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RO 23-6240 (fleroxacin), pefloxacin, augmentin, cefaclor, cef-uroxime, ceftazidime, vancomycin, piperacillin and amikacin were tested against a wide variety of gram-positive and gram-negative bacteria. The MICs of fleroxacin were very similar to those of pefloxacin. Against all the bacterial groups tested, the quinolones compared favorably with the other antimicrobials tested, particularly against the more resistant species such as Corynebacterium group JK and D2 and methicillin-resistant staphylococci.
Antibiotics are heavily used in Chinese mariculture, but only a small portion of the added antibiotics are absorbed by living creatures. Biofilm processes are universally used in mariculture wastewater treatment. In this study, removal of antibiotics (norfloxacin, rifampicin, and oxytetracycline) from wastewater by moving bed biofilm reactors (MBBRs) and the influence of antibiotics on reactor biofilm were investigated. The results demonstrated that there was no significant effect of sub-μg/L-sub-mg/L concentrations of antibiotics on TOC removal. Moreover, the relative abundance of antibiotic resistance genes (ARGs) and antibiotic resistance bacteria (ARB) in MBBR biofilm increased because of selective pressure of antibiotics. In addition, antibiotics decreased the diversity of the biofilm bacterial community and altered bacterial community structure. These findings provide an empirical basis for the development of appropriate practices for mariculture, and suggest that disinfection and advanced oxidation should be applied to eliminate antibiotics, ARGs, and ARB from mariculture wastewater.
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Emergence of resistance to fluoroquinolones was observed in two clinical isolates of Pseudomonas aeruginosa after ciprofloxacin or norfloxacin monotherapy. In the first case, the resistant variants exhibited quinolone-imipenem cross-resistance (MIC of norfloxacin and ciprofloxacin: 16 mg/L; MIC of imipenem: 8 mg/L), although the patient had never received imipenem treatment, while the strain from the second case remained imipenem-susceptible (MIC of norfloxacin or ciprofloxacin: 8 mg/L; MIC of imipenem: 2 mg/I). The frequency of in-vitro emergence of variants resistant to imipenem and fluoroquinolones was studied for the two strains, with imipenem or fluoroquinolones as selecting agents. Ciprofloxacin and three other quinolones (norfloxacin, temafloxacin and tosufloxacin) selected imipenem-resistant variants in a similar way to imipenem for the first strain, but not for the other. In contrast, imipenem did not select quinolone-resistant variants from either strain. For both strains, killing curves demonstrated that a bactericidal effect could be obtained with a drug combination (2 x MIC of ciprofloxacin and 2 x MIC of imipenem) without any selection of resistant mutants after 24 h, thereby suggesting the possible use of this combined regimen for treating severe P. aeruginosa infection.
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Quinobenzoxazine A-62176, developed from the antibacterial fluoroquinolones, is active in vitro and in vivo against murine and human tumors. It has been previously claimed that A-62176 is a catalytic inhibitor of mammalian topoisomerase II that does not stabilize the cleaved complex. However, at low drug concentrations and pH 6-7, we have found that A-62176 can enhance the formation of the cleaved complex at certain sites. Using a photocleavage assay, mismatched sequences, and competition experiments between psorospermin and A-62176, we pinpointed the drug binding site on the DNA base pairs between positions +1 and +2 relative to the cleaved phosphodiester bonds. A 2:2 quinobenzoxazine-Mg2+ self-assembly model was previously proposed, in which one drug molecule intercalates into the DNA helix and the second drug molecule is externally bound, held to the first molecule and DNA by two Mg2+ bridges. The results of competition experiments between psorospermin and A-62176, as well as between psorospermin and A-62176 and norfloxacin, are consistent with this model and provide the first evidence that this 2:2 quinobenzoxazine-Mg2+ complex is assembled in the presence of topoisomerase II. These results also have parallel implications for the mode of binding of the quinolone antibiotics to the bacterial gyrase-DNA complex.
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A total of 14,272 urine specimens were examined over one year to determine the validity of direct antimicrobial agent susceptibility testing against ampicillin, amoxicillin-clavulanic acid, cephalothin, gentamicin, norfloxacin, and trimethoprim. A comparison between direct and standardized disk diffusion tests was made for a total of 1,106 urine specimens containing > or = 10(5) organisms per ml in pure culture. There were 5,821 individual organism-antimicrobial agent challenges compared for the two testing methods, and there was complete agreement of susceptibility category in 5,492 comparisons (94.3%). Initially, discordant results were reduced from 5.7 to 2.1% when the intermediate category was considered susceptible. Intralaboratory variation was assessed by testing another 453 organisms by the standard National Committee for Clinical Laboratory Standards (NCCLS) method on two consecutive days; there was complete agreement in 96.1% of comparisons. When results of direct and standardized testing were simply classified as susceptible or resistant, there was 1.1% discordance. When simple same-day tests were used together with predictable patterns of susceptibility and resistance, 536 (48.5%) of 1,106 isolates could be identified satisfactorily to the genus or species level. For laboratory reporting purposes, the direct method is equivalent to the standard method when the urine being tested is infected with > or = 10(5) organisms of a single type per ml. The presence or absence of preexisting antimicrobial agents in urine did not appreciably influence the results. This procedure allows the earlier reporting of susceptibility results and facilitates less expensive identification of many organisms. Costs and benefits need to be determined in each institution.
