Trypan Blue Stain 0.4% was obtained from Gibco® (Life Technologies Corporation, Gaithersburg, MD, USA). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reagent used to check the cell viability was ABT-888 purchased from Duchefabiochemie, Haarlem, The Netherlands. Dimethyl sulfoxide (DMSO) with high purity grade of 99.9% was acquired from Sigma-Aldrich. Tissue culture flasks and microplates for cell seeding and growth were purchased from BD Falcon™, Winston-Salem, NC, USA and SPL Life Sciences, Pocheon-si, Gyeonggi-do, Korea.

Characterization THZ1 mw Variable pressure field emission scanning electron microscope (FE-SEM) EVO® LS10 equipped with energy-dispersive X-ray spectroscopy (EDS) obtained from Carl Zeiss SMT., Ltd., Oberkochen, Germany, was used to investigate the morphology and elemental detection of nanofibers. Before viewing, the samples were pasted on a carbon tape and sputter-coated using a thin layer of gold palladium for 120 s for two consecutive cycles at 45 mA with the Ion Sputter 1010, Hitachi, Chiyoda-ku, Japan. After sample coating, the micrographs from each samples were taken at an accelerating voltage of 2 KV and with magnifications of 15 K. The EDS images were captured at an accelerating voltage of 10 KV and with magnifications of 15 K. The average nanofiber diameters

were calculated using the software Innerview 2.0, Dong, Bundang Daeduk Plaza, Korea, after measuring 100 diameters per sample from FE-SEM images. Transmission electron microscopy (TEM) was done by JEOL JEM-2200FS operating at 200 KV, JEOL Ltd., Akishima-shi, Japan. The samples for TEM were MGCD0103 prepared by dispersing 10 mg of nanofibers in 200 μl of ethanol and subsequently dispersed by bath sonicator using locally supplied ultrasonic cleaner (60 kHz, Shenzhen Codyson Electrical Co., Ltd., Shenzhen, Guangdong, China) for 120 s. After dispersing the nanofibers, 20 μl of dispersion was pipetted out by micropipette and carefully poured on 200 mesh copper grid. The extra solution was removed using Kimwipes supplied by Kimberly-Clark Professional, GA, USA, and the grid was allowed to dry overnight at room temperature. Information

about the phases and crystallinity was obtained using PANalytical diffractometer (HR-XRD, X’pert-pro MPD, Almelo, 17-DMAG (Alvespimycin) HCl The Netherlands) with Cu, Cr (λ = 1.540 A) radiation over Bragg angle ranging from 10° to 60°. To identify the vibrations caused due to functional groups in nanofibers, Fourier transform infrared spectroscopy (FT-IR) analysis was done using BIO-RAD (Cambridge, MA, USA). The samples were directly loaded on ATR window, and spectra were collected using Excaliber Series by averaging 32 scans with the resolution of 4 cm−1. The thermal analysis of the synthesized nanofibers was carried out with a thermal analysis system, (TA Instruments, New Castle, DE, USA) by ramping the samples at 10°C/min, and heating was started from 30°C to 700°C.

, LTD) and inserted into pMD18-T vectors (TAKARA BIOTECHNOLOGY (DALIAN) CO., LTD). The recombinant plasmids {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| were transformed into E.coli DH5α. DNA sequencing of the plasmids was done by Beijing Youbo Gene Technology Co. Ltd. Nucleotide sequences were assembled and edited with Gap4 which is a part of the STADEN package (http://​staden.​sourceforge.​net/​) software. The sequences were compared with those of the reference organisms by Blast search. Selection of

a medium for Ferroptosis inhibitor clinical trial polymyxin production Among the seven media used in our survey, Katznelson and Lochhead (KL) medium [48], Landy medium [49], Landy medium either supplemented with yeast extract, D, L-alanine and phenylalanine (Landy GA) or with yeast extract and phenylalanine (Landy G), GSC medium [45], brain-heart infusion (BHI) medium and tryptic soy broth yeast extract (TSBYE) medium, the GSC medium was optimal for production of polymyxin. Antibacterial activity

assay To investigate its antibacterial spectrum, P. polymyxa M-1 was grown in GSC medium under aerobic conditions at 30°C for 72 h. Then the culture was centrifuged at 6000 rpm at 4°C for 10 min to remove cells. Fresh indicator bacteria plates were prepared for the assay. When the concentration of indicator bacteria grown in LB medium at appropriate temperature was up to 4 × 107 CFU/mL, 0.5 mL bacteria suspension was mixed with 20 mL melting LB agar and cooled below 60°C Temsirolimus to prepare the plates. 50 μL M-1 GSC culture supernatant were loaded into a well punched in indicator bacteria plate which was then incubated at 30°C overnight to observe the growth inhibition effect. GSC medium without bacteria was also loaded as a negative control. The diameters of inhibition zones were then measured and recorded. The inhibiting activity of M-1 against E. amylovora Ea273 and E. carotovora was also tested

