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Ponstel (Mefenamic Acid)
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Ponstel

Ponstel is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Ponstel is used for treating menstrual pain. It may be used for short-term (not more than 7 days) treatment of mild to moderate pain. Ponstel blocks the effect of certain substances in the body that are associated with pain and inflammation.

Other names for this medication:

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Celebrex, Voltaren, Dolobid, Lodine, Motrin, Indocin, Orudis, Toradol, Naproxen, Ibuprofen, Diclofenac, Voltaren, Aleve, Advil, Celecoxib, Naprosyn, Motrin, Ketoprofen

 

Also known as:  Mefenamic Acid.

Description

Ponstel is used for treating menstrual pain. It may be used for short term (not more than 7 days) treatment of mild to moderate pain.

Ponstel blocks certain substances in the body that are linked to inflammation. NSAIDs treat the symptoms of pain and inflammation.

Ponstel is also known as Mefenamic acid, Ponstan.

Generic name of Ponstel is Mefenamic Acid.

Brand name of Ponstel is Ponstel.

Dosage

Take Ponstel orally.

Take Ponstel with or without food.

Take Ponstel with a full glass of water.

If you want to achieve most effective results do not stop taking Ponstel suddenly.

Overdose

If you overdose Ponstel and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Ponstel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Ponstel if you are allergic to Ponstel components or to aspirin.

Do not take Ponstel if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Ponstel if you have had a severe allergic reaction (e.g., severe rash, hives, trouble breathing, growths in the nose, dizziness) to aspirin or a nonsteroidal anti-inflammatory drug (NSAID) (e.g., ibuprofen, celecoxib).

Do not take Ponstel if you have had recent or will be having bypass heart surgery.

Do not take Ponstel if you have kidney problems.

Do not take Ponstel if you have ulcers or inflammation of the stomach or bowel.

Do not use Ponstel with aspirin.

Be careful with Ponstel when it is used by children younger than 14 years old and by elderly people.

Avoid machine driving.

Avoid drinking alcohol.

It can be dangerous to stop Ponstel taking suddenly.

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Case reports and small case series suggest increased central nervous system (CNS) toxicity, especially convulsions, after overdose of mefenamic acid, compared with other nonsteroidal anti-inflammatory drugs (NSAIDs), although comparative epidemiological studies have not been conducted. The current study compared rates of CNS toxicity after overdose between mefenamic acid, ibuprofen, diclofenac and naproxen, as reported in telephone enquiries to the UK National Poisons Information Service (NPIS).

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To screen for and characterize compounds that protect corneal endothelial cells against unfolded protein response (UPR) and oxidative stress.

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Stimuli such as u.v. light or trauma which induce recurrence of herpes simplex may act by affecting virus replication in the skin. Such stimuli release pharmacologically active agents in the skin, including prostaglandins (PGs) such as PGE2. These agents, and other compounds which alter levels of adenosine cyclic monophosphate (cyclic AMP), were tested for their effect on the replication of herpes simplex virus (HSV) in Vero cells. Prostanglandin E2 (PGE2) and prostaglandin F2alpha both increase the size of HSV plaques; PGE2 also increases the yield of virus inoculated at low m.o.i. Moreover, inhibitors of prostanglandin synthesis decrease plaque size and inhibit the growth of virus inoculated at low m.o.i.; such inhibition can be partially overcome by adding PGE2. Analysis of the results suggest that prostaglandins can enhance cell-to-cell spread of HSV, but that cyclic AMP is probably not involved in this effect.

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Optimum conditions for the preparation of non-magnetic and magnetic microspheres of albumin-globulin mix (alglomix) containing mefenamic acid have been standardized. The effect of various parameters has been investigated with regard to the appearance, yield, drug content and encapsulation efficiency. The physicochemical parameters of the microspheres such as density, particle size distribution, surface topography and wall thickness, as well as the magnetite contained within the magnetic microspheres, have been determined. The infrared spectroscopic analysis confirmed the encapsulation of the drug and absence of free drug on the surface of the microspheres. The X-ray diffraction analysis confirmed that the crystallinity of the drug remained unchanged indicating thereby that no complex formation had taken place between core and coat materials. The in vitro release profiles of the microspheres have been studied. An attempt has also been made to check the in vivo efficacy in rats.

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The study design was a multi-center randomized control trial and included 144 patients. The diagnosis of TTH was based on the criteria of the International Classification of Headache Disorders-1 and all patients were diagnosed with episodic tension-type headache (ETTH). Changes in the severity of headache and shoulder pain were graded using a Visual Analogue Scale (VAS) before and after administration of drugs. Patients were randomized into NSAID alone (NSAID, mefenamic acid, 250 mg) group and NSAID (mefenamic acid, 250 mg) plus etizolam (0.5 mg) (NSAID-ET) group prior to treatment.

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It has been reported that ibuprofen interferes with the antiplatelet effect of low-dose aspirin. This interaction is ascribed to steric hindrance at the active site of cyclooxygenase-1 by ibuprofen, when aspirin is administered after ibuprofen. However, whether other non-steroidal anti-inflammatory drugs (NSAIDs) interact with aspirin similarly is not well defined. The aim of this study was to assess the influence of nine NSAIDs on the antiplatelet effect of aspirin.

