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At least 199 records · Page 11Linked to original sources
PubMed1983

Cefoxitin versus erythromycin, neomycin, and cefazolin in colorectal operations. Importance of the duration of the surgical procedure.

Perioperative parenteral cefoxitin was compared with oral erythromycin, neomycin and parenteral cefazolin in a prospective, double-blind, randomized evaluation of 119 patients undergoing colorectal operations. Patients receiving cefoxitin had a higher wound infection rate than patients receiving erythromycin-neomycin-cefazolin (12.5% v 3.2%, respectively, p = .06). A direct correlation existed between the duration of the operation and the infection rate. Cefoxitin prophylaxis was as effective as erythromycin-neomycin-cefazolin in patients undergoing surgical procedures of 4 hours or less (infection rates of 4.8% and 4.0%, respectively). However, for surgical procedures lasting more than 4 hours, 5 of 14 patients (37.5%) receiving cefoxitin developed a wound infection v 0 of 13 patients receiving erythromycin-neomycin-cefazolin (p less than .05). It is speculative as to whether frequent two-gram doses of cefoxitin given during the operation would provide prophylaxis equivalent to erythromycin-neomycin-cefazolin.

Cefazolin↗
PubMed1999

The bacterial Neo gene confers neomycin resistance to mammalian cochlear hair cells.

The aminoglycoside antibiotics are important agents in the treatment of bacterial infection. At pharmacological doses they also preferentially damage the sensory hair cells of the inner ear, leading to ototoxic hearing loss. However, it has been suggested that the mechanism of ototoxicity is different from that of bacterial toxicity. The bacterial neomycin phosphotransferase gene (Neo) confers resistance to this and related aminoglycoside antibiotics. To determine whether the Neo gene also confers resistance to vertebrate ototoxicity, the sensitivity of cochlear hair cells to neomycin was evaluated in mice with a targeted insertion of Neo. Organotypic cultures of the organ of Corti, isolated from neonatal wild-type mice and two strains of mice carrying the Neo gene, were cultured for 72 h in the absence (controls) or in the presence of 200 microM neomycin. Organs from wild-type mice showed no remaining outer hair cells and <25% of inner hair cells when incubated with neomycin. In contrast, organs from mice carrying the Neo gene showed no loss of hair cells after neomycin treatment.

Animals↗
PubMed2006

Prospective randomised single-blind controlled trial of glacial acetic acid versus glacial acetic acid, neomycin sulphate and dexamethasone spray in otitis externa and infected mastoid cavities.

OBJECTIVES: The literature reports the merits of antibacterial, antibiotic and steroid agents in treating otological infections but no controlled clinical trial has directly compared 2% glacial acetic acid (EarCalm; Stafford-Miller Ltd, Brentford, UK) against 2% glacial acetic acid, 0.1% dexamethasone and 3250 U/ml of neomycin sulphate (Otomize; Stafford-Miller Ltd) in the treatment of otitis externa and infected mastoid cavities. DESIGN: Prospective, single-blind randomised controlled trial. SETTING: Outpatients, Derby Royal Infirmary, Derby, UK. PATIENTS: Emergency and GP referrals with acute otitis externa (n = 53) and infected mastoid cavities (n = 56). MAIN OUTCOME MEASURES: Otoscopy was performed at initial randomisation and then at 2 and 4 weeks, the ear assessed for active and inactive disease. RESULTS: Patients with active otitis externa, 71% (15/21) resolved with glacial acetic acid, dexamethasone and of neomycin sulphate after 2 weeks, increasing to 86% (18/21) after 4 weeks treatment. Patients on glacial acetic acid had only 38% (12/32) resolution after 4 weeks (P < 0.0005). Two per cent glacial acetic acid, dexamethasone and neomycin sulphate resolved only 30% (8/27) of infected mastoid cavities compared to only 10% (3/29) on glacial acetic acid (P < 0.07). A further 2 weeks treatment this increased to 67%, (18/27) with glacial acetic acid, dexamethasone and neomycin sulphate and 48% (14/29) with glacial acetic acid. These results are not statistically significant. CONCLUSION: Glacial acetic acid, dexamethasone and neomycin sulphate is significantly more effective in treating otitis externa when compared with glacial acetic acid. This effect failed to be significant in the infected mastoid cavities group. We therefore recommend that in conjunction with aural toilet, antibiotic/steroid combination is more effective than an antibacterial agent for otitis externa. Larger numbers of infected mastoid cavities are required to be studied.