by spotting bacterium on an indicator bacteria plate prepared by the method described above. E. coli DH5α used as a negative control was also spotted onto the lawn of indicator strains. Then the plates were incubated at 30°C overnight to observe the growth inhibition effect. To analyze the antibacterial activity of the HPLC ADAMTS5 fractions, a 50-μL aliquot of each fraction was loaded onto sterilized paper disks. 50 μL M-1 GSC culture supernatant used as a positive control and 50 μL sterile distilled water used as a negative control were also loaded. After being air dried in a clean bench, the disks were transferred onto E. amylovora Ea273 and E. carotovora plates prepared by the method described above and incubated at 30°C overnight to observe growth inhibition effect. Separation of antibacterial compounds by RP-HPLC The chromatographic system consisted of an Agilent 1100 liquid chromatograph equipped with a diode-array detector (Agilent Technologies, Waldbronn, Germany).

Therefore, we directly micropipetted a colloidal silica sphere solution on the substrate squares with an area of 5 × 5 mm2. The selleck products solution contained enough silica spheres to give a full monolayer of colloidal silica spheres. A small droplet of water (approximately 10 μl) was also placed on top of the colloidal solution on the substrates. The solution on top of STO has been dried under continuous sonication. AFM images of deposited silica layers were acquired with a Bruker AFM model Icon (Bruker, the Netherlands). The silicone cantilevers were purchased from MikroMasch

(Wetzlar, Germany) with a force constant of 14 N m−1. All images were acquired using tapping mode under ambient laboratory conditions. An epitaxial Cilengitide in vivo platinum film with a thickness of 8 nm was evaporated by e-beam evaporation using a three-step deposition technique [7]. A monolayer of silica beads was removed by sonication in hot concentrated potassium hydroxide aqueous solution. The nanocrystal arrays were characterized by X-ray diffraction

(XRD) to confirm the orientation of crystalline platinum islands with respect to the substrate. The diffraction experiments were performed at the Advanced Photon Source (APS) using the four-circle diffractometer with a vertical scattering geometry at beamline 12BM. The incident energy was 11.5 keV, and beam defining slits were set to 1 mm with an under-focused beam. From our experience, intense synchrotron X-ray beam in the presence of

oxygen from air causes damage to platinum single crystal surfaces. Most likely, this damage is a result of interaction between MDV3100 research buy reactive free radicals generated from oxygen and platinum metal. We protected delicate nanocrystal arrays click here from X-ray damage by flowing ultra-high purity nitrogen gas into a polypropylene bag placed over the sample. For the STO (001) substrates, the Pt (004) and four (113) Bragg peaks were found. It is necessary to use a θ-offset of 0.15° to 0.30° for the θ-2θ scans so that the STO Bragg peak does not saturate the scintillation detector and to reduce background around the platinum Bragg peaks (STO and Pt (004) are separated by approximately 0.3° at 11.5 keV). The samples were also characterized by a high-resolution Hitachi Model S4700 scanning electron microscope (Hitachi, Tokyo, Japan) at the Electron Microscopy Center, Argonne National Laboratory. Results and discussion Microscopy characterization of silica monolayers and platinum nanoparticle arrays Ordered silica bead monolayers, which later served as templates for the platinum metal deposition, were made by depositing solutions containing either 450- or 150-nm silica beads. We used AFM and optical microscopy to characterize deposited layers. Figure 1 shows optical microscopy image of 150-nm silica spheres deposited on STO.

gingivalis, one of the systems of heme acquisition consists of HmuR and HmuY proteins [12]. HmuR is an outer-membrane TonB-dependent receptor involved in heme transport through the outer membrane [13–16], whereas HmuY is a heme-binding lipoprotein associated with the outer membrane of the selleck compound bacterial cell [17–21]. A detailed characterization of the HmuY-heme complex demonstrated that heme, with a midpoint potential of 136 mV, is in a low-spin Fe(III)

