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Chelation interactions between drugs/supplements that contain large amounts of multivalent ions and the fluoroquinolones have been known for quite some time. However, there has been a lack of taking this interaction into account when they may be coadministered with foods that have been fortified with amounts of multiple multivalent ions that equal or exceed many supplement products. A previous study demonstrated that 12 ounces of calcium-fortified orange juice significantly decreased the bioequivalence of a dose of ciprofloxacin. This study examined, in 16 healthy volunteers, whether 12 ounces of orange juice with and without calcium fortification would demonstrate the same chelation interaction with single doses of levofloxacin. The results of the study demonstrated that both types of juice decreased levofloxacin Cmax values by 14% to 18% and prolonged tmax values by approximately 50%, with calcium-fortified orange juice decreasing Cmax enough to lose bioequivalence as compared to the control arm (89% [78.1%, 99.8%]). Due to the lack of change in overall exposure, it is thought that rather than a chelation interaction, levofloxacin and components of the orange juices competed for intestinal transport mechanisms such as P-glycoprotein and organic anion-transporting polypeptides, which resulted in the discovered interaction. These results further confirm the need to adjust regulatory studies to include bioequivalence/bioavailability studies that contain fortified foods more than high-calorie/high-fat foods to better reflect current American consumption habits.
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We isolated and detected bacteria from phlegm, throat swabs, urine, wound or wound secretions, blood, and fecal samples from 221 liver transplant patients in our hospital from January 2007 to April 2010. All isolated bacterial strains were identified and tested by minimal inhibitory concentration (MIC) drug-sensitive detection using the BioMerieux ATB bacterial identification instrument and repetitive extragenic palindromic-polymerase chain reaction (REP-PCR) detection of bacterial homology. Risk factors were calculated by multivariate Logistic regression analysis.
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We developed a case-control study in order to identify risk factors associated with pharyngeal colonization by Streptococcus pneumoniae with reduced susceptibility to fluoroquinolones (ciprofloxacin MIC, > or =4 microg/ml). A total of 400 patients were studied for colonization by quinolone-nonsusceptible S. pneumoniae (QNSP) isolates and risk factors for this colonization. Isolate susceptibility was determined by the agar dilution method. Forty patients were colonized by QNSP (case patients), and 360 patients were not colonized by QNSP (control patients). The MIC range of ciprofloxacin for QNSP isolates was 4 to 8 microg/ml. No isolates were resistant to levofloxacin and moxifloxacin. Risk factors significantly associated with QNSP colonization, according to univariate analysis, were recent hospitalizations (odds ratio [OR], 3.43; 95% confidence interval [CI], 1.6 to 7.2; P < 0.01) and prior exposure to fluoroquinolones (OR, 6.04; 95% CI, 3.0 to 12.0; P < 0.01). Other factors such as chronic obstructive pulmonary disease (OR, 1.94; 95% CI; 0.7 to 5.0), prior exposure to penicillins (OR, 1,68; 95% CI, 0.8 to 3.3) and prior exposure to macrolides (OR 2; 95% CI, 0.6 to 6.2) were more frequent among patients colonized with QNSP, but there was no statistical significance. Multivariate analysis showed that exposure to fluoroquinolones was the only independent factor associated with colonization by QNSP (OR, 4.2; 95% CI, 1.8 to 9.4; P < 0.01). Throat colonization by QNSP is becoming frequent, though most of these isolates (all the isolates in this case) remain susceptible to newer fluoroquinolones. Previous treatment with fluoroquinolones seems to be the main risk factor associated with colonization by QNSP.
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Although gatifloxacin is no longer available, other fluoroquinolones may significantly interfere with glucose homeostasis. The objective of the present study was to compare the risk of severe hypo- and hyperglycemia in a cohort of patients treated with gatifloxacin, levofloxacin, ciprofloxacin, or azithromycin.
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DS-8587 is a novel broad-spectrum fluoroquinolone with extended antimicrobial activity against both Gram-positive and Gram-negative pathogens. In this study, we evaluated the in vitro and in vivo antibacterial activity of DS-8587 against multidrug-resistant (MDR) Acinetobacter baumannii. The MIC range of DS-8587 against MDR A. baumannii was 0.25-2 mg/L. These DS-8587 MICs were a minimum of 16-fold or 8-fold more potent than ciprofloxacin or levofloxacin, respectively. Bactericidal activity, a 3 log10 reduction from the initial bacterial counts, was observed within 2 h for 1593644 and 4 h for 1593684 after exposure to DS-8587. Therapeutic efficacy of DS-8587 in the murine calf muscle model was observed at 256 mg/kg. The analysis of the pharmacokinetic and pharmacodynamic index revealed that the AUC/MIC ratio showed the best correlation with efficacy. The total and free drug AUC/MIC value required for a static effect was 29.4 and 14.1, respectively. These data indicate DS-8587 would be an effective agent against MDR A. baumannii infection.
