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During recent years, there has been growing interest in the use of nanoemulsion as a drug-carrier system for topical delivery. A nanoemulsion is a transparent mixture of oil, surfactant and water with a very low viscosity, usually the product of its high water content. The present study investigated the modification of nanoemulsions with different hydrocolloid gums, to enhanced drug delivery of ibuprofen. The in vitro characterization of the initial and modified nanoemulsions was also studied.
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The possible contribution of pulmonary metabolism to the putative first-pass metabolism of 2-arylpropionic acid nonsteroidal antiinflammatory drugs has not been documented. Isolated perfused rabbit lungs, perfused with 4.5% bovine serum albumin or 5% dextran, were used to study the pulmonary elimination of (R)- and rac-ibuprofen, fenoprofen, and flurbiprofen. In the absence of protein binding, ibuprofen was metabolized via inversion and other pathways, whereas fenoprofen metabolism was essentially restricted to inversion of the (R)-enantiomer; fraction inverted (+/- SE) was 0.37 +/- 0.05 for (R)-ibuprofen and 0.85 +/- 0.03 for (R)-fenoprofen. In the presence of protein, neither ibuprofen nor fenoprofen was metabolized. Flurbiprofen did not undergo pulmonary elimination under any condition studied. This study illustrates that even though a tissue is capable of metabolism, particularly inversion of 2-arylpropionics, the quantitative importance of such elimination pathways may be minimal in the presence of the high degree of protein binding that is characteristic of these drugs.
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Included were 201 premature babies (< or = 32 weeks gestational age), from January 2001 to June 2007, with PDA who received primary medical treatment with ibuprofen. Number of ibuprofen cycles, gestational age, body weight, and presence of symptomatic hypotension requiring vasoactive/inotropic drugs were related to hospital outcome, including hospital mortality, presence of necrotizing enterocolitis, acute renal failure, intraventricular hemorrhage, retinopathy and bronchopulmonary dysplasia at week 36. Data were analyzed with a logistic regression model.
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Fractures and severe sprains generate moderate to severe pain (>3/10). Despite this fact, pain management in children presenting to the Emergency Department (ED) with a musculoskeletal trauma is still suboptimal. Few studies have focused on the efficacy of a combination of an opioid with an anti-inflammatory drug to relieve this type of pain.
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Bielschowsky staining and Aβ(1-40) expression show few nerve connections and Aβ(1-40) expression in an Aβ sample, preserved neuronal cells and Aβ(1-40) expression lowering in an IBU sample, mostly in IBU-LA. The Ngb level decreases in Aβ samples, compared to control and IBU-LA samples. p-Akt/Akt and p-CREB/CREB ratios reveal a reduction in Aβ sample, going back to the basal level in control and IBU-LA samples. Cytochrome C/Apaf 1 co-immunoprecipitate occurs and TUNEL-positive nuclei percentage decreases in Aβ sample. Probe test performance shows an increased spatial reference memory in the IBU-LA compared to the Aβ sample; no significant differences were seen between the IBU-LA and IBU samples.
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Free radicals have been implicated in the development of injury to the immature retina. Asphyxia increases free radicals as well as prostaglandins (PG) in neural tissues. We assessed whether in the retina the cyclooxygenase pathway contributes to free radical formation after oxidative insults such as asphyxia, which in turn disrupts retinal function. Newborn pigs were treated with either saline, ibuprofen (194 mumol/kg i.v.), or allopurinol (1 mmol/kg i.v.), and retinal malondialdehyde (MDA), hydroperoxides, PGE2 and PGF2 alpha levels, and the amplitudes and implicit times of the a- and b-waves of the full-field electroretinogram were measured before and 1 h after a 5-min period of asphyxia. In saline-treated animals, asphyxia caused a marked increase (p < 0.01) in MDA, hydroperoxides, PGE2, and PGF2 alpha concentrations in the retina. This was associated with a significant decrease (p < 0.01) in the b-wave amplitude measured under scotopic and photopic conditions and an increase in the b-wave implicit times. Ibuprofen and another cyclooxygenase inhibitor, indomethacin (28 mumol/kg i.v.), decreased PGE2 and PGF2 alpha levels and prevented the increase in MDA and hydroperoxides after asphyxia. Allopurinol maintained low concentrations of MDA and hydroperoxides after asphyxia. Both ibuprofen and allopurinol prevented the postasphyxial changes in the b-wave amplitude and diminished the delay in implicit time observed after asphyxia in saline-treated pigs. Our findings suggest that in the retina after asphyxia free radicals appear to originate primarily from the cyclooxygenase pathway and contribute to the deterioration in retinal electrophysiologic function of the newborn animal. Cyclooxygenase inhibitors, like free radical scavengers, may protect retinal function from deteriorating after oxidative stresses.