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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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The accumulated experience was 515 woman-months. There were no pregnancies, neither ectopic nor intrauterine: Adverse events (AE) were mild. Some patients complained of a yellow discharge and itching. Fifty percent experienced mild abdominal discomfort which was easily managed with mefenamic acid.

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The marketed formulations of 6 analgesic preparations were compared in the treatment of patients suffering from acute exacerbations of low back pain using a crossover trial of balanced incomplete block design. Sixty out-patients with symptoms resulting from a mechanical or degenerative condition were each prescribed 3 drugs which were administered consecutively for 1 week each. The medications (and daily dosages) were coded as A --aspirin (3600 mg), B --dextropropoxyphene plus paracetamol (260 mg plus 2600 mg), C --indomethacin (150 mg), D --mefenamic acid (1500 mg), E --paracetamol (4000 mg), and F --phenylbutazone (300 mg). Daily pain scores were significantly lower (p less than 0.05) during treatment D than during treatments E and B, and significantly lower (p less than 0.05) during treatment A than during treatment B. There were large and significant differences between treatments in the percentages of recommended doses acceptable to the patients and in the number of defaults from the prescribed regimens. The patients chose F and D significantly more (p less than 0.05) often than A. Overall, there were consistently superior performances by mefenamic acid and phenylbutazone with little to choose between the two.

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We investigated the antiplatelet effect of NSAIDs using steady-state plasma concentration reported after usual doses. We studied the in vitro antiplatelet effect of NSAID alone, aspirin alone, aspirin before NSAID addition and aspirin after NSAID addition to platelet-rich plasma. The rates of platelet aggregation induced by collagen were determined. The final concentration of aspirin used was the 50% effective concentration (EC(50)) previously estimated in vitro.

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A total of 571 women with HMB. A purposeful sample of 27 women who were randomised or ineligible owing to treatment preference participated in semistructured face-to-face interviews around 2 and 12 months after commencing treatment.

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We report in this paper using measurement of intracellular free Ca2+ with fura-2, that flufenamic acid and several related blockers of the 25 pS Ca(2+)-activated non-selective cation channel cause release of Ca2+ from an intracellular store other than the endoplasmic reticulum, possibly from mitochondria. A new compound, 4'-methyl-DPC, is found to be as effective in blocking non-selective cation channels as other flufenamate analogs but, like the parent compound, the non-selective cation channel blocker DPC, it does not cause release of Ca2+ from intracellular stores. DPC and 4'-methyl-DPC are thus the most suitable of the available blockers of non-selective cation channels for use in studies on the role of these channels in normal cell function.

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To review the mechanisms and clinical significance of adverse interactions between warfarin and nonsteroidal anti-inflammatory drugs (NSAIDs) and discuss how these interactions can be avoided.

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Hematological analysis showed that mefenamic acid significantly reduced white blood cell count, red blood cell (RBC) count, hemoglobin content, lymphocytes levels, and neutrophils levels in healthy mice as compared with control, suggesting the immunosuppressive activity of mefenamic acid. Treatment with mefenamic acid also significantly reduced all the hematological parameters in cyclophosphamide-induced neutropenic mice, as compared with positive control group. We found that treatment with mefenamic acid significantly suppressed DTH after 24 h, 48 h, and 72 h, as compared with positive control group. Mefenamic acid treated groups showed a significant reduction in antibody titer against sheep RBCs as compared to control group, similar to the effect of cyclophosphamide. We also found increased mice lethality rate in mefenamic acid treated groups, as compared with positive control group.

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The effects of mefenamic acid and Bay K 8644 on voltage-dependent nifedipine-sensitive inward Ba2+ currents in pig urethral myocytes were investigated by use of conventional whole-cell configuration patch clamp. Mefenamic acid increased the peak amplitude of voltage-dependent nifedipine-sensitive inward Ba2+ current without shifting the position of the current-voltage relationship. Mefenamic acid (300 microM) caused little shift in the activation curve although the voltage dependence of the steady-state inactivation was shifted to more positive potentials by 11 mV in the presence of mefenamic acid. Bay K 8644 (> or = 100 nM) enhanced voltage-dependent nifedipine-sensitive inward Ba2+ currents in a concentration- and voltage-dependent manner, shifting the maximum of the current-voltage relationship by 10 mV in the hyperpolarizing direction. Bay K 8644 (1 microM) significantly shifted the voltage dependence of the activation curve to more negative potentials by approximately 9 mV although Bay K 8644 caused little shift in the steady-state inactivation curve. These results indicate that mefenamic acid increased voltage-dependent nifedipine-sensitive inward Ba2+ currents through the activation of L-type Ca2+ channels with different kinetics from those of Bay K 8644 in pig urethral myocytes.