hexa-coordinate environment [20]. In that report we also identified histidines 134 and 166 as potential heme ligands. Recent crystallographic analysis of the HmuY-heme complex confirmed these data and showed that the protein exhibits a unique structure composed of an all-β fold [21]. Our studies also showed that HmuY may be functional in the form of dimers/tetramers [19, 21]. It seems that dimeric HmuY takes up heme and this leads to tetramerization under occlusion of the heme binding sites. Tetrameric HmuY would protect heme from host scavengers and delivered it to HmuR. On the basis of our mutational analysis of HmuY heme ligands [20], an initial step in Androgen Receptor agonist inhibitor heme transfer could involve disruption of only one of the two axial histidine ligands, as found for Serratia marcescens hemophore HasA [22]. Once bound by HmuR, heme is translocated across the outer membrane into the periplasm with the assistance of TonB and further heme transport

requires the presence of binding proteins to escort it across the periplasm to the cytoplasm. This step might be performed by other hmu operon proteins, so far not characterized [17, 19]. HmuY, especially in the form associated with the outer membrane, may also store heme and protect the bacterial cell from damage induced by free hemin. It is likely that HmuY lipoprotein may play a role not only in heme acquisition, but also in the host pathogen response. GNA12 Therefore the aim of this study was to analyze the surface exposure and expression of HmuY protein in P. gingivalis. In find more addition, in this report we examined the participation of HmuY protein in biofilm formation. Results and Discussion HmuY is a unique P. gingivalis protein Preliminary studies demonstrated that HmuY

shows high identity to proteins identified in several P. gingivalis strains [17, 19]. Here we compared the amino-acid sequences of putative HmuY homologues deposited in databases. Interestingly, we found that HmuY is similar to proteins encoded in several different species belonging to the Bacteroidetes phylum, which consists of three classes: Bacteroidetes, Flavobacteria, and Sphingobacteria [23]. The Bacteroidetes class consists of anaerobes which are often found in high numbers in the intestinal tracts of animals and which may infect different human tissues, including periodontal tissues (see Additional file 1). Members of the other two classes are mainly aerobic and abundant in many freshwater and marine systems (data not shown).

Lukehart SA: Activation of macrophages by products of lymphocytes from normal and syphilitic rabbits. Infect Immun 1982,37(1):64–69.PubMed 47. Gayet-Ageron A, Ninet B, Toutous-Trellu L, Lautenschlager S, Furrer H, Piguet V, Schrenzel J, Hirschel B: Assessment of a real-time PCR test to diagnose syphilis from Evofosfamide price diverse biological samples. Sex Transm Infect 2009, 85:264–269.PubMedCrossRef 48. Grange PA, Gressier L, Dion PL, Farhi D, Benhaddou N, Gerhardt P, Morini JP, Deleuze J, Pantoja C, Bianchi A, Lassau F, Avril MF, Janier M, Dupin N: Evaluation of a PCR test for detection of Treponema pallidum in swabs and blood. J Clin Microbiol 2012,50(3):546–552.PubMedCrossRef 49. Martin IE, Tsang RSW,

Sutherland selleck K, Tillay P, Read R, Anderson B, Roy C, Singh AE: Molecular characterization of syphilis in pacients in Canada: Azitromycin resistance and detection of Treponema pallidum DNA in whole-blood samples versus ulcerative swabs. J Clin Microbiol 2009,47(6):1668–1673.PubMedCrossRef 50. Woznicová V, Šmajs

D, Wechsler D, Matějková P, Flasarová M: Detection of Treponema pallidum subsp. pallidum from skin lesions, serum, and cerebrospinal fluid in an infant with congenital syphilis after clindamycin treatment of the mother during pregnancy. J Clin Microbiol 2007, 45:659–661.PubMedCrossRef 51. Stamm LV, Bergen HL: A point mutation associated with bacterial macrolide resistance is present in both 23S rRNA genes of an erythromycin-resistant Treponema pallidum clinical isolate. http://www.selleck.co.jp/products/Metformin-hydrochloride(Glucophage).html Antimicrob Agents Chemother 2000, 44:806–807.PubMedCrossRef 52. Lukehart SA, Godornes C, Molini BJ, Sonnett P, Hopkins S, Mulcahy F, Engelman J, Mitchell SJ, Rompalo AM, Marra CM, Klausner JD: Macrolide resistance in Treponema pallidum in the

United States and Ireland. N Engl J Med 2004, 351:154–158.PubMedCrossRef 53. Matějková P, Flasarová M, Zákoucká H, Bořek M, Křemenová S, Arenberger P, Woznicová V, Weinstock GM, Šmajs D: Macrolide treatment failure in a case of secondary syphilis: a novel A2059G mutation in the 23S rRNA gene of Treponema pallidum subsp. pallidum . J Med Microbiol 2009, 58:832–836.PubMedCrossRef 54. Preacher KJ: ACY-1215 ic50 calculation for the chi-square test: An interactive calculation tool for chi-square tests of goodness of fit and independence [Computer software]. 2001. http://​quantpsy.​org Competing interests The authors declare that they have no competing interests. Authors’ contributions LM and PP participated in the study design, carried out PCR testing, analyzed results and prepared a draft version of the manuscript. VW, IK and HZ participated in sample collection and serology testing. DS planned and coordinated the study, and wrote the final version of the manuscript. All authors read and approved the final manuscript.”
“Background Methionine is an essential amino acid in mammalian cells, although most bacteria, fungi and plants synthesize this amino acid de novo from aspartate [1].