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We report an unusual and emerging cause of profound hypokalaemia associated with a severe myopathy, attributable to misuse of Nurofen Plus, a readily available over-the-counter medication containing ibuprofen and codeine, and excessive ingestion of the caffeine-containing energy drink, Red Bull. The mechanism of the hypokalaemia may be ascribed to ibuprofen-mediated type 2 renal tubular acidosis, and caffeine-mediated antagonism of adenosine receptors or intercompartmental shift of potassium into the intracellular space. Practitioners should be aware that patients with codeine addiction who misuse Nurofen Plus may present with severe hypokalaemia complicated by myopathy.
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We considered all completed randomised or non-randomised controlled clinical trials, published or unpublished, where pharmacological or physical strategies or both to reduce temperature were applied in patients with acute ischaemic stroke or intracerebral haemorrhage. Outcome measures were death or dependency (modified Rankin Scale score >/= 3) at the end of follow up, and adverse effects.
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All neonates weighing < 1500 g at birth who received ibuprofen to close patent ductus arteriosus and were admitted to Seoul National University Children's Hospital's neonatal intensive care unit in 2010-2014 were eligible for this study. The study population was divided into the PAH and non-PAH groups, and medical records were retrospectively reviewed.
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The aim of the study was to investigate the effects of subchronic exposure of zebrafish to ibuprofen, using selected oxidative stress parameters as a target.
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To study changes in electrical behavior from inflammation, the conduction properties of six normal canine right atrial appendages were quantified as a function of the direction of impulse propagation with and without 80 mum arachidonic acid. To study the effect of topical anti-inflammatory drugs, 24 adult mongrel dogs were prepared according to the model of sterile talc pericarditis. Nine dogs received talc alone (T), seven received talc combined with 600 mg ibuprofen (T + I), and eight received talc combined with 10 mg methylprednisolone (T + M). Three days following preparation, programmed electrical stimulation was performed to quantify conduction characteristics and to attempt the induction of atrial fibrillation (AF).
To assess quantitatively the analgesic efficacy and adverse effects of single-dose dipyrone in randomised trials in moderate to severe postoperative pain. To compare the relative efficacy of dipyrone with other drugs assessed in the same way.
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Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID), treatment with which has been shown to delay the onset, slows the cognitive decline, and decreases the incidence of Alzheimer׳s disease (AD) in epidemiological and clinical studies. However, a comprehensive understanding of its mechanism of action remains unclear. To elucidate the prophylactic effect of ibuprofen on the onset of the learning and memory disturbances of AD, we performed proteomic analysis of the hippocampus of chronic ibuprofen-treated mice using two-dimensional gel electrophoresis (2-DE) followed by mass spectrometry. Twenty-eight proteins and seven phosphoproteins were identified to be significantly changed in the hippocampus of chronic ibuprofen-treated mice: translationally controlled tumor protein, thioredoxin-dependent peroxide reductase, and peroxiredoxin 6 were increased, and glial fibrillary acidic protein, dihydropyrimidinase-related protein 2, EF-hand domain-containing protein D2, and 14-3-3ζ were decreased. These identified proteins and phosphoproteins could be classified as cytoskeletal, neuronal development, chaperone, metabolic, apoptosis, neurotransmitter release, ATP synthase, deubiquitination, proteasome, NOS inhibitor, adapter, vesicle transport, signal transduction, antioxidant enzyme, proton transport, synaptogenesis, and serine/threonine phosphatase types. Western blot analysis showed the changes in dihydropyrimidinase-related protein 2, heat shock protein 8, ubiquitin carboxyl-terminal hydrolase PGP9.5, and γ-enolase levels in the hippocampus of chronic ibuprofen-treated mice. These findings showed that the chronic treatment with ibuprofen changed the levels of some proteins and phosphoproteins in the hippocampus. We propose that these identified proteins and phosphoproteins play an important role in decreasing the incidence of AD, especially impaired learning and memory functions.