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Fenamate NSAIDs are inhibitors of cyclooxygenases, antagonists of non-selective cation channels, subtype-selective modulators of GABA(A) receptors, weak inhibitors of glutamate receptors and activators of some potassium channels. These pharmacological actions are all implicated in the pathogenesis of ischemic stroke. The aim of this study was to investigate the hypothesis that the fenamate, mefenamic acid, is neuroprotective in an in vitro and in vivo model of stroke. Embryonic rat hippocampal neurons were cultured and maintained for up to 14 days in vitro. At 9 or 14 days, cells were exposed to glutamate (5microM) or glutamate (5microM) plus mefenamic acid (10-100microM) or the control agent, MK-801 (10microM) for 10min. 24h later, cell death was determined by measuring lactate dehydrogenase (LDH) levels in the culture media. In vivo, male Wistar rats (300-350g) were subjected to 2h middle cerebral artery occlusion (MCAO) followed by 24h reperfusion. Animals received either a single i.v. dose of MFA (10mg/kg or 30mg/kg), or MK-801 (2mg/kg) or saline prior to MCAO or, four equal doses of MFA (20mg/kg) at 1h intervals beginning 1h prior to MCAO. Ischemic damage was then assessed 24h after MCAO. In vitro, mefenamic acid (10-100microM) and MK-801 (10microM) significantly reduced glutamate-evoked cell death compared with control cultures. In vivo, MFA (20mg/kgx4) significantly reduced infarct volume, total ischemic brain damage and edema by 53% (p< or =0.02), 41% (p< or =0.002) and 45% (p< or =0.002) respectively. Furthermore, mefenamic acid reduced cerebral edema when measured as a function of brain water content. MK-801 was also neuroprotective against MCAO brain injury. This study demonstrates a significant neuroprotective effect by a fenamate NSAID against glutamate-induced cell toxicity, in vitro and against ischemic stroke in vivo. Further experiments are currently addressing the mechanism(s) of this neuroprotection.

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Ibuprofen and mefenamic acid are weak, competitive inhibitors of cyclooxygenase-2 (COX-2) oxygenation of arachidonic acid (AA) but potent, noncompetitive inhibitors of 2-arachidonoylglycerol (2-AG) oxygenation. The slow, tight-binding inhibitor, indomethacin, is a potent inhibitor of 2-AG and AA oxygenation whereas the rapidly reversible inhibitor, 2'-des-methylindomethacin, is a potent inhibitor of 2-AG oxygenation but a poor inhibitor of AA oxygenation. These observations are consistent with a model in which inhibitors bind in one subunit of COX-2 and inhibit 2-AG binding in the other subunit of the homodimeric protein. In contrast, ibuprofen and mefenamate must bind in both subunits to inhibit AA binding.

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Auricular acupuncture (AA) has been shown to alleviate acute and chronic pain. We investigated the effects of auricular electroacupuncture (AE) on pain and analgesic drug consumption in the first 48 h after unilateral mandibular third molar tooth extraction under local anesthesia in a prospective, randomized, double-blind, placebo-controlled study in 149 patients.

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Day-case laparoscopic subtotal hysterectomy may be considered as a potential treatment option in symptomatic women with major congenital uterine anomaly, in whom fertility potential is no longer an issue. Accurate pre-operative assessment of the upper urinary tract is considered essential.

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Substantial differences in management exist between practices when investigating and prescribing for menorrhagia in primary care. Rates of prescribing of effective medical treatment remain low. The decision to refer a woman impacts markedly on her chances of subsequently being operated on. Effective management in primary care may not reduce referral or hysterectomy rates.

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Trials with random or alternate allocation, testing interventions for the prevention or treatment of bleeding irregularities associated with the use of progestin-only contraceptives were eligible.

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Niflumic acid, 2-{[3-(trifluoromethyl)phenyl]amino}pyridine-3-carboxylic acid (NFA), a nonsteroidal anti-inflammatory drug that blocks cyclooxygenase (COX), was shown previously to activate [Na(+)](i)-regulated Slo2.1 channels. In this study, we report that other fenamates, including flufenamic acid, mefenamic acid, tolfenamic acid, meclofenamic acid, and a phenyl acetic acid derivative, diclofenac, also are low-potency (EC(50) = 80 μM to 2.1 mM), partial agonists of human Slo2.1 channels heterologously expressed in Xenopus oocytes. Substituent analysis determined that N-phenylanthranilic acid was the minimal pharmacophore for fenamate activation of Slo2.1 channels. The effects of fenamates were biphasic, with an initial rapid activation phase followed by a slow phase of current inhibition. Ibuprofen, a structurally dissimilar COX inhibitor, did not activate Slo2.1. Preincubation of oocytes with ibuprofen did not significantly alter the effects of NFA, suggesting that neither channel activation nor inhibition is associated with COX activity. A point mutation (A278R) in the pore-lining S6 segment of Slo2.1 increased the sensitivity to activation and reduced the inhibition induced by NFA. Together, our results suggest that fenamates bind to two sites on Slo2.1 channels: an extracellular accessible site to activate and a cytoplasmic accessible site in the pore to inhibit currents.

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During hypertonic saline induction, the evolution of intrauterine pressure, the oxytocin response and abortion were delayed in naproxen-treated patients. The PG synthesis inhibitors naproxen, mefenamic acid and ibuprofen decreased the high uterine resting pressure ('tone'), the frequency of contractions but not always the active pressure ('amplitude') in dysmenorrheic patients, with a coincident decrease in pain. The naproxen-sodium treatment decreased prostaglandins F and E in menstrual blood and uterine jet washings by 60--80 per cent.

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The native fluorescence of mefenamic, flufenamic and meclofenamic acids is more useful for determination of these drugs than is the fluorescence of the derivative substituted acridones and benzoxazines obtained from these drugs by treatment with sulphuric acid or formaldehyde respectively.

