Active Ingredient: Ciprofloxacin
A near confluent culture of NIH 3 T 3 cells was detached using a trypsin solution according to standard procedures and diluted 1:5 in fresh cell culture medium. All experiments were conducted in triplicates and the results are given as mean values with the standard deviation.
The results were in agreement with data from clinical analyses, with the exception that no gyrA 87 and no gyrB mutations were found in ciprofloxacin-resistant P. Pseudomonas aeruginosa is capable of growing in a wide variety of niches with a preference for moist environments.
In addition. Thus. As human P. In particular. As a consequence, this antibiotic has lost its effectiveness.
Fluoroquinolones have been widely used for the treatment of P. Besides the acquired fluoroquinolone resistance. The targets of quinolones are considered to be the type II topoisomerases DNA gyrase and topoisomerase IV, which are essential enzymes for controlling the topological state of DNA during replication and transcription Levine et al.
Alterations in DNA gyrase and topoisomerase IV caused by mutations appear to play a major role in fluoroquinolone resistance in clinical isolates of P.
They found changes in the GyrB subunits of P. A novel mutation in the parE gene in P.
Many studies have focused on the characterization of clinical isolates from patients with P. The aim of this study was to quantify the occurrence of ciprofloxacin-resistant P.
In order to quantify the occurrence of P.