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The objectives of this study were to assess the prescribing of non-steroidal anti-inflammatory drugs (NSAIDs) by general practitioners and to determine their attitudes to problems caused by this class of drugs. The study consisted of two parts. The first was a questionnaire survey among general practitioners in Fife and Tayside, and the second was an analysis of NSAID prescribing over 12 months among the doctors in the Carnoustie Health Centre, using duplicate prescriptions. In the questionnaire survey 61% of the general practitioners responded. The three most preferred drugs were buprofen (56%), naproxen (20%) and mefenamic acid (7%); choice of drug was determined by efficacy and personal experience. Gastrointestinal side effects were most frequently encountered, although there was little consensus amongst respondents as to their management. The duplicate prescription study showed that 14% of patients (1607 individuals) received at least one NSAID prescription in the year of study. Ibuprofen (31%), naproxen (20%) and piroxicam (15%) were most frequently prescribed and up to 16% of the patients were co-prescribed a gastroprotective agent; ranitidine (75%) was the most commonly prescribed. Despite the introduction of newer NSAIDs, ibuprofen and naproxen are still the most commonly prescribed drugs. Furthermore, although gastrointestinal side effects are commonly encountered, there is some uncertainty about their management.
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The heats of reaction have been measured directly by flow microcalorimetry.
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This was an observational, multicentre, prospective survey. A total of 616 patients (38% male and 62% female) from the Italian Stomatology Clinics of the Universities of Bologna, Brescia, Cagliari, Chieti, Pavia, Pisa, Siena and Varese and from the Department of Oral and Maxillo-Facial Surgery of Semmelweis University, Budapest, were eligible for the study. Patients were evaluated over the 7 days following surgical extraction. NSAIDs were prescribed according to the normal prescribing habits of the centre and physician involved. The main outcomes of interest in the survey were the efficacy, onset and duration of analgesic effect, duration of therapy, and tolerability of the NSAIDs prescribed.
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Before and after 21-month trial with one study site and two control sites and a questionnaire that was sent to 203 clinicians.
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Five percent of cases and 1.9% of controls had a history of treatment for alcohol abuse. The presence of either NSAID use or a history of alcohol abuse led to an odds ratio (OR) of 2.9* for severe GI events, whereas the presence of both risk factors simultaneously led to an OR of 10.2* (additive would be 5.8). Similarly, the presence of ibuprofen and naproxen use, which are OTC in the USA, without alcohol abuse led to an OR of 1.9*, whereas alcohol abuse by itself led to an OR of 2.4*. The presence of both OTC NSAIDs and alcohol abuse simultaneously, led to an OR of 6.5 (additive would be 4.3). Thus with both risk factors present, the resulting risk ratio is greater than the additive risk of the separate risk factors.
A 23-month-old girl with TAR syndrome was treated with recombinant IL-6 (Sigosix; Serono Laboratories, Norwell, MA) at a dose of 7 micrograms/kg subcutaneously daily. Complete blood counts were monitored weekly. The child was closely monitored for any toxicity.
To evaluate risks of discontinuity of pharmaceutical care at paediatric hospital discharge and assess potential improvement strategies, using two complementary methods: a prospective risk analysis and a spontaneous incident reporting system.
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Skeletal muscle wasting is a prominent feature of cancer cachexia and involves decreased muscle protein synthesis and increased activity of the ubiquitin-proteasome pathway of protein degradation. We report that both indomethacin and ibuprofen improved body weight and weight of the gastrocnemius muscle in tumor-bearing mice. Ibuprofen increased the soluble protein content of the muscle without affecting muscle levels of phosphorylated p70 S6 kinase, a ribosomal kinase involved in protein synthesis. Paradoxically, indomethacin increased levels of ubiquitin-conjugated proteins. Further study is needed to understand the mechanism of action by which indomethacin and ibuprofen preserve body weight and muscle mass in the tumor-bearing mice. The data suggest that ibuprofen may have beneficial effects in the treatment of cancer cachexia.