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A spectrophotometric procedure for the simultaneous determination of mefenamic acid and paracetamol in a mixture is described. Using 0.01 M methanolic hydrochloric acid as solvent, the absorbance of the mixture is measured at 248, 279 and 351 nm. The concentration of each component can be calculated by solving two equations using two wavelengths, either 248 and 279 nm or 248 and 351 nm.

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Synthesis of the ester was carried out using mefenamic acid, guaiacol. N. N'-dimethylaminopyridine, and N,N'dicyclohexylcarbodiimide. The hydrolysis of the ester was investigated in aqueous buffer solutions pH 1-12 as well as in Caco-2 homogenate, human plasma, and porcine liver esterase. Caco-2 cell monolayers were utilized for transport studies. Due to the high lipophilicity of the ester with a calculated logP of 6.15, bovine serum albumin (BSA, 4%) was included in the receiver compartment to obtain a good in vitro-in vivo correlation. Permeation of the ester was assessed with or without the exposure of cells to PMSF, an inhibitor of esterase.

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No currently marketed NSAID, even those that are COX-2 selective, spare gastric COX activity at therapeutic concentrations. Thus, all NSAIDs should be used cautiously until safer agents are developed.

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This study of sparingly soluble model drugs assesses (a) how pH and the aqueous boundary layer factors may affect in vitro and in vivo absorption, (b) to what extent single excipients (sodium taurocholate, hydroxypropyl-beta-cyclodextrin, KCl, propylene glycol, methylpyrrolidone, and polyethylene glycol 400) can mitigate adverse absorption effects, and (c) how a novel rank-order visualization tool can be applied in high-throughput screening to identify promising single-excipient effects on the absorption potential of test compounds. The products of accurately measured solubility and artificial-membrane permeability (PAMPA) values at pH 5.0, 6.2, and 7.4, fully taking into account factors such as aqueous boundary layer resistance, membrane retention, and the formation of drug dimers and trimers, were used to define a flux function. A "self-organized" data visualization tool based on the flux function was mined for the promising excipient-drug combinations. In excipient-free solutions, most of the compounds studied formed aggregates. The presence of an excipient predominantly lowered permeability, but most often not by the same amount as solubility was elevated. The compounds with absorption potential most helped by excipients were: clotrimazole>griseofulvin>progesterone>dipyridamole>glibenclamide>mefenamic acid>butacaine>astemizole. The HP-beta-CD effect observed for albendazole and glibenclamide appeared to follow Cmax trends in published pharmacokinetics studies. A surprising outcome of the in vitro measurements was that the classical pH Partition Hypothesis can be "inverted" in its monotonicity by sparingly soluble compounds.

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In the absence of objective symptoms, it is difficult to assess an adverse reaction during drug provocation testing. We evaluated the value of serum tryptase levels to distinguish between positive, negative and, even more important, so-called 'hysterical' reactions (conversion symptoms). The latter are occasionally observed in drug provocation tests when the patient experiences ambiguous subjective symptoms.

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buy ponstel online 2015-02-08

Groups were similar in age, parity, vaginal birth or relevant medical history. A buy ponstel statistically significant difference in pain scores was noted among the 3 groups during the procedure (group I, 4.13+/-1.28; group II, 5.93+/-1.26; group III, 5.58+/-1.51), (P<0.001); as well as 30 minutes later (group I, 1.78+/-0.89; group II, 2.53+/-0.81; group III, 2.23+/-0.94), (P<0.001) and 60 minutes later (group I, 1.2+/-0.46; group II, 1.98+/-0.83; group III, 1.68+/-0.75), (P<0.001). VAS at different time intervals among the groups was also statistically significant. No adverse effects were observed.

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Patent ductus arteriosus (PDA) with significant buy ponstel left to right shunt in preterm infants increases morbidity and mortality. Early closure of the ductus arteriosus may be achieved pharmacologically using cyclooxygenase inhibitors, or by surgery. The efficacy of both treatment modalities is well established. However, the preferred initial treatment of a symptomatic PDA in a preterm infant, surgical ligation or trial of indomethacin, has not been well established.

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This report describes a scoping study conducted in order to establish whether pharmaceutical compounds may be present in UK estuaries. Surface water samples collected from five UK estuaries were analysed for the presence of 14 pharmaceutical compounds selected from the priority lists of the UK Environment Agency and the Oslo and Paris Commission (OSPAR). The pharmaceutical compounds/metabolites clofibric acid, clotrimazole, dextropropoxyphene, diclofenac, ibuprofen, mefenamic acid, propranolol, tamoxifen and trimethoprim were detected at measurable concentrations in the samples collected. The concentrations of erythromycin, lofepramine, paracetamol, sulfamethoxazole and acetyl-sulfamethoxazole were all below the limits of detection of the methods used (between 4 and 20 ng l(-1)). The anti-fungal agent clotrimazole was the most frequently detected at a maximal concentration of Tegretol Cost 22 ng l(-1) and a median concentration of 7 ng l(-1). The analgesic compound ibuprofen was detected at a maximal concentration of approximately 930 ng l(-1) and a median concentration of 48 ng l(-1), whilst the other pharmaceutical compounds were detected between the limits of detection of the method used and 570 ng l(-1).