Acetic Acid↗
PubMed1994

In vitro interactions of neomycin sulfate, bacitracin, and polymyxin B sulfate.

BACKGROUND: Neomycin sulfate, bacitracin, and polymyxin B sulfate have been combined in topical preparations to provide a complementary antimicrobial spectrum for the prevention of minor wound infections. The advisability of the inclusion of neomycin sulfate has been questioned since it may cause contact sensitization. METHODS: To assess the value of neomycin, microdilution checkerboard titrations were used to determine the in vitro interactions between two-antibiotic and three-antibiotic combinations against reference strains of bacteria commonly associated with wound infections. Using Fractional Inhibitory Concentration (FIC) indices (< 0.5 indicates synergism with two-drug combinations), the combination of neomycin/bacitracin was synergistic for both S. aureus and Ps. aeruginosa; neomycin/polymyxin B was synergistic for E. faecalis, and the bacitracin/polymyxin B combination was synergistic against Ps. aeruginosa. A three-drug combination of neomycin/bacitracin/polymyxin B had FIC values of < 1 for all organisms, indicating synergy and substantiating the clinical role of neomycin sulfate in current topical formulations. RESULTS: Neomycin has the lowest safety profile of the drugs in this combination. A replacement agent should ideally have similar or superior synergistic capabilities with the remaining drugs and contribute to the therapeutic efficacy of the preparation. Additionally, because of the strongly synergistic tendencies displayed by the three-drug combination, it may be possible to reduce the antibiotic concentrations present in current formulations. CONCLUSION: By developing this concept, there is potential for the formulation of topical preparations to be based on a sound theoretical and clinical rationale.

Bacitracin↗
PubMed1988

Neomycin inhibits platelet functions and inositol phospholipid metabolism upon stimulation with thrombin, but not with ionomycin or 12-O-tetradecanoyl-phorbol 13-acetate.

Gel-filtered human platelets that had been pre-labelled with [32P]Pi were stimulated with thrombin, ionomycin or the phorbol ester 12-O-tetradecanoyl-phorbol 13-acetate (TPA). The effect of the hexacationic aminoglycoside antibiotic, neomycin, on platelet physiological responses, such as aggregation and secretion, as well as changes in phosphoinositide metabolism was studied. Neomycin strongly inhibited thrombin-induced aggregation and secretion whereas the antibiotic had no effect on ionomycin- or TPA-induced platelet functions. The thrombin-induced enhancement of inositol phospholipid metabolism was strongly inhibited by the presence of neomycin whereas the TPA- or ionomycin-induced increase in inositol [32P]polyphospholipids remained unaffected. The inhibitory effect of some other aminoglycoside antibiotics was compared to that of neomycin and the data demonstrate that the inhibition of platelet secretion and phosphatidic acid production was dependent on the cationic charge of the antibiotic. It is suggested that neomycin inhibits signal transduction in platelets at a level prior to the inositol-phospholipid-specific phosphodiesterase.

Blood Platelets↗
PubMed1997

The effect of neomycin on the kidney function of the horse.

The toxic effect of neomycin on the horse kidney was studied. Twelve horses were used, and were divided at random into three groups of four. The first group was treated twice a day with 10 mg/kg I.M. for 15 days and then euthanised; kidney and liver samples were studied and no histopathological changes were observed. Group 2 was treated with neomycin sulphate as in group 1, and group 3 was used as control. Blood samples were taken at 8.00 h and 20.00 h daily from both neomycin treated and control horses. Serum creatinine, potassium, sodium and urinary creatinine remained without change. On day 6 of treatment plasma urea (Urea)p decreased to 5.6 +/- 2.0 mmol/L (P < 0.001) as compared with controls (8.0 +/- 2 mmol/L). Urinary excretion of GGT increased on the third day of treatment to 118.6 +/- 1 IU/L for treated and 89 +/- 8 IU/L for controls (P < 0.001). Thereafter, GGT continued to be elevated significantly for the duration of the experiment, as compared with controls. The (GGT)/(Cr)u ratio increased significantly on the 9th day of treatment, and continued to be elevated for 6 days after treatment. Neomycin kinetics were similar during treatment. It was concluded that neomycin, in the dose used, was not harmful to kidney function in the horse.