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Platelet activating factor (PAF) is considered a key mediator in eliciting the immunologic and metabolic consequences of endotoxic shock and sepsis. Release of oxygen-derived radicals is one of the important and relevant actions of PAF. This study examines the direct and priming effects of PAF on superoxide anion release by perfused liver, isolated Kupffer cells and blood neutrophils. One hour after PAF infusion at a dose of 2.2 micrograms/kg body weight a significant amount of superoxide release (0.71 +/- 0.1 nmol/min/g liver) was measured in the perfused liver compared with the control livers (0.2 +/- 0.01). In the in vitro presence of either phorbol ester or opsonized zymosan, superoxide release following PAF treatment in vivo was significantly increased to 1.36 +/- 0.2 and 4.29 +/- 0.36, respectively. The administration of PAF receptor antagonist (SDZ 63-441) almost completely inhibited the release of this radical. Kupffer cells (KC1, KC2, KC3) and blood neutrophils isolated from PAF-treated rats were also primed for increased production when these cells were challenged in vitro by the activator of protein kinase C, opsonin-coated zymosan as well as the chemotactic factors, complement 5a and F-met-leu-phe. PAF added in vitro to the perfused livers, isolated Kupffer cells or neutrophils from normal animals stimulated the release of superoxide with or without the above agonists. The direct stimulatory effect of PAF on superoxide release was inhibited by the PAF receptor antagonist in vitro. The role of PAF in the LPS-induced superoxide release by the perfused liver was also examined by the administration of PAF antagonist in endotoxic rats. The antagonist inhibited the LPS-mediated superoxide release at 1 hr, but not at 3 hr post-treatment. These results indicate that PAF stimulates and primes the hepatic elements to release superoxide. PAF may be an important factor during the early phase of endotoxemia, while other bioactive substances may take over at a later phase. Therefore, PAF is a key mediator that can directly enhance the release of toxic oxygen-derived radicals which may contribute to organ failure during endotoxemia or sepsis.
We have previously reported that a single meal of an arginine-free diet rapidly induces hyperammonemia in young ferrets and that aspirin administration in conjunction with influenza B infection and arginine-free diet results in clinical and biochemical alterations consistent with Reye's syndrome. The objective of the present study was to test whether ibuprofen administration, either alone or in combination with influenza infection and arginine-free diet, produces a similar effect. Two-mo-old ferrets were inoculated intranasally with influenza B virus, treated with therapeutic doses of ibuprofen, and fed a single meal of an arginine-free diet. Arginine-free diet caused a significant increase in plasma ammonia and a small increase in plasma aspartate aminotransferase activity. All ferrets fed an arginine-free diet recovered within 6 to 7 h after ingesting the diet. Ibuprofen treatment, either solely or in combination with influenza infection, did not produce significant change in the plasma levels of aspartate or ornithine aminotransferase activities. A combination of ibuprofen treatment, influenza infection, and arginine-free diet caused a significant increase in the mortality and plasma ammonia levels. Plasma aspartate aminotransferase and ornithine carbamyl transferase activities were elevated, and liver ornithine carbamyl transferase activity was decreased. However, other mitochondrial enzymes such as ornithine aminotransferase were not altered, whereas the activity of cytoplasmic enzymes such as arginase were decreased. These results suggest that ibuprofen administration resulted in generalized hepatopathy rather than specific mitochondrial injury and Reye's syndrome-like changes associated with aspirin in our previous model.
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We describe our experience with cluster headache in eleven children who all presented before the age of 16.
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A total of 867 patients provided postbaseline data and were included in the intent-to-treat population (CYC5, n = 288; CYC5/IBU400, n = 286; CYC5/IBU800, n = 293). All three treatment groups demonstrated significant improvements from baseline in PGIC, spasm, pain, ODI, and medication helpfulness (p < 0.001 for all comparisons) after 3 and 7 days of therapy. There were no significant differences in mean PGIC among groups after 3 days of therapy (p = 0.65 for treatment effect) or after 7 days of therapy (primary endpoint; p = 0.41). A PGIC responder analysis of changes from baseline showed that 88% and 93% of patients reported at least mild improvement after 3 and 7 days of therapy, respectively. All three treatments were well tolerated, with no significant differences between treatments regarding the number of adverse events (AEs) reported or number of patients reporting AEs. The most common AEs in all groups were fatigue, somnolence, dizziness, sedation, and nausea. Limitations of this study include an unblinded design and possible introduction of bias into efficacy and safety results by use of a voluntary telephone reporting system.