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Non-steroidal anti-inflammatories (NSAIDs) are analgesic, antipyretic, and, as their name implies, anti-inflammatory drugs, which are widely used for the treatment of a variety of human and veterinary disease conditions in which control of pain and inflammation is desired. Acetaminophen (ACE) is a common over-the-counter analgesic. Detection of a variety of widely used NSAIDs and ACE in fluid and tissue samples is an important diagnostic tool. A sensitive and selective analytical method has been developed for simultaneous screening of 12 NSAIDs and ACE by liquid chromatography-mass spectrometry with an atmospheric pressure chemical ionization interface set to operate in the negative ion mode of MS. Following sample preparation, all analytes were separated on a C18-reversed-phase column with a gradient elution of acetonitrile and acetic acid. Full-scan mass spectral fragmentation profiles were established for each analyte and individual extracted ion chromatograms were used for quantitation. Linearity of detection was observed over the 0.05-25.0 microg/mL range of standard concentrations. The instrument limits of detection (LOD), based on an individual analyte quantitation ions, fell between 0.05 and 1.0 microg/mL for all compounds. The matrix LODs were determined to be 0.05 microg/mL for phenylbutazone (m/z 307); 0.1 microg/mL for indomethacin (m/z 312), flunixin (m/z 295), and piroxicam (m/z 330); 0.5 microg/mL for ACE (m/z 150), diclofenac (m/z 250), ketoprofen (m/z 209), and mefenamic acid (m/z 240); 1.0 microg Paracetamol Suppository Child Dose /mL for oxyphenbutazone (m/z 323); 5.0 microg/mL for ibuprofen (m/z 205), salicylic acid (m/z 137), and tolmetin (m/z 212); and 10 microg/mL for naproxen (m/z 185).

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A rapid method has been developed to analyse carprofen (CPF), diclofenac (DCF), mefenamic acid (MFN), niflumic acid (NIFLU), naproxen (NAP), oxyphenylbutazone (OXYPHEN), phenylbutazone (PBZ) and suxibuzone (SUXI) residues in bovine milk. Milk samples are extracted with acetonitrile and sample extracts were purified on Evolute ABN solid phase extraction Cystitis Bactrim Dose cartridges. Aliquots were analysed by rapid resolution liquid chromatography tandem mass spectrometry (RRLC-MS/MS) with a runtime of 6.5 min. The method was validated in bovine milk, according to the criteria defined in Commission Decision 2002/657/EC. CCalpha values of 0.46, 1.08, 0.92, 1.26, 1.29, 2.12, 0.55 and 2.86 ng mL(-1) were determined for CPF, DCF, MFN, NIFLU, NAP, OXYPHEN, PBZ and SUXI, respectively. CCbeta values of 0.79, 1.85, 1.56, 2.15, 2.19, 3.62, 0.94 and 4.87 ng mL(-1) were determined for CPF, DCF, MFN, NIFLU, NAP, OXYPHEN, PBZ and SUXI, respectively. The measurement uncertainty of the method was estimated at 9, 28, 28, 45, 46, 45, 10 and 39% for CPF, DCF, MFN, NIFLU, NAP, OXYPHEN, PBZ and SUXI. Fortifying bovine milk samples (n=18) in three separate assays, show the accuracy of the method to be between 82 and 108%. The precision of the method, expressed as RSD values for the within-lab reproducibility at the three levels of fortification (5, 7.5 and 10 ng mL(-1)) was less than 16%, respectively. The advantage of the method is that low ng mL(-1) levels can be detected and quantitatively confirmed rapidly in milk and that 3 batches of samples can be analysed within a single day using RRLC-MS/MS with a runtime of 6.5 min.

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A patent ductus arteriosus (PDA) complicates the clinical Feldene Dosage 40 Mg 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 gut. Ibuprofen, another cyclo-oxygenase inhibitor, may be as effective with fewer side effects.

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This work deals with the spectroscopic (supported by quantum chemistry calculations), structural, and morphological characterization of mefenamic acid (2-[(2,3-(dimethylphenyl)amino] benzoic acid) polymorphs, known as forms I and II. Polymorph I was obtained by recrystallization in ethanol, while form II was reached by heating form I up to 175 °C, to promote the solid phase transition. Experimental and theoretical vibrational band assignments were performed considering the presence of centrosymmetric dimers. Besides band shifts in the 3345-3310 cm(-1) range, important vibrational modes to distinguish the polymorphs are related to out-of-phase and in-phase N-H bending at 1582 (Raman)/1577 (IR) cm(-1) and 1575 (Raman)/1568 (IR) cm(-1) for forms I and II, respectively. In IR spectra, bands assigned to N-H bending out of plane are observed at 626 and 575 cm(-1) for polymorphs I and Eldepryl Reviews II, respectively. Solid-state (13)C NMR spectra pointed out distinct chemical shifts for the dimethylphenyl group: 135.8 to 127.6 ppm (carbon bonded to N) and 139.4 to 143.3 ppm (carbon bonded to methyl group) for forms I and II, respectively.

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Sixteen RCTs were identified that fulfilled the inclusion criteria for this review. The reviewers extracted the data independently and odds ratios for dichotomous Motrin 800 Mg Dosage outcomes and weighted mean differences for continuous outcomes were estimated from the data of nine trials. The remaining seven trials were of crossover design with data unsuitable for pooling and their individual results were described in text form.