Animals↗
PubMed1989

Comparison of the effects of calcium and the calcium channel stimulant Bay k 8644 on neomycin-induced neuromuscular blockade.

The effects of calcium and the calcium channel stimulant Bay k 8644 on neomycin-induced neuromuscular blockade were evaluated using rat phrenic nerve-hemidiaphragm preparations in vitro. neomycin showed maximum potency in inducing neuromuscular blockade when the calcium concentration in the bath was 1 mM. Higher calcium concentrations (1.5, 2 and 4 mM) produced a gradual decrease in neomycin potency, manifested as a progressive shift to the right of neomycin concentration-response curves. Bay k 8644 (0.1 and 1 microM) did not significantly modify indirectly elicited diaphragm contractions per se, nor did it antagonize neomycin-induced neuromuscular blockade. A higher concentration of Bay k 8644 (10 microM) antagonized indirectly elicited contractions. In conclusion, our results show that Bay k 8644, at concentrations causing calcium channel stimulation at the cardiac and vascular level, did not exert stimulant effects in a nerve-skeletal muscle preparation, suggesting that its action may be tissue-selective to a certain degree.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Inhibition by lithium of neomycin-induced release of N-acetyl-beta-glucosaminidase in the rat heart.

The effects of neomycin, lithium and concurrent therapy of these drugs on subcellular distribution of lysosomal enzyme, N-acetyl-beta-glucosaminidase (NAG) in the heart was studied. Released activity of NAG was used as a marker for assessing myocardial lysosomal integrity. The activity of NAG was determined in non-sedimentable and sedimentable fractions after centrifugation of the tissue extracted for assessment of the subcellular distribution of the lysosomal enzyme. Daily intraperitoneal injection of 100 mg/kg/day of neomycin increased the ratio of the non-sedimentable activity (free) to the non-sedimentable plus sedimentable activities (total) of NAG. Daily intraperitoneal injection of lithium decreased the total activity of NAG but did not affect the ratio of free: total activities of the enzyme. Lithium in doses of 2 and 4 mM/kg/day one hour prior to neomycin reduced the neomycin-induced enhancement of the ratio of free: total activity of NAG. Neomycin like other aminoglycosides altered the acidic phospholipid metabolism in lysosomal membranes and/or impairment of some important lysosomal functions. In this regard, the protective effects of lithium may be due to interference of this ion with phosphoinositide cycle.

Acetylglucosaminidase↗
PubMed2005

Binding of PLCdelta1PH-GFP to PtdIns(4,5)P2 prevents inhibition of phospholipase C-mediated hydrolysis of PtdIns(4,5)P2 by neomycin.

AIM: To investigate the effects of the pleckstrin homology (PH) domain of phospholipase C(delta1) (PLC(delta1)PH) on inhibition of phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] by neomycin. METHODS: A fusion construct of green fluorescent protein (GFP) and PLC (delta1)PH (PLC(delta1)PH-GFP), which is known to bind PtdIns(4,5)P2 specifically, together with laser-scanning confocal microscopy, was used to trace PtdIns(4,5)P2 translocation. RESULTS: Stimulation of the type 1 muscarinic receptor and the bradykinin 2 receptor induced a reversible PLC(delta1)PH-GFP translocation from the membrane to the cytosol in COS-7 cells. PLC inhibitor U73122 blocked the translocation. Wortmannin, a known PtdIns kinase inhibitor, did not affect the translocation induced by ACh, but blocked recovery after translocation, indicating that PtdIns(4,5)P2 hydrolysis occurs through receptor-mediated PLC activation. Neomycin, a commonly used phospholipase C blocker, failed to block the receptor-induced PLCd1PH-GFP translocation, indicating that neomycin is unable to block PLC-mediated PtdIns(4,5)P2 hydrolysis. However, in the absence of PLCd1PH-GFP expression, neomycin abolished the receptor-induced hydrolysis of PtdIns(4,5)P2 by PLC. CONCLUSION: Although PLCd1PH and neomycin bind to PtdIns(4,5)P2 in a similar way, they have distinct effects on receptor-mediated activation of PLC and PtdIns(4,5)P2 hydrolysis.

