these similarity measures [23].
Antimicrobial activity of compounds was quantified as the diameter of the clear zones surrounding the filter papers after subtraction of filter papers diameter (1 A.U. = 0.1 mm).
The interaction of two compounds was quantified by determining the combination index (CI), in accordance with the following classic isobologram [ 18]: CI = (D 1/(Dx)1 + (D 2/(Dx)2 Where Dx is the dose of one drug alone required to produce an effect, and (D 1 and (D 2 are the doses of compounds 1 and 2, respectively, in combination that produce the same effect.
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Tars are collected, and six compounds are quantified.
Compound identification was based on the comparison of mass spectra and/or reference compounds, and compounds were quantified using external calibration curves.
Arginine and related compounds were quantified in plasma, wound fluids and multiple tissues.
Attomoles of labeled compounds are quantified in milligram‐sized samples, such as 20 μl of blood.
Three different compounds were quantified by stable isotope dilution assay (SIDA): β-damascenone, β-ionone and α-ionone.
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