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Auricular acupuncture (AA) has been Strattera Brand Name shown to alleviate acute and chronic pain. We investigated the effects of auricular electroacupuncture (AE) on pain and analgesic drug consumption in the first 48 h after unilateral mandibular third molar tooth extraction under local anesthesia in a prospective, randomized, double-blind, placebo-controlled study in 149 patients.

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To determine the effificacy and safety Motrin 500 Mg of fenugreek seed and dry cupping on intensity of pain in primary dysmenorrhea.

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Mefenamic acid was more Retrovir Drug Class effective than placebo in short-term treatment of irregular bleeding and spotting associated with Implanon use.

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1. The perforated patch and conventional whole-cell recording techniques were used to study the action of flufenamic, mefenamic and niflumic acid on calcium-activated chloride and potassium currents in rabbit portal vein smooth muscle cells. 2. In K-conditions at a holding potential of -77 mV flufenamic acid and mefenamic acid decreased the amplitude of spontaneous transient inward currents (STICs, calcium-activated chloride currents, ICl(Ca)) in a concentration-dependent manner. The potency sequence was niflumic > flufenamic > mefenamic acid. 3. At -77 mV 1 x 10(-5) M flufenamic acid increased the STIC exponential decay time constant (tau). At higher concentrations the STIC decay was described by 2 exponentials with an initial decay (tau f) faster than the control tau value and a second exponential (tau s) which had a time constant slower than the control tau value. Low concentrations of mefenamic acid had no effect or decreased the tau value whereas in higher concentrations biphasic currents were recorded. 4. In K-free conditions the inhibitory effect of both High Dose Oral Prednisone Ms flufenamic and mefenamic acid on STIC amplitude was greater at +50 mV compared to -50 mV, showing that the effect of these agents was voltage-dependent. 5. In cells held at 0 mV in K-containing conditions the fenamates reduced both the frequency and amplitude of spontaneous transient outward currents (STOCs, calcium-activated potassium currents, IK(Ca)). The concentration range to produce these effects was higher than that to decrease STIC amplitude and the potency sequence was flufenamic > niflumic > or = mefenamic acid. 6. All these compounds in concentrations greater than 5 x 10(-5) M evoked a 'noisy' potassium current at 0 mV which reached a maximum after approximately 3 min. This current was readily reversible on washout of the drug and could be elicited several times in the same cell. The current-voltage relationship of the fenamate-evoked current exhibited pronounced outward rectification characteristic of IK(Ca). 7. The current evoked by 2 x 10(-4) M flufenamic acid and 5 x 10(-4) M niflumic acid was not affected by 1 x 10(-5) M glibenclamide but was markedly inhibited by 1 x 10(-3) M tetraethylammonium. Furthermore, large currents were activated by flufenamic and niflumic acid in the presence of caffeine and cyclopiazonic acid (an inhibitor of the sarcoplasmic reticulum Ca-ATPase) to deplete intracellular Ca-stores. 8. Conventional whole-cell recording was performed with pipette solutions in which the ability to buffer changes in intracellular calcium was varied by altering the concentration of the calcium chelator (2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA). Flufenamic acid (2 x 10(-4) M) and niflumic acid (5 x 10(-4) M) both evoked large outward currents when recordings were made with either 1 x 10(-4) M or 1 x 10(-2) M BAPTA. Furthermore, bathing the cells in nominally calcium-free extracellular solution did not reduce the amplitude of the evoked currents. 9. It is concluded that both flufenamic and mefenamic acid inhibit ICl(Ca) by a mechanism similar to niflumic acid, possibly open channel blockade. Furthermore, at concentrations greater than 5 x 10(-5) M all three fenamates inhibited STOC activity and evoked directly an outward current which resembled IK(Ca).

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Mice were dosed intraperitoneally with mefenamic acid either one day at 100mg/kg and 200mg/kg, or 14 days dosing at 50mg/kg/day and 100mg/kg/day. Plasma was taken for alanine aminotransferase activity. Mice were sacrificed Cymbalta Brand Name at the end of the study. Livers were removed and weighed. Liver samples were taken for histology. results: One-day doses of mefenamic acid revealed dose-dependent hepatocyte degeneration in the liver parenchyma. There were no significant changes in plasma alanine aminotransferase activity. Interestingly, 14-day daily doses induced hepatocellular necrosis, massive degeneration and inflammation. This was accompanied by a significant increase in plasma alanine aminotransferase activity and significant increase in the liver weight in the 100mg/kg/day mefenamic acid-dosed mice.

