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As expected, the target was validated in a mouse model of bubonic plague.
Similar results were obtained in a mouse model of bubonic plague using a yopJ deletion mutant of the Kimberley53 strain [25].
In a model of bubonic plague, mice were injected subcutaneously with 1×105 cfu of either Kim53ΔnlpD or the Y. pestis EV76 prototype vaccine strain.
DGC activity was also required for the Hms-independent autoaggregation phenotype of Y. pestis, but was not required for virulence in a mouse model of bubonic plague.
In addition, a recent study in a rat model of bubonic plague has shown that YopJ was not essential for the manifestation of virulence [11].
In this work, we show that deletion of the catalytic domain of the yscN gene in Y. pestis CO92 attenuated the strain over three million-fold in the Swiss-Webster mouse model of bubonic plague.
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The expression pattern of the genes was evaluated along with their respective contributions to Y. pestis virulence using mouse models of bubonic and pneumonic plague.
On the other hand, to assess the animal models of bubonic plague, pathological characteristics during bubonic infection have been investigated in mice [6], cats [7] and guinea pigs [3].
To test the contribution of SurE, Pcm, NlpD and RpoS to Y. pestis pathogenesis, we evaluated the virulence of Kimberley53-deletion mutants in mouse models of bubonic plague (s.c. infection) and pneumonic plague (intranasal infection).
Moreover, in this work, we found that both genes in the dapAX operon contributed to virulence of Y. pestis in mouse models of bubonic and septicemic plague, thereby reducing the potential for spontaneous reversion of virulence.
In the present study, we have further characterized the Y. pestis pcm locus genes and analyzed their expression and involvement in the pathogenesis of Y. pestis using mouse models of bubonic and pneumonic plague.
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