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The results indicate that the synthesized prodrug (MA-NH) is better in terms of analgesic and antiinflammatory activities and with less GI toxicity than the parent drug.
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As predicted, dissolution of class II drugs proved to be in general much more dependent on the medium than class I drugs. With the array of compendial and physiological media available, it should be possible to design a suitable set of tests to predict the in vivo dissolution of both class I and II drugs from immediate release formulations.
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An analytical method based on high-performance liquid chromatographic (HPLC) was developed for the determination of montelukast in human plasma using mefenamic acid as an internal standard. After precipitation of plasma proteins with acetonitrile, chromatographic separation was carried out using a Zorbax Eclipse XDB C8 (150 mm x 4.6 mm i.d., 5 microm) with mobile phase consisted of methanol-acetonitrile-0.04M disodium hydrogen orthophosphate (22:22:56, v/v, pH 4.9). The wavelengths of fluorescence detection were set at 350 nm for excitation and 450 nm for emission. The linearity was confirmed in the concentration range of 5-1000 ng/ml in human plasma. Intra- and inter-day accuracy determined from quality control samples were 101.50 and 107.24%, and 97.15 and 100.37%, respectively. Intra- and inter-day precision measured as coefficient of variation were < or =4.72 and < or =9.00%, respectively. Extraction recoveries of drug from plasma were >48.14%. The protocol herein described was employed in a pharmacokinetic study of tablet formulation of montelukast in healthy Thai male volunteers.
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To evaluate the efficacy of pain relief by oral diazepam, acetaminophen, mefenamic acid, intramuscular ketorolac tromethamine, and peribulbar anaesthesia in panretinal photocoagulation (PRP).
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Pharmaceuticals are a class of chemicals whose fate in the environment has received increasing attention in the past few years. A quantitative method was developed for the determination of acidic pharmaceuticals (ibuprofen, naproxen, ketoprofen, mefenamic acid, and diclofenac), caffeine and the antibacterial triclosan in wastewater effluent. The compounds were extracted from wastewater samples on Waters Oasis HLB solid-phase extraction columns, derivatized with N,O-bis [Trimethylsilyl] trifluoroacetamide (BSTFA) and analyzed using gas chromatography-mass spectrometry. Estimated method detection limits ranged from 6 to 45 ng/L based on replicate analyses (n = 10). This method was applied to the analysis of effluent from a wastewater treatment plant and compounds were detected at concentrations of 18-72 ng/L.
In this study, we designed an in vitro binding assay as well as computational methods using MOPAC 7 package for evaluation of competitive potency of tamoxifen for TBG binding in comparison with well-known TBG competitors (including furosemide, mefenamic acid and diclofenac).
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Whenever a dentist is dealing with abscess formation in the oral and maxillofacial region, it is mostly from dental origins. However, sometimes uncommon (co-)factors are present and responsible for major complications. Many general conditions or medications can significantly influence the course of an inflammation. It might spread faster and wider and also be resistant to "correct" therapy. This case report should raise awareness about general conditions supporting inflammation and demonstrate the importance of interdisciplinary treatment in these situations. A 76-year-old patient was referred to the maxillofacial surgery clinic after extraction of two teeth resulted in therapy-resistant painful swelling. Her dentist already had initiated "standard" therapy including Ponstan® (mefenamic acid) and Clamoxyl® (amoxicillin) without success. Initial blood testing came back with severe agranulocytosis. Immediately all potentially myelosuppressing drugs were stopped while myelosupporting drugs were prescribed. Under close interdisciplinary treatment conditions, healing was then uneventful without the necessity of surgical intervention. The challenge in inflammation treatment is to identify patients with uncommonly severe, fast-progressing, or therapy-resistant disease as early as possible. Further examination including blood workup for several medical parameters is indispensable in those patients.
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The effect of acetylsalicylic (250 mg/kg) and mephenamic (50 mg/kg) acids on the process of skin cytoarchitectonics restoration was studied in rats with acute local cryogenic traumas induced by acting with a stream of ethyl chloride upon epilated back skin area (1.5 cm2). The animals were killed under narcosis on the 12th day of post-treatment observation. Both acetylsalicylic and mephenamic acids were administered per os twice per day over various periods after cryogenic damage. The effect depended on the treatment duration. The normal skin cytoarchitectonics was restored by acetylsalicylic acid in half, and by mephenamic acid, in one-third of cases (for a "combined" administration scheme).