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The elimination of six acidic pharmaceuticals (clofibric acid, diclofenac, ibuprofen, ketoprofen, mefenamic acid, and naproxen) in a real wastewater treatment plant (WWTP) using an activated sludge system and membrane bioreactors (MBRs) was investigated by using a gas chromatography/mass spectrometry (GC/MS) system for measurement of the compounds. Limited information is available for some of the tested pharmaceuticals at present. Solid retention times (SRTs) of the WWTP and the two MBRs were 7, 15, and 65 days, respectively. The elimination rates varied from compound to compound. The MBRs exhibited greater elimination rates for the examined pharmaceuticals than did the real plant. Dependency Zithromax Buy Online of the elimination rates of the pharmaceuticals on SRTs was obvious; the MBR operated with a longer SRT of 65 days clearly showed better performance than did the MBR with a shorter SRT of 15 days. The difference between the two MBRs was particularly significant in terms of elimination of ketoprofen and diclofenac. Measurements of the amounts of adsorbed pharmaceuticals on the sludge and aerobic batch elimination experiments were carried out to investigate the elimination pathways of the pharmaceuticals. Results of the batch elimination tests revealed that the sludges in the MBRs had large specific sorption capacities mainly due to their large specific surface areas. Despite the sorption capacities of sludges, the main mechanism of elimination of the pharmaceuticals in the investigated processes was found to be biodegradation. Biodegradation of diclofenac, which has been believed to be refractory to biodegradation, seemed to occur very slowly.

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The human liver and kidney are important sites of MPA glucuronidation. MPA glucuronidation was inhibited to various extents by different NSAIDs and the four most effective inhibitors were niflumic acid, flufenamic acid, mefenamic acid and diflunisal. These drugs have similar molecular structures consisting of two aromatic rings bearing a carboxylic group.

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In isolated canine tracheal smooth muscle, repeated administrations of histamine result in a rapid reduction in contractile response to about 15% of the initial contraction (tachyphylaxis). Development of this tachyphylaxis is specific inasmuch as: 1) it does not develop to acetylcholine (10(-6) M or 10(-4) M), or serotonin (10(-5) M; and 2) maximally developed histamine tachyphylaxis is not associated with a parallel reduction in response to acetylcholine. Pretreatment with propranolol (10(-5) M) or phentolamine (10(-4) M) does not prevent tachyphylaxis: however, pretreatment with atropine (10(-4) M) does prevent tachyphylaxis in about 50% of the animals tested. Tachyphylaxis to histamine can be reversed in a dose- and time-dependent fashion with prostaglandin synthesis inhibiting agents. The order of potency obtained with such compounds (indomethacin greater than mefenamic acid greater than oxyphenbutazone greater than acetylsalicylic acid) is consistent with potencies for inhibition of prostaglandin synthesis found in the literature. Also, in indomethacin pretreated strips in which tachyphylaxis to histamine was prevented, exogenous addition of PGE2 (1.42 x 10(1-) M to 2.84 x 10(-9) M) and PGA2 in a high concentration (2.9 x 10(-9) M) are capable of selectively reducing the response to histamine without an effect on acetylcholine-induced contractions. These data suggest that the mechanism of histamine tachyphylaxis in the canine tracheal smooth muscle preparation involves prostaglandin synthesis.

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Randomised controlled trials in women of reproductive age treated with progesterone or progestogen-releasing intrauterine devices versus no treatment, placebo, or other medical or surgical therapy for heavy menstrual bleeding within primary care, family planning or specialist clinic settings were eligible for inclusion. Women with postmenopausal bleeding, intermenstrual or irregular bleeding, or pathological causes of heavy menstrual bleeding were excluded.

ponstel buy 2015-07-12

N-(2-Methyl-3-chlorophenyl)anthranilic acid (tolfenamic acid) and its metabolites in serum and urine were analyzed by a reversed-phase ion-pair HPLC method. The major metabolites were N-(2-methyl-3-chloro-4-hydroxyphenyl)anthranilic acid, and one of the minor metabolites was N-(2-formyl-3-chlorophenyl)anthranilic acid, i.e., products resulting from hydroxylation in either the methyl group or the methylchlorophenyl group of tolfenamic acid, and further oxidation of the hydroxymethyl group to a formyl group.

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We found that zooxanthellatoxin-B from a symbiotic marine alga, Symbiodinium sp., caused a concentration-dependent contraction of the rabbit isolated aorta at concentrations of 10(-7)-10(-5) M. Verapamil (10(-6) M) and mefenamic acid (10(-5) M) significantly attenuated the contractile response to zooxanthellatoxin-B at lower concentrations (10(-7)-10(-6) M) but not at higher concentrations (3 X 10(-6)-10(-5) M). The response to zooxanthellatoxin-B was partly inhibited by phentolamine (10(-6) M), whereas it was potentiated by ouabain (10(-5) M). Tetrodotoxin (10(-6) M), methysergide (10(-6) M), chlorpheniramine (10(-6) M) or indomethacin (3 X 10(-6) M), however, did not affect it. The zooxanthellatoxin-B-induced contraction was abolished by incubation in Ca2+-free solution. The contractile response increased in a concentration-dependent fashion with Ca2+ (0.03 and 10 mM) or Sr2 + (0.10 and 10 mM). After treatment with verapamil (10(-6) or 5 X 10(-6) M), the concentration-contractile response curves for Ca2+ and Sr2+ in the presence of zooxanthellatoxin-B were shifted to the right in parallel. MgCl2 (10 mM) shifted the concentration-response curve for Ca2+ more markedly than did verapamil. Zooxanthellatoxin-B increased tissue Na+ and reduced tissue K+ contents in the aorta, suggesting that zooxanthellatoxin-B increases Na+ and K+ permeability across the plasma membrane. These results suggest that the zooxanthellatoxin-B-induced contraction of the aorta is caused mainly by a direct action on smooth muscle, i.e., an increase in Ca2+ permeability that occurs at least partly through voltage-sensitive Ca2+ channels as well as through nonselective cation channels in the cell membrane of smooth muscle.

