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Variants of the Helicobacter pylori cag pathogenicity island (cagPAI) and certain virulence genotypes have been proposed to be associated with different gastric disorders.
The aim of the present work was to analyze whether the location of the dental biofilm was associated with shifts in the membrane fatty acid profile, and whether such shifts could affect certain virulence factors of strains of Streptococcus mutans.
In order to find optimal HMM sets, we designed multiple HMM sets for certain virulence protein families.
It has also been speculated that certain virulence factors can play important roles in the persistence of H. pylori in the gastric mucosa [18].
As a result, certain virulence factors are maintained on mobile elements, including GIs, which are thought to be related to phage [17].
Interestingly, these prokaryotes form mixed biofilms [39] and P. aeruginosa is known to promote B. cepacia pathogenesis by upregulating certain virulence factors [40].
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With respect to gene content differences, there was no significant association between the presence of certain virulence-associated genes and the source of the strain, i. e., whether it was isolated from a healthy carrier or from a case of invasive meningococcal disease.
Most probably, certain virulence-associated genes are specific for fitness in the host and have little or no function in vitro.
Expansion of certain virulence-associated gene families often occurs in the sub-telomeric regions of Candida species – such as with the EPA gene family of adhesins of C. glabrata (Kaur et al., 2007).
The study provides support for certain hypothetical virulence factors while rejecting others.
We also observed that certain known virulence factors were upregulated during Sz35246 infection, for example, streptokinase (SeseC_02411) and fibronectin-binding protein (sfs, SeseC_00464).
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