Acetylcholine↗
PubMed1978

Nonvalue of neomycin instillation after intermittent urinary catheterization.

This study evaluated weekly urine cultures of patients with neurogenic bladder disease who underwent intermittent urinary catheterization for bladder retraining. One group of 53 patients in 1974 received regular instillations of 0.1% neomycin after each catheterization. A similar group of 55 patients in 1975 did not receive neomycin and constituted a control group. Distribution of age, sex, diagnosis, and duration of bladder retraining was comparable in both groups. Quantitative bacterial colony counts of 10(4) to 10(5) or greater per ml of urine were considered significant. There was no difference in the incidence of bacteriuria between the neomycin-treated group and the control group (53 versus 49%, respectively), and most patients in each group had colony counts >10(5)/ml. Escherichia coli was seen less frequently in neomycin-treated patients (43.4 versus 62.5%), but a greater percentage of infections due to Pseudomonas aeruginosa, group D streptococci, and yeasts was noted in the neomycin-treated group than in the control group (41.5 versus 22.5%).

Bacteriuria↗
PubMed1973

Two enzymes which phosphorylate neomycin and kanamycin in Escherichia coli strains carrying R factors.

Two enzymes which phosphorylate neomycin and kanamycin have been detected in Escherichia coli strains carrying R factors. Neomycin-kanamycin phosphotransferase I can phosphorylate neomycin and kanamycin, but not butirosin. Neomycin-kanamycin phosphotransferase II can phosphorylate all three antibiotics. The enzymes also differ in their response to certain inhibitors of phosphorylation. Neomycin-kanamycin phosphotransferase II is found in certain strains of Pseudomonas aeruginosa.

Drug Resistance, Microbial↗
PubMed1973

Selective isolation of leptospiras from contaminated material by incorporation of neomycin to culture media.

Incorporation of neomycin to the culture medium was found to be effective in inhibiting Escherichia coli contaminants without interfering with the growth of serotype L. autumnalis. The growth of 12 other Leptospira serotypes was unaffected by the addition of 300 mug of neomycin per ml to Ellinghausen medium or 5 mug/ml to Fletcher medium. Neomycin-containing medium was found to be of value in the isolation of leptospiras from cultures of blood from infected laboratory animals. A higher percentage of isolates was obtained in swine kidneys from an abattoir in medium containing neomycin than resulted from the same medium without antibiotic or with 5-fluorouracil. Contaminated leptospiral cultures growing in media with 5-fluorouracil were purified by subculturing into neomycin-containing media.

Animals↗
PubMed1970

Stability of neomycin resistance in Staphylococcus aureus.

A strain of Staphylococcus aureus isolated from the skin of a subject with eczema showed a loss in resistance to neomycin and tetracycline after treatment with neomycin was stopped. Seven out of 22 strains of neomycin-resistant Staph. aureus showed a loss in resistance to neomycin and streptomycin after storage in nutrient broth for 14 days at room temperature, and it seems probable that resistance in these unstable strains was controlled by extrachromosomal elements or plasmids. Strains of phage types 84/85 and 29/77 and related types were frequently isolated in general hospital wards and showed no loss in resistance on similar storage in nutrient broth. Five of the neomycin-unstable strains were isolated from patients with eczematous lesions. Multiple-resistant and antibiotic-sensitive strains of Staph. aureus of similar phage type were isolated from patients in a ward for patients with skin disease, and the possibility of transfer of resistance in vivo is discussed.

Drug Resistance, Microbial↗
PubMed1993

Bioactive polymers 68--controlled release of neomycin-furazolidone bicomponent system from xanthan hydrogel.

The neomycin-furazolidone-xanthan complex has been synthesized. Neomycin is covalently linked to xanthan, while furazolidone is inserted in the hydrogel formed by the reaction between neomycin and xanthan. The content of neomycin and furazolidone depends on the drug rate in the reaction medium. Thus, a zero-order kinetics is obtained for the release of both neomycin and furazolidone in basic medium. The complex's antimicrobial activity is intensified.

Delayed-Action Preparations↗
PubMed2004

Neomycin inhibits glioma cell migration.

