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The spatial structure of resistance genes influences epidemic intensity in many systems [30], and the effect of this spatial structure, itself, has the potential to vary across gradients [31].
In our setting, overall host density in the area determined epidemic intensity before resistance deployment (parameter ).
They found that epidemic intensity was the main factor explaining resistance breakdown.
This was true regardless of the choice of R gene and, to a lesser extent, of epidemic intensity.
The landscape composition (cropping ratio between the susceptible and resistant cultivars) was also found to be crucial but even its influence was determined by epidemic intensity.
It defined thresholds for epidemic intensity below which relative damages were identical for both strategies (i.e., the solid and dashed lines merge in Fig. 4).
Similar(41)
However, for higher epidemic intensities, relative damage increased steeply, whatever the resistance gene.
CYS yield marked disease control only for the lower range of epidemic intensities.
In situations in which within-field infections predominated, relative damages for CSS were always 100% for epidemic intensities >0.6 (Fig. 4A).
When two mutations are required, high levels of disease control (i.e. relative damage < 10%) were achieved for the entire range of epidemic intensities explored.
At best, damage is decreased by more than 90% only when epidemic intensities are <0.35 before the deployment of resistance (Fig. 1B, C).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com