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In the present study, a novel strategy was developed to construct lipid prodrug of norfloxacin. N-Mannich base of norfloxacin was synthesized. The prodrug was obtained by covalently coupling this N-Mannich base with fatty acid hydrazide. The synthesized prodrug was characterized by spectral as well as other physical analysis. The hydrolytic studies of prodrug in buffers (pH 1.2 and 7.4), simulated gastric and intestinal fluid by HPLC analysis were undertaken. The studies revealed that prodrug liberates only about 2% of norfloxacin in HCl buffer (pH 1.2) as compared to about 8% in phosphate buffer (pH 7.4) in first 3 h. The synthesized prodrug was found to exhibit improved partition coefficient (1.15) when compared with parent drug, norfloxacin (0.46). The results of antimicrobial evaluation indicates remarkable antibacterial activity with MICs of 8.5 µg/ml, 20 µg/ml, 10 µg/ml against S. aureus MTCC 96, P. aeruginosa MTCC 1688 and E. coli MTCC 443 respectively when compared with standard drugs. Moreover the prodrug showed promising antifungal activity having MICs 250 µg/ml, 75 µg/ml and 100 µg/ml against C. albicans MTCC 227, A. niger MTCC 282 and A. clavatus MTCC 1323 respectively.
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The in-vitro activity of fleroxacin (Ro23-6240), a new synthetic quinolone, was compared with that of three other quinolones against 665 clinical isolates of aerobic bacteria by the agar dilution technique. Fleroxacin showed similar activity to norfloxacin, enoxacin and pefloxacin against most isolates of Enterobacteriaceae, Neisseria meningitidis, N. gonorrhoeae, Haemophilis influenzae, Staphylococcus spp. and streptococcus faecalis. Fleroxacin was the most active quinolone against Enterobacter spp. Fleroxacin was not as active against Pseudomonas aeruginosa, but the MIC90 (4 mg/l) is still below the reported peak serum level after a standard oral dose of 400 mg.
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An indirect competitive enzyme-linked immunosorbent assay (ELISA) was developed to detect ciprofloxacin (CPFX) in food animal edible tissues. CPFX was converted by an active ester method into conjugates CPFX-bovine serum albumin (CPFX-BSA) and CPFX-human serum albumin (CPFX-HSA), which both allowed production of CPFX-specific rabbit antisera. In the ELISA, CPFX-HSA was coated onto the microtiter plate, followed by incubation with standard CPFX and anti-CPFX antibody. The indirect competitive ELISA revealed that the antisera have no cross-reactivity with penicillin, gentamicin, neomycin, sulfadiazine, and chlortetracycline. The antisera cross-reacted with enrofloxacin and norfloxacin about 69.8 and 44.6% as much as they did with CPFX. This ELISA was highly sensitive (0.32 ng/mL) to CPFX determination. Recovery of CPFX at 40 microg/kg was 75.58% in pork, 81.29% in chicken, and 84.30% in milk. The coefficients of variation varied from 3.7 to 9.2% over the range of CPFX concentrations studied. The linear detection range was between 1.6 and 1000 ng/mL. The results suggest that this ELISA is a specific, accurate, and convenient method for the detection of CPFX residues in food animal edible tissues.
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It was a cross-sectional descriptive community based study to collect ABR data from Out Patient Department (OPD) of two leading Teaching Hospitals in Colombo district. The indicator organism Escherichia coli (E. coli) was obtained from the urine specimens of patients who were suspected to have urinary tract infections. Antibiotic susceptibility testing was performed for commonly used oral antibiotics using disc diffusion method. The antibiotic consumption aggregate data were collected from the OPD pharmacies of the said hospitals and expressed as Defined Daily Doses (DDD) per 1000 inhabitants per 1000 day.
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While cell-based screens have considerable power in identifying new chemical probes of biological systems and leads for new drugs, a major challenge to the utility of such compounds is in connecting phenotype with a cellular target. Here, we present a systematic study to elucidate the mechanism of action of uncharacterized inhibitors of the growth of Escherichia coli through careful analyses of interactions with compounds of known biological activity. We studied growth inhibition with a collection of 200 antibacterial compounds when systematically combined with a panel of 14 known antibiotics of diverse mechanism and chemical class. Our work revealed a high frequency of synergistic chemical-chemical interactions where the interaction profiles were unique to the various compound pairs. Thus, the work revealed that chemical-chemical interaction data provides a fingerprint of biological activity and testable hypotheses regarding the mechanism of action of the novel bioactive molecules. In the study reported here, we determined the mode of action of an inhibitor of folate biosynthesis and a DNA gyrase inhibitor. Moreover, we identified eight membrane-active compounds, found to be promiscuously synergistic with known bioactives.