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We studied healthy volunteers in a double-blind double-dummy randomized crossover study. Each subject took, over four separate 10-day dosing periods, ibuprofen 400 mg t.d.s., ketoprofen 12.5 mg t.d.s., ketoprofen 25 mg t.d.s. or ketoprofen 50 mg t.d.s. Mucosal injury was assessed by endoscopy at baseline and on the 3rd and 10th day of each dosing period. Ex vivo gastric mucosal prostaglandin (PG) E2 evoked by vortex mixing was measured by radioimmunoassay. Serum thromboxane was also measured by radioimmunoassay.
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Patent ductus arteriosus (PDA) is one of the most common problems in the care of premature infants, especially the extremely premature. There is no real consensus regarding the diagnostic criteria or treatment of a hemodynamically significant PDA. Its diagnosis, assessment, and treatment still remain challenges. Therefore, we investigated clinical practices in French tertiary neonatology centers regarding the management of PDA to compare their similarities and differences. We sent a questionnaire by email to the PDA specialist in every French tertiary neonatal intensive care unit. It contained 27 items regarding the unit's structure, method of diagnosing PDA, and treatment choices. The completed questionnaire were returned via email and analyzed blindly. The questionnaire response rate was 87.5%, which allowed us to draw some conclusions regarding French clinical practices in the care of neonates with PDA. Although the diagnostic criteria are quite similar, the therapeutic practices are rather different across neonatal care units. We highlight the great variability in French clinical practices when it comes to treating PDA and underscore the necessity for harmonization of these practices, which could be achieved using multicenter, randomized studies to identify the advantages of one approach compared with another.
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We measured cardiac output, regional blood flow, and total systemic shunt flow in dogs using radiolabeled 15-microns microspheres. These parameters were assessed in control (N = 10) and endotoxin-treated animals (N = 7). Additional endotoxin-treated animals (N = 7) were also pretreated with ibuprofen.
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In this paper, the implementation of the CS-FE/MT model introduced in article 1 is discussed, and computer simulations are performed to evaluate the feasibility of the new theoretical approach. As discussed in article 1, making predictions of surfactant/solubilizate aqueous solution behavior using the CS-FE/MT model requires evaluation of DeltaDeltaG for multiple surfactant-to-solubilizate or surfactant-to-cosurfactant transformations. The central goal of this article is to evaluate the quantitative accuracy of the alchemical computer simulation method used in the CS-FE/MT modeling approach to predict DeltaDeltaG for a single surfactant-to-solubilizate or for a single surfactant-to-cosurfactant transformation. A hybrid single/dual topology approach was used to morph the ionic surfactant sodium dodecyl sulfate (SDS) into the ionic solubilizate ibuprofen (IBU), and a dual topology approach was used to morph the nonionic surfactant octyl glucoside (OG) into the nonionic solubilizate p-aminobenzoate (PAB). In addition, a single topology approach was used to morph the nonionic surfactant n-decyl dimethylphosphine oxide (C10PO) into the nonionic cosurfactant n-decyl methyl sulfoxide (C10SO), the nonionic surfactant octylsulfinyl ethanol (C8SE) into the nonionic cosurfactant decylsulfinyl ethanol (C10SE), and the nonionic surfactant n-decyl methyl sulfoxide (C10SO) into the nonionic cosurfactant n-octyl methyl sulfoxide (C8SO). Each DeltaDeltaG value was computed by using thermodynamic integration to determine the difference in free energy associated with (i) transforming a surfactant molecule of type A into a cosurfactant/solubilizate molecule of type B in a micellar environment (referred to as DeltaG2) and (ii) transforming a surfactant molecule of type A into a cosurfactant/solubilizate molecule of type B in aqueous solution (referred to as DeltaG1). CS-FE/MT model predictions of DeltaDeltaG for each alchemical transformation were made at a number of simulation conditions, including (i) different equilibration times at each value of the coupling parameter lambda, (ii) different data-gathering times at each lambda value, and (iii) simulation at a different number of lambda values. For the three surfactant-to-cosurfactant transformations considered here, the DeltaDeltaG values predicted by the CS-FE/MT model were compared with DeltaDeltaG values predicted by an accurate molecular thermodynamic (MT) model developed by fitting to experimental CMC data. Even after performing lengthy equilibration and data gathering at each lambda value, physically unrealistic values of DeltaDeltaG were predicted by the CS-FE/MT model for the transformations of SDS into IBU and of OG into PAB. However, more physically realistic DeltaDeltaG values were predicted for the transformation of C10PO into C10SO, and reasonable free-energy predictions were obtained for the transformations of C8SE into C10SE and C10SO into C8SO. Each of the surfactant-to-cosurfactant transformations considered here involved less extensive structural changes than the surfactant-to-solubilizate transformations. As computer power increases and as improvements are made to alchemical free-energy methods, it may become possible to apply the CS-FE/MT model to make accurate predictions of the free-energy changes associated with forming multicomponent surfactant and solubilizate micelles in aqueous solution where the chemical structures of the surfactants, cosurfactants, and solubilizates differ significantly.