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Mefenamic acid showed potential ability to prevent growth of dermatophytes. This ability increased due to the presence of Co.
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We have assessed the role of mefenamic acid, a non-steroidal anti-inflammatory drug known to inhibit both the synthesis and actions of prostaglandins, as an analgesic in migraine by comparing it with the established analgesic paracetamol (acetaminophen) in a double-blind cross-over trial. Forty ambulant migraine patients were supplied with oral medication for six consecutive attacks; metoclopramide 10 mg was administered in all attacks, and paracetamol 500 mg and mefenamic acid 500 mg for three attacks each. The patients recorded the intensity of the headache at the time the medication was taken, and again after 3 hours, on a linear analogue scale. Twenty-two patients completed the trial satisfactorily. Seven had insufficient attacks and the remainder were lost to follow-up. The mean reduction in headache intensity was 36 +/- 11% on mefenamic acid and 27 +/- 10% (both mean +/- SEM) on paracetamol. While this difference is not quite statistically significant (0.1 greater than P greater than 0.05) there still remains a 28% probability that mefenamic acid is twice as potent as an analgesic. The responses in each individual patient to the two drugs were very closely correlated (P much less than 0.001). Our failure to demonstrate a convincing difference between the two analgesics leads us to speculate that peripheral prostaglandin mediated pain pathways, in which paracetamol is inactive, may be less important than central pathways, which are inhibited by both drugs.
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The menstrual pain was significantly decreased in both groups after three-cycle intervention. Significant changes were observed in VAS (p<0.001) and VMSS (p<0.001) in the experimental group. There is a significant (p<0.001) reduction in duration of pain in both the groups. Associated symptoms and QOL were markedly improved after treatment (p<0.001).
Reports concerning the quantitative analysis of pharmaceuticals in marine ecosystems are somewhat limited. It is necessary to determine pharmaceutical fate and assess any potential risk of exposure to aquatic species and ultimately, seafood consumers. In the work presented herein, analytical methods were optimised and validated for the quantification of pharmaceutical residues in wastewater effluent, receiving marine waters and marine mussels (Mytilus spp.). Selected pharmaceuticals included two non-steroidal anti-inflammatory drugs (NSAIDs) (diclofenac and mefenamic acid), an antibiotic (trimethoprim), an antiepileptic (carbamazepine) and a lipid regulator (gemfibrozil). This paper also presents the results of an in situ study in which caged Mytilus spp. were deployed at three sites on the Irish coastline over a 1-year period. In water samples, pharmaceutical residues were determined using solid phase extraction (SPE) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). The extraction of pharmaceuticals from mussel tissues used an additional pressurised liquid extraction (PLE) step prior to SPE and LC-MS/MS. Limits of quantification between 15 and 225 ng·L(-1) were achieved in wastewater effluent, between 3 and 38 ng·L(-1) in marine surface water and between 4 and 29 ng·g(-1) dry weight in marine mussels. Method linearity was achieved for pharmaceuticals in each matrix with correlation coefficients of R(2)≥0.976. All five selected pharmaceuticals were quantified in wastewater effluent and marine surface waters. This work has demonstrated the susceptibility of the Mytilus spp. to pharmaceutical exposure following the detection of pharmaceutical residues in the tissues of this mussel species at measurable concentrations.
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Two rat liver cytosolic aldehyde dehydrogenases, ALDH1 and ALDH3c, are of particular interest because they are inducible by different classes of xenobiotics. ALDHI is mainly increased by phenobarbital-type inducers; polycyclic aromatic hydrocarbons (PAHs), such as 3- methylcholanthrene (3MC), increase ALDH3c enzyme activity in all rat species currently tested. In addition, ALDH3c has been found to reflect the subfamily CYPIA of cytochrome P-450, as well as other enzymes functionally related to the aryl hydrocarbon receptor (the "Ah-receptor enzyme battery"), which is activated by the same type of inducers. In the present study we investigated whether the induction of ALDH3c might be connected with a chemically produced aseptic inflammation of the hepatocyte. To answer this question, we examined the relationship between the induction of ALDH3c by 3MC and the arachidonic acid cascade. Different non-steroid anti-inflammatory drugs (NSAIDs) were tested in combination with 3MC and in post-treatment. The 3MC-induced ALDH3c activity was significantly diminished by the co-administered anti-inflammatory agents. Two microsomal enzyme activities (ethoxyresorufin-O-deethylase, EROD; aryl-hydrocarbon-hydroxylase, AHH) were also decreased. Similar results were obtained with NSAIDs administered to animals pre- treated with 3MC, as far as the ALDH3c activity was concerned, but not for the microsomal enzyme activity (EROD and AHH). In conclusion, the induction of ALDH3c, after PAH treatment, may be related to an aseptic inflammation of the hepatocytes. This effect is reduced by commonly used steroid and non-steroid anti- inflammatory drugs, and although the mechanism of inhibition has not yet been elucidated, it appears likely that ALDH3c and CYP1A activities are associated with the "acute phase" response.
