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For example, Staphylococcus aureus, a common source of skin infections, used to be easily treated with penicillin, but today many strains are resistant to that and several other antibiotics, making a minor scratch potentially life-threatening.
For example Staphylococcus epidermidis adhesion and growth were markedly higher on rough titanium surfaces than on smooth surfaces (Cheng et al. 2013).
For example, Staphylococcus sequences belonging to subfamily II were more closely related to Lactobacillales and Clostridiales sequences than to sequences of other Bacillales (Figures 2 3, and Figures S3 S6).
For example, Staphylococcus aureus employs fibronectin as a pathogenic mechanism to adhere, modulate the intracellular signaling pathway, and invade host cells [ 7, 9].
For example, Staphylococcus species give a respiratory response to N-sources but we have never been able to get them to grow on single N-sources.
For example, Staphylococcus aureus has an average volume of about 1.76 μm (0.5 1 μm cell diameter) while Mycobacterium tuberculosis has a volume of about 8.4 μm (2 4 μm in length and 0.2 0.5 μm in width).
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Despite the apparent redundancy in vitro, effects of uppP knockouts in vivo are significant, with, for example, deficient Staphylococcus aureus and Streptococcus pneumoniae showing attenuated virulence in mouse models of infection9 and uppP-deficient Mycobacterium tuberculosis showing impaired biofilm formation10.
For example, the Staphylococcus aureus α-toxin has been demonstrated to bind to caveolin 1, and mutant α-toxins that are disrupted in the ability to bind caveolin 1 are non-hemolytic [68], [69], [70].
Where the genetic diversity of human pathogens has been intensively studied, for example in Staphylococcus aureus [12] and Neisseria meningitides [13] (two human commensal bacteria which cause sporadic outbreaks of disease), the number of studies focusing on disease isolates far outnumbers those of the more diverse carrier populations.
For example, in Staphylococcus aureus, ethanol supplementation stimulated the expression of genes involved in stress response, and biofilm formation [ 42].
The physiological role of Th17 cells lies in bacterial defense - for example, against Staphylococcus aureus - as shown in experimental pneumonia and the hyper-IgE syndrome [ 55, 56].
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