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Although testosterone replacement rescued the mutant hypogonadal and spermatogenetic defects, the majority of mutant mice were still infertile.
In addition, we observed the majority of mutant mice failed to impregnate their mates, because vaginal plugs were not found after mating.
The results suggested the majority of mutant bacteria trafficked into the lysosomes and potentially were in the process of lysosomal degradation.
Our preliminary screen showed that the majority of mutant mRNAs were able to recapitulate wildtype Elk-1 mediated cell death suggesting that their respective sites were not essential in the cell death process.
The p120-catenin homozygotes are viable and fertile; p120ctn308 mutation has been reported to induce a delayed, but complete DC and subtle irregularities of the leading edge in the majority of mutant embryos [60].
The lower value for KC in mutant than in wild type carboxysomes was surprising in view of the normal appearance of the large majority of mutant carboxysomes and the low abundance of the CsoS4 proteins in wild type organelles.
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The majority of mutants, except X2345 and X34512, showed decreased activity toward pNPX compared with the wild-type enzyme X12345.
The majority of mutants were found in the N1 and N2 subtypes, which showed 57 (2.7%) and 55 (3.2%) mutants, respectively.
The majority of mutants that alleviate silencing (and concomitantly function) of the centromere are specific for only one of the domains.
This, however, is not surprising: knockout growth rates tend to be bi-modal, with the majority of mutants being either (nearly) lethal or showing little reduction in fitness.
The majority of mutants had far-UV CD spectra almost identical to the wild-type protein with slight variations in ellipticity only (Fig. 1B).
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