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It has been recently described that some non-steroidal anti-inflammatory drugs (NSAIDs) are able to induce the shedding of L-selectin in neutrophils, an adhesion molecule that plays an essential role in the inflammatory response. We have found that, according to this capability, NSAIDs could be grouped into three categories. A high releaser group (flufenamic, meclofenamic, and mefenamic acids, diclofenac and aceclofenac), a group of moderate releasers (aspirin, indomethacin, nimesulide, flurbiprofen, and ketoprofen), and a non-releaser group (phenylbutazone and the oxicams, piroxicam and meloxicam). Only NSAIDs from the high releaser group shared diphenylamine in their chemical structure. The amine group of this chemical agent proved to be essential for the anti-L-selectin activity of diphenylamine-based NSAIDs. The presence of a carboxylic acid group in the diphenylamine (N-phenylanthranilic acid) highly increased its ability to reduce the L-selectin surface expression in neutrophils. Diphenylamine and N-phenylanthranilic acid neither affected COX activity in platelets nor modified the activation state of neutrophils. Diphenylamine-related compounds, which include the diphenylamine-based NSAIDs caused a variable reduction in the neutrophil intracellular ATP concentration, which correlated with the differential ability of such compounds to trigger L-selectin shedding (r = 0.97, p < 0.01). Diphenylamine-related compounds failed to down-regulate L-selectin in a tumor necrosis factor-alpha-converting enzyme (TACE)-deficient murine monocytic cell line. Our data indicate that diphenylamine seems to be the structural core of NSAIDs accounting for their down-regulatory activity of L-selectin leukocyte expression. Diphenylamine and its related compounds exert this action on L-selectin through a prostaglandin-independent, TACE-dependent mechanism that seems to be linked to the capability of these agents to uncouple the mitochondrial oxidative phosphorylation.
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Gemfibrozil, a fibrate hypolipidemic agent, is eliminated in humans by glucuronidation. A gemfibrozil glucuronide has been reported to show time-dependent inhibition of cytochrome P450 2C8. Comprehensive assessment of the drug interaction between gemfibrozil and cytochrome P450 2C8 substrates requires a clear understanding of gemfibrozil glucuronidation. However, the primary UDP-glucuronosyltransferase (UGT) isozymes responsible for gemfibrozil glucuronidation remain to be determined. Here, we identified the main UGT isozymes involved in gemfibrozil glucuronidation. Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity. The kinetics of gemfibrozil glucuronidation in pooled human liver microsomes (HLMs) follows Michaelis-Menten kinetics with high and low affinity components. The high affinity K(m) value was 2.5 microM, which is similar to the K(m) value of gemfibrozil glucuronidation in recombinant UGT2B7 (2.2 microM). In 16 HLMs, a significant correlation was observed between gemfibrozil glucuronidation and both morphine 3-OH glucuronidation (r = 0.966, p < 0.0001) and flurbiprofen glucuronidation (r = 0.937, p < 0.0001), two reactions mainly catalyzed by UGT2B7, whereas no significant correlation was observed between gemfibrozil glucuronidation and either estradiol 3beta-glucuronidation and propofol glucuronidation, two reactions catalyzed by UGT1A1 and UGT1A9, respectively. Flurbiprofen and mefenamic acid inhibited gemfibrozil glucuronidation in HLMs with similar IC(50) values to those reported in recombinant UGT2B7. These results suggest that UGT2B7 is the main isozyme responsible for gemfibrozil glucuronidation in humans.
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Human serum albumin monomer and dimer obtained by fractionation of a commercial preparation were immobilized on CH-Sepharose 4B by covalent coupling. For salicylic acid, warfarin, phenylbutazone, mefenamic acid, sulphamethizole and sulphonylureas, the binding capacities of the monomer and dimer were compared by continuous frontal affinity chromatography. The salicylate-binding capacities of both monomer and dimer were essentially retained upon immobilization. For these drugs, the dimer showed only about 10-30% less capacity per monomeric unit than that of the monomer, the reduction being associated for most drugs with the intrinsic binding constant rather than with the number of binding sites.