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A 26-year-old male presented with symptoms of acute esophageal obstruction immediately after swallowing an 800-mg ibuprofen tablet. Multiple attempts to extract the pill with a variety of traditional endoscopic retrieval devices were unsuccessful. We successfully destroyed the pill using a threaded-tip biliary stent retrieval device to drill a hole in the center of the pill, which allowed us to use a rat-tooth forceps to crush the pill. This case report demonstrates a novel use of this device in a challenging esophageal pill extraction.
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This study assessed the relative bioavailability of two formulations of ibuprofen. The first formulation was Doloraz(®), produced by Al-Razi Pharmaceutical Company, Amman, Jordan. The second forumulation was Brufen(®), manufactured by Boots Company, Nottingham, UK.
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A prospective, convenience sample of emergency department patients were enrolled. Data were recorded using a standardised questionnaire over 4 months.
Stadol NS significantly reduced pain (by 50%) after third molar extraction within 15 minutes after administration. It had a high level of patient acceptance, 81% on day 1, and was well tolerated.
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Ketoprofen and ibuprofen topical gels were compounded with decyl methyl sulfoxide and the terpenes d-limonene, (-)-menthone, terpinen-4-ol, and a-terpineol as penetration enhancers. Transdermal penetration profiles for both ketoprofen and ibuprofen were determined using full-thickness human skin, modified Franz diffusion cells and an isotonic (pH7.4) phosphate buffer solution. Human skin was used in these experiments to approximate the therapeutic use of these gels. Ibuprofen was found to have superior transdermal kinetics when compared to ketoprofen. Ibuprofen is a smaller and more lipophilic molecule than ketoprofen, which gives it better penetration properties. All enhancers tested significantly increased the penetration (except (-)-menthone) and skin retention (except terpinen-4-ol) of ketoprofen. None of the enhancers tested significantly increased the penetration or retention of ibuprofen. Despite the lack of enhancer activity, ibuprofen still demonstrated higher skin penetration and retention than enhanced delivery of ketoproen. The results of these studies suggest that the addition of penetration enhancers can significantly increase the amount of ketoprofen penetration, while enhancers demonstrated no significant increase (and can actually decrease) the amount of ibuprofen penetrating into and through the skin.
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Ibuprofen is the most palatable analgesic medicine for children, suggests a UK study of young people's opinions on the taste of commonly used medicines in liquid form.
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Tertiary care center in Philadelphia, Pennsylvania, United States.
There was no difference in closure of the ductus arteriosus or occurrence of adverse effects between the two dose regimens.
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The results show that the efficacy of fish oil is better than ibuprofen on treatment of severe pain in primary dysmenorrhea.
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The occurrence and removal rate of seven pharmaceuticals (ibuprofen, naproxen, diclofenac, fluoxetine, ofloxacin, norfloxacin, ciprofloxacin), two metabolites (norfluoxetine, clofibric acid), one degradation product (4-isobutylacetophenone) and 3 estrogens (17alpha-ethinylestradiol, 17beta-estradiol, estrone) were studied in the inlet and outlet of a tertiary sewage treatment plant (STP) in Sweden as well as between different treatment steps in the STP which includes a conventional activated sludge step. Pharmaceuticals in raw household and raw hospital sewage streams leading to the STP were as well investigated. Hydraulic retention times (HRT) of each treatment step was considered for sampling and for the calculation of the removal rates. These rates were above 90%, except for diclofenac, clofibric acid, estrone and ofloxacin. However, only diclofenac and naproxen showed significant effluent loads (>145 mg/d/1000 inh). Diclofenac was not eliminated during the treatment and in fact even higher concentrations were found at the effluent than in the inlet of the STP. 17alpha-Ethinylestradiol was not detected in any of the samples. Results indicate that a STP such as the one in Kristianstad, Sweden, with a tertiary treatment is sufficient to remove significantly most of the investigated pharmaceuticals. The chemical treatment improved the removal of several pharmaceuticals especially the antibiotics, which showed step removal rates between 55 and 70%. The expected concentration levels of the pharmaceuticals in the surface water (dilution 1 to 10) close to the outlet of the STP are below the no-observed effect-concentration (NOEC). However, despite that this would imply no important effects in the aquatic environment one cannot rule out negative consequences nearby the STP because most of the NOEC values are derived from acute toxicity data. This may underestimate the real impact of pharmaceuticals in the aquatic ecosystem.