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Apolipoprotein-E (apoE) has been shown by noncovalent binding and photoaffinity labeling with [125I]T4 to possess a single L-T4 binding site with a K5 of about 3 x 10(7) M-1 and a relative affinity for analogs of L-T4 = D-T4 = rT3 = triiodothyroacetic acid > L-T3. T4 binding was not affected by the flavonoid EMD 21388 or heparin, but was inhibited by diclofenac = mefenamic acid > furosemide. Localization of the T4 site to the N-terminal 62-amino acid region of the mature peptide coded by exon 3 was deduced from the following evidence. 1) The N-terminal 15- to 26-kilodalton (kDa) fragments (within residues 1-160 to 210), but not the approximately 10- to 11-kDa fragments (within residues approximately 220-299), were labeled by [125I]T4. 2) Variants apoE2 and apoE4, with nonconservative mutations at positions 112 and 158 (the latter unable to interact with the apoB/E receptor), maintained the ability to bind T4. 3) Monoclonal antibodies MAb 1D7 and 3H1 (epitopes at positions 139-169 and 243-272, respectively) failed to inhibit T4 binding, but MAb 6H7 (epitope at 1-125) decreased labeling by about 24%. 4) Polymers of apoE were specifically labeled despite the interaction between amphipathic alpha-helices of the exon 4-encoded region (63-299). We conclude that apoE, as previously observed with apoA-I and apoB, possesses a T4-binding domain separate from the lipid-binding domain and distinct from both the heparin- and the cell receptor-binding sites. Thyroid hormone binding by apoE may facilitate uptake of the hormone by cells through apoB/E receptors, which are widely distributed in tissues.

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This study was performed in Iran on 92 single 18-24 year old students with BMI :19-25 and obtaining pain intensity score of 5-8 in Visual Analogue Scale that were randomly classified and included in two groups of 46 persons. The participants received two capsules of Mefenamic Acid and Rosa damascena with the similar physical properties in two consecutive cycles per 6 hours for 3 days in a cross-over form. The data were collected through the questionnaire of demographic characteristics and check-list of visual analogue scale. Descriptive statistics and repeated measurement test and independent samples t test by using SPSS (13/win) were used in order to determine and compare the effects of two drugs on dysmenorrheal pain intensity of the groups.

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The primary objective of this review was to investigate the effectiveness of non-steroidal anti-inflammatory drugs (NSAIDs) in achieving a reduction in menstrual blood loss in women of reproductive years HMB.

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The aim of this investigation was to study the inhibition of 11 nonsteroidal anti-inflammatory drugs (NSAIDs) on the human liver phenol sulfotransferases (HL-PST) and catechol sulfotransferase (HL-CST).

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This open-label randomized controlled trial was designed to compare the efficacy of acupuncture and combined oral contraceptive (COC) pill in treating moderate-to-severe primary dysmenorrhea. Fifty-two participants were randomly assigned to receive either acupuncture (n = 27) or COC (n = 25) for three menstrual cycles. Mefenamic acid was prescribed as a recue analgesic drug with both groups. The statistical approach used for efficacy and safety assessments was intention-to-treat analysis. By the end of the study, both treatments had resulted in significant improvement over baselines in all outcomes, that is, maximal dysmenorrhea pain scores, days suffering from dysmenorrhea, amount of rescue analgesic used, and quality of life assessed by SF-36 questionnaire. Over the three treatment cycles, COC caused greater reduction in maximal pain scores than acupuncture, while improvements in the remaining outcomes were comparable. Responders were defined as participants whose maximal dysmenorrhea pain scores decreased at least 33% below their baseline. Response rates following both interventions at the end of the study were not statistically different. Acupuncture commonly caused minimal local side effects but did not cause any hormone-related side effects as did COC. In conclusion, acupuncture is an alternative option for relieving dysmenorrhea, especially when COC is not a favorable choice.

buy ponstel online 2015-03-20

Mefenamic acid (MEF) is a non-steroidal anti-inflammatory drug indicated for relief of mild to moderate pain, and for the treatment of primary dysmenorrhea. The presence of MEF in raw and sewage waters has been detected worldwide at concentrations exceeding the predicted no-effect concentration. In this study, using experimental designs, different oxidative processes (H2O2, H2O2/UV, fenton and Photo-fenton) were simultaneously evaluated for MEF degradation efficiency. The influence and interaction effects of the most important variables in the oxidative process (concentration and addition mode of hydrogen peroxide, concentration and type of catalyst, pH, reaction period and presence/absence of light) were investigated. The parameters were determined based on the maximum efficiency to save time and minimize the consumption of reagents. According to the results, the photo-Fenton process is the best procedure to remove the drug from water. A reaction mixture containing 1.005 mmol L(-1) of ferrioxalate and 17.5 mmol L(-1) of hydrogen peroxide, added at the initial reaction period, pH of 6.1 and 60 min of degradation indicated the most efficient degradation, promoting 95% of MEF removal. The development and validation of a rapid and efficient qualitative and quantitative HPLC/UV methodology for detecting this pollutant in aqueous solution is also reported. The method can be applied in water quality control that is generated and/or treated in municipal or industrial wastewater treatment plants.