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Microxin (Norfloxacin)
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Norfloxacin

Microxin is a fluoroquinolone antibiotic. Other fluoroquinolones include ciprofloxacin (Cipro), levofloxacin (Levaquin), and ofloxacin (Floxin). Microxin works by blocking DNA gyrase enzyme, which is responsible for production and repair of bacterial DNA. Blocking of DNA gyrase leads to bacteria death and prevents worsening of infection. Microxin treats infections caused by gram-positive and gram-negative bacteria like Enterococcus faecalis, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus saprophyticus, Streptococcus agalactiae, Citrobacter freundii, Enterobacter aerogenes, Enterobacter cloacae, Escherichia coli, Klebsiella pneumonia, Neisseria gonorrhoeae, Proteus mirabilis, Proteus vulgaris, Pseudomonas aeruginosa, and Serratia marcescens. FDA approved the brand name Microxin (Microxin) in October 1986.

Other names for this medication:
Norfloxacin, Noroxin, Ambigram, Baccidal, Barazan, Bexinor, Chibroxin, Chibroxine, Danilon, Epinor, Firin, Flox, Floxatral, Grenis, Janacin, Lexinor, Loxone, Microxin, Nalion, Noflo, Nolicin, Noprose, Noracin, Norax, Norbactin, Norflohexal, Norilet, Normax, Noroxine, Norsol, Norzen, Nufloxib, Oranor, Renor, Respexil, Senro, Shinun, Trizolin, Uritracin, Uroxacin, Utinor, Zoroxin,

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An experimental study confirmed that bias due to the presence of the sampling line is small. However, the lower therapeutic benefit and the high proportion of topical steroid use indicate a need for optimized therapy. Pulsing of dendritic cells with cell lysates from either B16 melanoma or MCA-106 fibrosarcoma yields equally effective vaccines against B16 tumors in mice. These results, obtained with a modified fixation procedure, which is described, have been checked by supravital observation.

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Cultured human fibroblasts display age-dependent transcriptomic differences. Side effects of these agents are consistent with the physiological effects of ovarian suppression, such as vasomotor instability, vaginal dryness, and headaches. Three cases of psychogenic G-force intolerance are presented with a discussion of common factors. In addition, our results raise interesting issues about evaluating the significance of rare genetic variants in disease and their role in causation.

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