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As we suggest, evolutionary explanations predict that genetic variation in the susceptibility to antibiotics will arise in biofilms, and that the frequency of antibiotic resistant cells will increase through time.
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These concepts derive from the spatial nature of maps, and may be conceptual constraints that suggest evolutionary misconceptions.
Though it is difficult to pin-point their exact function immediately, the highly conserved associations do suggest evolutionary constraint on these connections.
Statistically significant enrichments at specific classes of sites could suggest evolutionary preservation.
These phylogenetic relationships suggest evolutionary conservation of the basal architecture of the CDPK family.
Combined, these observations suggest evolutionary divergence is the most plausible explanation for the inconsistencies in this group.
However, differences in gene numbers, diversity, and in the function of Ppd-H1 suggest evolutionary modification of clock related components.
Our data reinforce the evolutionary structural genomic relationships among channel ortholog genes, which can suggest evolutionary gene duplication and further specialization of channel functioning.
We suggest an evolutionary algorithm with adapted operators.
We suggest that evolutionary tinkering in the timing and spatial expression of steroidogenic genes in the CAM could lead to novel endocrine functions in communication with the maternal uterus; thus, facilitating the endocrine role of the chorioallantoic placenta.
Yet, we suggest that evolutionary changes in the structure of the Y chromosome in the chimpanzee lineage might have an impact on its interactions with the X chromosome in male meiotic prophase, thereby affecting chromatin structure and transcriptional dynamics of the X chromosome in spermatogenesis, leading to a quantitative and qualitative improvement of sperm production.
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