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Host indexes (lists of diseases known to occur on certain hosts in regions, countries, or continents) are valuable in diagnosis.
For example, black flies and mosquitoes will feed preferentially on certain hosts [79] [81].
Traditional means for determining mosquito host-preferences in the field are to estimate the proportion of blood meals on certain hosts [1] or, more specifically, to calculate a feeding index, where the proportion of blood meals acquired from a specific host is assessed in relation to the abundance of that host within the community of potential hosts [2], [3].
Field surveys suggest that different morphotypes tend to differ in their host associations and that sexual lineages are disproportionately common on certain hosts [ 8, 23, 24].
To determine if the seemingly nonessential 39.2 gene of T4 is in fact essential for bacteriophage growth on certain hosts, we constructed an isogenic T4 strain with an in-frame deletion of 39.2, using the insertion/substitution system of Selick et al. (1988).
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However, recent years have seen great progress in understanding of the molecular mechanisms that enable insect to feed on certain host plants.
In the following, we thus derive and empirically test approaches that could be applied directly (or after minor modifications) to all kind of associate character data, be it morphological or sequence data of individuals in certain geographic areas or habitats, parasites or mutualists on certain host organisms, or genes and sequence variants present in certain individuals.
Similarly, isolated foci of some vector-borne diseases that rely on the continued presence of certain hosts and vectors could disappear if movement of either is restricted.
Using custom-designed glycospheres, we developed an assay platform for high-throughput functional characterization of clinical influenza isolates based on their ability to bind to certain host-specific glycan motifs.
Findings indicate that preferential feeding by C. pipiens mosquitoes on certain avian hosts is likely to be inherent, and we discuss the implications innate host preferences may have on enzootic WNV transmission.
Finally, as proof of principle that Gp39.2 is essential for bacteriophage growth on certain bacterial hosts, we constructed a T4 39.2 deletion strain and showed that, unlike the isogenic wild-type parent, it is incapable of propagating on certain groEL mutant hosts.
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