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These results suggest that the observed rRNA cleavage is caused by L. pneumophila infection rather than a general host cell stress response.
These data indicate that the host damage by E.coli is a characteristic of this system and not a general host damage in all conditions.
We conclude that the increased level of miR-17 family members seen in Toxoplasma-infected cells is Toxoplasma-specific and is not a general host response to apicomplexan infection.
The abundance of mature miR-17 family members, which are derived from these two miRNA clusters, remains unchanged in host cells infected with the closely related apicomplexan Neospora caninum; thus, the Toxoplasma-induced increase in their abundance is a highly directed process rather than a general host response to infection.
More likely, genotype-3a infected hosts who are treatment non-responsive show evidence of a general host resistance to the effects of IFN therapy.
An alternative to targeting a general host factor is to target the viral membrane, a task that has been accomplished recently with the aryl methyldiene rhodanine derivative LJ001.
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These findings suggest that oxidative stress is more a function of the general host response to sepsis rather than attributable to a specific microorganism.
The NS1 proteins of most influenza A virus strains bind the nuclear-localized 30 kDa subunit of cleavage and polyadenylation specificity factor (CPSF30) as a mechanism to suppress general host gene expression [2], [4], [13], [15].
Based on the annotation and gene pathway analysis it is suggested that these genes play a central role in general host defence against E. coli infections in the mammary gland.
The results presented in this study assume that resistant parasites spread to the general host population from a group of hosts representative of, but generally not mixing homogeneously with, the general host population.
Local and general host defenses play an important role in the progression from colonization to VAP [11].
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