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Experimental mosquitoes were derived from wild pupae collected in a dengue epidemic context.
The chance of two haplotypes being identical in state purely by chance is a maximum of 0.1×0.25×0.5 = 0.0125 assuming linkage disequilibrium between the loci (see later) and that separate clones in a human (and hence in the bloodmeal of mosquitoes) were derived from separate bites i.e. a human could not be infected by two genetically-related clones inoculated in the same bite.
Fold changes in gene expression between resistant and susceptible mosquitoes were derived by the comparative CT method using the 18S ribosomal protein gene as an internal control [ 52].
Fold-changes in gene expression between S and B mosquitoes were derived by the comparative CT method [ 73], using the constitutive gene rp49 (GenBank Acc. No.: AY539746; asEL003396) as the reference and four samples each for S and B mosquitoes.
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The isofemale lines of the mosquito were derived from a laboratory colony of A. aegypti maintained by J.J. Becnel (USDA, Gainesville, USA), had been maintained for more than 50 generations, and have previously been shown to differ in several life history traits and in their immune response (unpublished Masters theses).
The Aedes mosquitoes used in this study were derived from wild pupae collected from outdoor containers in the survey zone.
Environmental factors that might influence mosquito spatial distribution and WNV infection were derived from various data sources.
Similarly, mosquito orthologs were identified for a set of human and Drosophila genes associated with DENV and WNV that were derived from RNA interference screen [ 20].
Since the macrophages were derived from mice that are nonreactive to endotoxin, it is unlikely that results presented here are due to mosquito salivary gland contamination.
Samples were derived from blood.
Analytical results were derived manually.
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