Can J Clin Pharmacol 2009; 16: e400–6PubMed 12. Donato JL, Koizumi F, Pereira AS, et al. Simultaneous determination of dextromethorphan, dextrorphan and doxylamine in human plasma by HPLC coupled to electrospray ionization tandem mass spectrometry: application to a pharmacokinetic

study. J Chromatogr B Analyt Technol Biomed Life Sci 2012; 899: 46–56PubMedCrossRef”
“Introduction Levofloxacin 0.5% ophthalmic solution (Cravit® ophthalmic solution 0.5%; selleck kinase inhibitor Santen Pharmaceutical Co., Ltd., Osaka, Japan) is an antibacterial eye drop formulation, which selleck chemicals contains the active ingredient levofloxacin, a synthetic antimicrobial agent of the fluoroquinolone family.[1] Fluoroquinolones are known to exert antimicrobial activity through inhibition of DNA gyrase, an enzyme involved in bacterial DNA synthesis. They have been used extensively for the treatment of bacterial CYT387 infections in clinical practice because of their potent activity against a wide range of Gram-positive and Gram-negative microbes. Furthermore, topical fluoroquinolones, such as ophthalmic solutions containing norfloxacin or ofloxacin, have been widely prescribed

for the treatment of external ocular bacterial infections.[2] Levofloxacin, an L-isomer of ofloxacin, has two times greater antimicrobial activity than ofloxacin[3] and has high water solubility at a neutral pH, allowing for the preparation of high-concentration formulations. Clinical trials of levofloxacin 0.5% ophthalmic solution revealed that levofloxacin ophthalmic solution was superior to ofloxacin ophthalmic solution.[4–7] As a result, levofloxacin 0.5% ophthalmic solution was approved and marketed in Japan in 2000 for the treatment of bacterial conjunctivitis or other external ocular infections Sitaxentan and for perioperative use during ocular surgery.[1] It is approved for the treatment of bacterial conjunctivitis in the US (Quixin®)[8] and is also approved in several European countries for the treatment

of ocular infections (Oftaquix®).[9] Japanese regulatory authority policy required monitoring of the safety and efficacy of levofloxacin 0.5% ophthalmic solution for the treatment of ocular bacterial infections for up to 6 years after its approval. In accordance with this, surveillance was conducted on the use of levofloxacin 0.5% ophthalmic solution, initiated immediately after levofloxacin was launched on the market. In this article, we present the results of this post-marketing surveillance of levofloxacin 0.5% ophthalmic solution used in everyday clinical practice in a large patient population. Methods Patients This survey was designed to investigate the safety and efficacy of levofloxacin 0.5% ophthalmic solution in patients who received treatment for external ocular bacterial infections in regular clinical practice.

Figure 2 Structure and NVP-HSP990 manufacturer sequence comparison of the CYP61 gene from X . dendrorhous. (A) PCR-amplified DNA region that includes the CYP61 gene from X. dendrorhous. The nine exons of the CYP61 gene are shown in thick red arrows (E1 to E9) and the recognition site of primers used in this work are represented by thin arrows. (B) Sequence comparison of CYP61 genes from different X. dendrorhous strains: UCD 67–385 [GenBank: JX183236], CBS 6938 [GenBank: JX183240], VKM Y-2786 [GenBank: JX183238], UCD 67–210 [GenBank: JX183237], AVHN2 [GenBank: JX183239], ANCH03 [GenBank: JX183241], ANCH07 [GenBank: JX183242] and ANCH10 [GenBank: JX183243]. The base changes are shown indicating their position in bp, with

the adenine of the translation start codon as bp 1. The respective exon (E-1 to E-9) or intron (I-1 to I-8) where Thiazovivin cell line ARRY-438162 concentration the base changes occur is also indicated. The CYP61 gene from several X. dendrorhous strains (VKM Y-2786, CBS 6938, UCD 67–210, ANCH03, ANCH07, ANCH10 and AVHN2 (Table  2) was PCR-amplified using Pfu DNA pol, and each amplicon was sequenced [GenBank: JX183238, JX183240, JX183237, JX183241,