A rapid, sensitive and efficient analytical method based on the use of ionic liquids for determination of non-steroidal anti-inflammatory drugs (NSAIDs) in water samples was developed. High-performance liquid chromatography equipped with a diode array and fluorescence detector was used for quantification of ketoprofen, ibuprofen and diclofenac in tap and river water samples. This new method relies on the use of two ionic liquids with multiple functionalities: one functions as an extraction solvent (1-butyl-3-methylimidazolium hexafluorophosphate ([BMIM][PF6]), and the other changes the polarity in the aqueous medium (1-butyl-3-methylimidazolium tetrafluoroborate, ([BMIM][BF4]). Factors such as the type and volume of the ILs and dispersive solvent, sample volume, and centrifugation time were investigated and optimized. The optimized method exhibited good precision, with relative standard deviation values between 2% and 3%, for the three NSAIDs. Limits of detection achieved for all of the analytes were between 17 and 95 ng mL(-1), and the recoveries ranged from 89% to 103%. Furthermore, the enrichment factors ranged from 49 to 57. The proposed method was successfully applied to the analysis of NSAIDs in tap and river water samples.
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In this study, we investigated the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on 1-methyl-4-phenylpyridinium (MPP(+))-induced cell death in PC12 cells. Coincubation of PC12 cells with indomethacin, ibuprofen, ketoprofen, or diclofenac, but not aspirin or N-[2-(cyclohexyloxy)-4-nitrophenyl]methanosulfonamide (NS-398), significantly potentiated the MPP(+)-induced cell death. In contrast, these NSAIDs had no effect on rotenone-induced cell death. The potentiating actions of these NSAIDs were not suppressed by treatment with phenyl-N-butyl-nitrone, a radical scavenger; N-acetyl-l-cysteine, an antioxidant; Ac-DEVD-CHO, a selective caspase-3 inhibitor; or 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective antagonist of peroxisome proliferator-activated receptor gamma. Furthermore, we observed that DNA fragmentation, which is one of the hallmarks of apoptosis, was not induced by coincubation with MPP(+) and NSAIDs. We confirmed that coincubation of PC12 cells with 30 microM MPP(+) and 100 microM indomethacin, ibuprofen, ketoprofen, or diclofenac led to a significant increase in the accumulation of intracellular MPP(+) compared with incubation with 30 microM MPP(+) alone. In addition, these NSAIDs markedly reduced the efflux of MPP(+) from PC12 cells. (3-(3-(2-(7-Chloro-2-quinolinyl) ethenyl) phenyl ((3-dimethyl amino-3oxo-propyl) thio) methyl) propanoic acid (MK 571), which is an inhibitor of multidrug resistance proteins (MRPs), mimicked the NSAIDs-induced effects, increasing cell toxicity and promoting the accumulation of MPP(+). Moreover, some types of MRPs' mRNA were detected in PC12 cells. These results suggest that some NSAIDs might cause a significant increase in the intracellular accumulation of MPP(+) via the suppression of reverse transport by the blockade of MRP, resulting in the potentiation of MPP(+)-induced cell death.