Fifteen eligible trials were assessed by three reviewers and eight of these did not meet with the inclusion criteria. Of the seven remaining trials, four of these could be included within the meta-analysis. The remaining three trials had a crossover design and despite contacting the authors and appropriate companies, we were unable to extract the results in a format suitable to include these within the meta-analysis. However the results are included within the text of the review for discussion.
There was no significant difference between the groups in the time of first analgesic request. Likewise, there was no significant difference in the post-operative cumulative analgesic consumption between the four groups. The post-operative administration of ropivacaine resulted in significantly lower pain scores at certain time points compared with the other groups as measured both with the visual analogue scale and the numeric rating scale (at rest). It must be emphasized, that the pain scores both at rest and with exertion remain high and that the net analgesic consumption (per day) remains constant for the first 8 post-operative days.
Antiprostaglandin drugs have been found to provide significant relief from dysmenorrhea. Twelve patients taking ibuprofen or mefenamic acid experienced menstrual delay of several days to two weeks and dysfunctional uterine bleeding. Menstruation returned to normal with the next cycle after the cessation of drug use.
Carvedilol is administered orally as a racemic mixture of R(+)- and S(-)-enantiomers for treatment of angina pectoris, hypertension and chronic heart failure. We have reported that enzyme kinetic parameters for carvedilol glucuronidation by human liver microsomes (HLM) differed greatly depending on the substrate form, namely, racemic carvedilol and each enantiomer. These phenomena were thought to be caused by mutual inhibition between carvedilol enantiomers during racemate glucuronidation. The aim of this study was to clarify the mechanism of these phenomena in HLM and human intestinal microsomes (HIM) and its relevance to uridine 5'-diphosphate (UDP)-glucuronosyl transferase (UGT) 1A1, UGT2B4 and UGT2B7, which mainly metabolize carvedilol directly in phase II enzymes. HLM apparently preferred metabolizing (S)-carvedilol to (R)-carvedilol in the racemate, but true activities of HLM for both glucuronidation were approximately equal. By determination of the inhibitory effects of (S)-carvedilol on (R)-carvedilol glucuronidation and vice versa, it was shown that (R)-carvedilol glucuronidation was more easily inhibited than was (S)-carvedilol glucuronidation. UGT2B7 was responsible for (S)-carvedilol glucuronidation in HLM. Ratios of contribution to (R)-carvedilol glucuronidation were approximately equal among UGT1A1, UGT2B4 and UGT2B7. However, enzyme kinetic parameters were different between the two lots of HLM used in this study, depending on the contribution ratio of UGT2B4, in which (R)-glucuronidation was much more easily inhibited by (S)-carvedilol than was (S)-glucuronidation by (R)-carvedilol. Meanwhile, HIM preferred metabolizing (R)-carvedilol, and this tendency was not different between the kinds of substrate form.
It has been clear from the above result that R. emodi is an effective herb in alleviating symptoms of primary dysmenorrhoea. It can serve as an alternative treatment without any apparent side effects. These results deserve further investigations.
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A patent ductus arteriosus (PDA) complicates the clinical course of preterm infants, increasing their risks of developing chronic lung disease (CLD), necrotizing enterocolitis (NEC), and intraventricular hemorrhage (IVH). Indomethacin is used as standard therapy to close a PDA, but is associated with reduced blood flow to the brain, kidneys and gastrointestinal tract. Ibuprofen, another cyclo-oxygenase inhibitor, may be as effective as indomethacin, with fewer side effects.
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Studies have been carried out on the effect of pH (from pH 11.33 to H(O) = -4.65) on the UV spectrum of mefenamic acid. The dissociation constant pKa was found to be 4.55 +/- 0.06 and the protonation constant pK(2) was -1.78 +/- 0.18 in methanol-aqueous media. Mefenamic acid was determined spectrophotometrically by formation of a coloured complex (2:5) with Fe(III). At 495 nm Beer's law was followed for the concentration range 96.52 to 579.12 mug ml(-1).
To provide updated evidence-based recommendations for the preventive treatment of migraine headache. The clinical question addressed was: Are nonsteroidal anti-inflammatory drugs (NSAIDs) or other complementary treatments effective for migraine prevention?