JX183242, JX183243 and JX183239, respectively]. We found several base changes, but most of them were located in the intronic regions. Only four base changes produced amino acid replacements; the adenine, guanine, guanine and cytosine at positions 34, 79, 1,573 and 2,075 were converted to guanine, adenine, adenine and thymine (numeration according to the CYP61 gene translation start in strain UCD 67–385), resulting in T12A, A27T, R306K and P409S variations at the deduced amino acid sequence, respectively (Figure  2B). Table 2 Strains and Plasmids used and built in this work   Genotype or relevant features Source or reference Strains:     E. coli:     DH-5α F- φ80d lacZΔM15Δ (lacZY-argF) U169 deoR recA1 endA1 hsdR17(rk- mk+) phoA supE44l- thi-1 gyrA96 relA1 [52] X. dendrorhous:     UCD 67-385 ATCC 24230, wild type. ATCC Diploid strain [30] 385-cyp61 (+/−) (385-CYP61/cyp61 hph ). Heterozygote transformant derived from UCD 67–385 containing an allele of the CYP61 locus interrupted with

a hygromycin B resistance cassette. This work 385-cyp61 (−/−) (385-cyp61 hph /cyp61 BCKDHB zeo ). Homozygote transformant derived by transformation of 385-cyp61 +/− with both CYP61 alleles interrupted, one with a hygromycin B resistance cassette and the other with a zeocin resistance cassette. This work CBS 6938 ATCC 96594, wild type. ATCC CBS-cyp61 (−) (CBS-cyp61 hph ). Hemizygote transformant derived from CBS 6938. The single CYP61 locus was interrupted with a hygromycin B resistance cassette. This work AVHN2* Chilean native isolate, wild type. Our Lab collection Av2-cyp61 (−) (Av2-cyp61 zeo ). Hemizygote transformant derived from AVHN2. The single CYP61 locus was interrupted with a zeocin resistance cassette. This work UCD 67-210 ATCC 24202, wild type (Phaffia rhodozyma) ATCC VKM Y-2786 Wild-type strain.

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“Background Following emergence of resistance to inexpensive broad-spectrum antimicrobials across much of Africa, quinolone antibacterials have recently been introduced and are widely used. West African studies that sought quinolone resistance in

commensal or diarrhoeagenic Escherichia coli before 2004 reported no or very low incidences of resistance to nalidixic acid and the fluoroquinolones [1–4]. Thus, available data suggests that resistance to the quinolones was rare in West Africa until the first decade of the 21st century. More recent anecdotal reports and surveillance studies point to emergence of quinolone resistance among enteric pathogens and faecal enteric bacteria in Ghana and elsewhere in West Africa CP673451 solubility dmso [5–8]. In a study by Nys et al. (2004) faecal isolates of adult volunteers in eight different countries were assessed for susceptibility to antimicrobials in the same laboratory [8]. Resistance to broad spectrum first-generation antibiotics GSK2126458 research buy was common and ciprofloxacin resistance was found to be slowly emerging in Asian, South American and African countries, including Ghana [8]. Newman et al. (2004) collected 5099 clinical bacterial isolates (1105 of which were E. coli) from nine of the ten regions in Ghana and tested them for antimicrobial susceptibility. They found that over 70% of the isolates were resistant to tetracycline, trimethoprim-sulphamethoxazole,

ampicillin and chloramphenicol and reported that 11% of the isolates were ciprofloxacin-resistant [7]. Quinolones inhibit the activity of bacterial DNA gyrase and DNA topoisomerase enzymes, which are essential for replication. Selumetinib nmr Single nucleotide polymorphisms

(SNPs) in the quinolone resistance determining regions (QRDR) of gyrA and parC, the two genes that encode DNA gyrase and topoisomerase IV respectively, can lead to conformational changes in these enzymes that cause them to block quinolones from binding to the DNA- substrate complex, yet still preserve their enzymatic function [9]. In Escherichia coli and related Gram-negative bacteria, DNA gyrase is the first target for fluoroquinolones. If gyrA has resistance-conferring mutations, the primary target of fluoroquinolone switches from DNA gyrase to topoisomerase IV [10, ID-8 11]. Studies from other parts of the world have found that resistance-conferring mutations are typically selected in gyrA first, and then parC. Although mutations in the QRDR of gyrA and parC are the most commonly documented resistance mechanisms, resistance has also been known to be conferred by mutations in the second topoisomerase gene, parE. Another mechanism of quinolone resistance relies on upregulation of efflux pumps, which export quinolones and other antimicrobials out of the bacterial cell. For example, mutations in the gene encoding a repressor of the acrAB pump genes, acrR, are associated with quinolone resistance [12].