Cyclodextrin-modified microemulsion electrokinetic chromatography (CD-MEEKC) was used to simultaneously determine 14 active ingredients (thiamine nitrate, anhydrous caffeine, acetaminophen, riboflavin, guaifenesin, pseudoephedrine hydrochloride, ascorbic acid, ethenzamide, DL-methylephedrine hydrochloride, dihydrocodeine phosphate, ibuprofen, noscapine, carbinoxamine maleate, and bromhexine hydrochloride) in a cold medicine. Separation of the ingredients was optimized by changing the SDS concentration and oil type and the addition of 2-propanol and cyclodextrin (CD) to the separation solution. The separation selectivity was improved dramatically by changing CD type. All of the active ingredients and formulation excipients were successfully separated with the use of a separation solution consisting of 0.81% (w/w) pentane, 6.61% (w/w) 1-butanol, 2% (w/w) 2-propanol, 4.47% (w/w) SDS, and 86.11% (w/w) 10 mM sodium tetraborate solution with 3 mM 2,6-di-O-methyl-beta-CD. The established method was then validated and demonstrated to be applicable to the determination of the active ingredients in a model cold medicine. No interference from the formulation excipients was observed. Good linearities were obtained with correlation coefficients above 0.999. Recovery and precision ranged from 99.1 to 100.7% and from 0.5 to 2.8% R.S.D., respectively. The detection limit for ingredients ranged from 0.6 to 4.2 microg ml(-1). Good agreement was obtained between the established method and the traditional HPLC method. These results suggest that CD-MEEKC can be used for the determination of multiple ingredients in cold medicine.
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There was no difference in corticosteroid use between case and control mothers, although the number of exposed subjects was small. Odds ratio estimates for folic acid antagonists and vasoactive agents support previously reported associations, but they were not statistically significant.
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Sixty-three patients completed the study. There were no statistically significant differences between the groups in patient age, body weight and stone size, the mean (SD) of which was 6.52 (1.8) mm in group 1 vs. 6.47 (1.79) mm in group 2 (P = 0.9). The mean (SD) time to stone expulsion in group 1 was 7.7 (1.9) days, vs. 18 (1.73) days in group 2 (P < 0.001). The analgesic requirement (mean number of ketorolac injections) in group 1 was significantly less than in group 2, at 0.55 (0.8) vs. 1.8 (1.6) (P < 0.001). The stone-free rate was 87% in group 1 and 63% in group 2 (P = 0.025).
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There is currently no therapeutic intervention to stem neonatal brain injury after exposure to hypoxia-ischemia (HI). Potential neuroprotective treatments that can be delivered postinsult that target neuroinflammation and are safe to use in neonates are attractive. One candidate is ibuprofen. Ibuprofen is a nonsteroidal anti-inflammatory drug that inhibits cyclooxygenase enzymes and is used in neonates to treat patent ductus arteriosus. We investigated whether ibuprofen can inhibit neuroinflammation and attenuate neuronal damage manifested in a rodent model of preterm HI. Postnatal day 3 (P3) rat pups were subjected to HI (right carotid artery ligation, 30 minutes 6% O₂). Ibuprofen was then administered daily for 1 week (100 mg/kg P3 2 hours after HI, 50 mg/kg P4-P9; subcutaneously). Ibuprofen treatment prevented the P3 HI-induced reductions in brain serotonin levels, serotonin transporter expression, and numbers of serotonergic neurons in the dorsal raphé nuclei on P10. Ibuprofen also significantly attenuated P3 HI-induced increases in brain cyclooxygenase 2 protein expression, interleukin-1β, and tumor necrosis factor levels, as well as the increase in numbers of activated microglia. Thus, ibuprofen administered after an HI insult may be an effective pharmacologic intervention to reduce HI-induced neuronal brain injury in the preterm neonate by limiting the effects of neuroinflammatory mediators.
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The present study assessed (1) whether long-term use of nonselective NSAIDs (etodolac, nabumetone, ibuprofen, or naproxen) is associated with an increased risk for treatment-related CVEs (acute myocardial infarction [AMI], angina, cerebrovascular attack [CVA], and/or transient ischemic attack [TIA]) compared with long-term use of celecoxib and (2) which factors are associated with the risk for treatment-related CVEs in long-term users of nonselective NSAIDs in Taiwan.
Male Sprague-Dawley rats were pretreated either with saline (0.3 ml subcutaneously) or octreotide (0.001-1 ng/kg subcutaneously). After 30 minutes gastric ulcers were induced by the intragastric application of NSAIDs (20 mg/kg indomethacin, 200 mg/kg aspirin, 200 mg/kg ibuprofen, or 50 mg/kg diclofenac). Four hours later the rats were killed and gastric mucosal lesions were assessed by computed planimetry. To determine whether octreotide could prevent indomethacin induced injury in humans, 20 healthy volunteers were evaluated in a double blind, placebo controlled study.