In this study, we examined, using the technique of DNA pyrosequencing, mutations in the quinolone resistance-determining regions of the gyrA and parC genes of 38 clinical isolates of P. aeruginosa that were non-susceptible to at least one of the three fluoroquinolones tested. The most common origin of the isolates was sputum (44.7 %), followed by wounds (11 %), urine (5 %), and ear discharge (5 %). Serotypes O:11 (21 %), O:2 (18.4 %), and O:6 this website (7.8 %), were the most predominant. Among these 38 isolates,
11 were susceptible, 22 were resistant, and 5 were intermediate-resistant to ciprofloxacin. We found that 19 (50 %) of these strains had a mutation in the gyrA gene (Thr 83 Ile), one of them presented a new mutation (His 80 Arg), 8 (21.05 %) strains had an additional mutation in the parC gene (Ser 80 Leu), and one of these strains had two new mutations not previously reported (Gln 84 Asp, Ala 85 Gly). The ciprofloxacin-sensitive strains had no mutations in the sequence area examined. We found that 81.8 % of the isolates that were resistant to ciprofloxacin had a mutation in the gyrA gene. Some of these resistant strains also had a mutation in the parC gene. The results of this study suggest that pyrosequencing is a reliable technique for the determination of the antibiotic
resistance pattern of a given bacterial strain.”
“Purpose of review
Recent years have seen the advent and progress selleck inhibitor in our understanding of fibrosis and vasculopathy in systemic sclerosis, scleroderma (SSc) largely mediated through the development and study of novel animal models. The most well studied animal models of SSc involve the bleomycin model of induced fibrosis
and the Tsk/+ model. However, even though these models provide useful insights into the pathogenesis of fibrosis and vasculopathy, they do not mimic the disease accurately.
Recent Lazertinib research buy findings
Several mouse models have been developed that have specifically focused on the vasculopathy of SSc and have yielded relevant insights into this disorder further highlighting the novel mechanisms that may be responsible for this pathological feature. Furthermore, the contribution of the innate immune system mediated by the inflammasome in the induction of fibrosis has also demonstrated significant insights, possibly implicating an etiological mechanism of SSc. And recent transgenic or knockout animal models have emphasized the relevance of macrophage chemoattractant protein-1 (MCP-1), alpha-melanocyte stimulating hormone (alpha-MSH), and peroxisome proliferator-activated receptor-gamma (PPAR gamma) in fibrosis.
Summary
Recent advances in animal models of SSc have elucidated the involvement of relevant proteins that appear to mediate vasculopathy and also implicated the involvement of the innate immune system in fibrosis.