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To reveal with greater confidence the genomic features common to the typhoid agents but not seen in non-typhoidal Salmonella pathogens for the elucidation of the genetic basis of the typhoid pathogenicity, we included additional typhoid agents as well as non-typhoidal salmonellae in the genomic comparisons.
However, all 25 genomic features common in clinical stage and N status had identical association directions; 14 with direct associations and 11 with inverse associations.
To identify the genomic features common to all human gut microbiomes as well as those variable among them, we performed a large-scale comparative metagenomic analysis of fecal samples from 13 healthy individuals of various ages, including unweaned infants.
As all Salmonella share high levels of genetic similarity, it is possible to reveal genetic differences or similarities in pathogenicity among the Salmonella typhoid agents by focusing on genomic features common to some or all of the Salmonella typhoid agents.
To test our hypothesis, we combined in silico comparative genomic analyses with an array-based comparative genomic hybridization (CGH) approach to probe the genomic diversity of L. monocytogenes and to identify genomic features common in LI and LII but absent in LIII.
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Another genomic feature common to X. albilineans and X. fastidiosa is the absence of a type III secretion system (T3SS) of the Hrp1 and Hrp2 (hypersensitive response and pathogenicity-1 and 2, respectively) injectisome families that are used by most Gram negative phytopathogenic bacteria to deliver bacterial effector proteins or virulence factors into the host plant cell.
Characterization of conserved single-copy genes as well as their pangenome showed that these two high-abundance, low diversity Sulfurovum populations were very similar to each other, suggesting they possessed genomic features in common enabling them to rapidly grow to high abundance in their respective habitats.
Common genomic features can be distinguished by analysis of nucleic acid sequence patterns or motifs.
These data indicate that this mouse sarcoma model and human MFH share common genomic features.
This study identifies several promoter regions that have altered DNA methylation status three generations after the initial exposure and identifies common genomic features present in these regions.
Because human MFH and the LSL-KrasG12D; Trp53Flox/Flox mouse model of soft tissue sarcoma share common genomic features, we wanted to determine if these shared features could be used to identify diagnostic or prognostic factors for human MFH.
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