Blocking migration is an attractive strategy to inhibit glioma tumorigenesis. Previous studies have indicated that neomycin inhibits glioma cells proliferation. The purpose of this study was to expand on the preliminary research by investigating the antimigratory effect of neomycin. We used glioma C6 cells to investigate the role of neomycin in cell migration in vitro. Cell wounding assay showed that neomycin inhibits in a dose-dependent manner glioma cells migration into the wound. Taken together, these results suggest that neomycin is an attractive candidate for the development of novel antimigratory molecules useful for the treatment of gliomas.

Animals↗
PubMed2004

Differentiation-inducing activity of neomycin in cultured rat glioma cells.

Induction of cellular differentiation is an attractive therapeutic strategy against glioma cell proliferation and tumorigenicity. Preliminary in vitro studies have indicated that neomycin inhibits the proliferation of cultured glioma cells and induces changes in cellular morphology, making it potentially useful as a therapeutic agent for gliomas. The purpose of this work was to expand on the preliminary research by investigating the differentiation effect of neomycin in rat C6 glioma cells, using glial fibrillary acidic protein (GFAP) staining as a reliable marker of differentiation for normal astrocytes and for tumors of astrocytic lineage. Cell cultures were grown in the absence or presence of 10 mM neomycin sulfate for 48 hours. Neomycin treatment produced changes in cell morphology and GFAP expression indicative of cellular differentiation. These results suggest that neomycin is an attractive differentiation agent for the treatment of gliomas.

Animals↗
PubMed2006

Prophylaxis of irinotecan-induced diarrhea with neomycin and potential role for UGT1A1*28 genotype screening: a double-blind, randomized, placebo-controlled study.

OBJECTIVE: Delayed-type diarrhea is a common side effect of irinotecan and is associated with a bacterial-mediated formation of the active irinotecan metabolite SN-38 from its glucuronide conjugate in the intestine. Based on a pilot study, we hypothesized that concomitant administration of the antibiotic neomycin would diminish exposure of the gut to SN-38 and ameliorate the incidence and severity of diarrhea. PATIENTS AND METHODS: Patients were treated with irinotecan in a multicenter, double-blind, randomized, placebo-controlled trial. Eligible patients received irinotecan (350 mg/m(2) once every 3 weeks) combined with neomycin (660 mg three times daily for three consecutive days, starting 2 days before chemotherapy) or combined with placebo. Blood samples were obtained for additional pharmacokinetic and pharmacogenetic analyses. RESULTS: Sixty-two patients were evaluable for the toxicity analysis. Baseline patient characteristics, systemic SN-38 exposure, and UGT1A1*28 genotype status (i.e., an additional TA repeat in the promoter region of uridine diphosphate-glucuronosyltransferase isoform 1A1) were similar in both arms. Although distribution, severity, and duration of delayed-type diarrhea did not differ significantly between arms, grade 3 diarrhea tended to be less frequent in the neomycin arm. The presence of at least one UGT1A1*28 allele was strongly related to the incidence of grade 2-3 diarrhea. In the neomycin arm, grade 2 nausea was significantly more common. CONCLUSION: Our results do not suggest a major role for neomycin as prophylaxis for irinotecan-induced delayed-type diarrhea. It is suggested that the UGT1A1*28 genotype status could be used as a screening tool for a priori prevention of irinotecan-induced delayed-type diarrhea.

Adult↗
PubMed1995

Effect of repeated administrations of neomycin on the neuromuscular functions and the enhancement of d-tubocurarine action in mice.

Effects of repeated s.c. treatments with 50 mumol (approx. 31 mg)/kg/day of neomycin for 10 or 15 days were examined in mice. There were no significant differences between saline and neomycin treatment groups in the motor coordination assessed by rota-rod test and traction test. On tension recordings, an in vitro addition of d-tubocurarine inhibited the twitch tensions evoked by the nerve stimulations in both cases of saline or neomycin treatment. Neomycin treatments shifted the concentration-response curve between twitch tension and d-tubocurarine to the left, dependently on its injection days. These results suggest that repeated treatments with neomycin enhance the inhibitory effect of d-tubocurarine on the neuromuscular transmission in mice without eliciting motor incoordination and muscle relaxation.

Animals↗