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The interaction between pharmaceutical and protein is an important pharmacokinetic characteristic. Most kinds of drugs must reach the receptor to perform the pharmacological function by plasma. Albumins can serve as a depot protein and a transport protein for numerous endogenous and exogenous compounds. It is of great significance to investigate the binding interaction between albumin and drugs, since it can not only help understand the transportation and distribution of drugs but also elucidate the mechanism. Under the physiological condition of body, the interaction between levofloxacin (LVFX) and bovine serum albumin (BAS) was investigated by fluorescence spectra and ultraviolet absorbance (UV) spectra based on liquid drop. The experimental results showed that LVFX quenches the fluorescence of BAS by forming a LVFX-BSA complex. According to Lineweaver-Burk equation, the apparent binding constants (K(LB)) between LVFX and BSA were 1.694 9 x 10(5) L x mol(-1) (291 K) and 2.881 0 x 10(5) L x mol(-1) (310 K), and the binding sites (n) were 0.884 9 (291 K) and 0.808 9 (310 K). Thermodynamic parameters could be evaluated from the thermodynamic second law, with deltaH (enthalpy) being 20.94 kJ mol(-1) and deltaS (entropy) being 172.1 J x mol(-1). According to the relation between thermodynamic parameters and the interaction force, LVFX depended principally on the hydrophobic interaction to bind with BSA. The results showed that the quenching belonged to static fluorescence quenching with non-radiation energy transfer happening within single molecule. The binding locality was an area 2.68 nm away from tryptonphan residue-212 in BAS according to Forster's non-radiation energy transfer mechanism. The conformational changes of BSA were evaluated by measuring the synchronous fluorescence intensity of protein amino acid residues, both before and after the addition of LVFX. A slightly stronger blue-shift of tryptophan fluorescence upon the addition of drug was observed, and the emission maximum of tyrosine kept its position. It was suggested that the environments of tryptophan residues in pure albumin solution are relatively polar. Binding of LVFX changes the environments to apolar ones. The shift in polarity is brought about by confirmation changes due to the interaction between albumin and ligand molecule.
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Because the treatment of inhalational anthrax cannot be studied in human clinical trials, it is necessary to conduct efficacy studies using a rhesus monkey model. However, the half-life of levofloxacin was approximately three times shorter in rhesus monkeys than in humans. Computer simulations to match plasma concentration profile, area under the concentration-time curve (AUC), and time above MIC for a human oral dose of 500 mg levofloxacin once a day identified a dosing regimen in rhesus monkeys that would most closely match human exposure: 15 mg/kg followed by 4 mg/kg administered 12 h later. Approximately 24 h following inhalational exposure to approximately 49 times the 50% lethal doses of Bacillus anthracis (Ames strain), monkeys were treated daily with vehicle, levofloxacin, or ciprofloxacin for 30 days. Ciprofloxacin was administered at 16 mg/kg twice a day. Following the 30-day treatment, monkeys were observed for 70 days. Nine of 10 control monkeys died within 9 days of exposure. No clinical signs were observed in fluoroquinolone-treated monkeys during the 30 treatment days. One monkey died 8 days after levofloxacin treatment, and two monkeys from the ciprofloxacin group died 27 and 36 days posttreatment, respectively. These deaths were probably related to the germination of residual spores. B. anthracis was positively cultured from several tissues from the three fluoroquinolone-treated monkeys that died. MICs of levofloxacin and ciprofloxacin from these cultures were comparable to those from the inoculating strain. These data demonstrate that a humanized dosing regimen of levofloxacin was effective in preventing morbidity and mortality from inhalational anthrax in rhesus monkeys and did not select for resistance.
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Using a simple model, we analyzed the transport of organic cation in kidney epithelial cell line, LLC-PK1. This method can be useful for the analysis of cation transport and drug interactions in the apical and basolateral membranes of renal tubules.
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The use of chalazion forceps is effective in treating chronic suppurative lacrimal canaliculitis. The forceps may offer an alternative treatment technology in the management of suppurative lacrimal canaliculitis.
In single-drug experiments, at 48 hours, tinidazole alone did not show significant killing of the entire bacterial population, whereas reductions in the initial inocula > or =2.09 log(10) CFU/ml with clindamycin, > or =3.26 log(10) CFU/ml with amoxicillin/clavulanic acid, and > or =3.83 log(10) CFU/ml with levofloxacin were obtained. When combined with tinidazole, reductions were significantly higher for all antibiotics: > or =5.28 log(10) CFU/ml with clindamycin, > or =4.78 log(10) CFU/ml with amoxicillin/clavulanic acid, and > or =6.17 log(10) CFU/ml with levofloxacin.