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Pharmaceuticals in the aquatic environment have received great attentions from the general and scientific community due to their potential impacts on ecological and human health. We investigated the occurrence of twelve acidic pharmaceuticals and herbicides (salicylic acid, clofibric acid, ibuprofen, gemfibrozil, fenoprofen, naproxen, ketoprofen, mefenamic acid, tolfenamic acid, diclofenac, meclofenamic acid and indomethacin) in surface waters of the Yellow River, Hai River and Liao River in north China during the wet and dry seasons and assessed the potential risks to aquatic organisms posed by these acidic compounds. Seven acidic compounds were detected in the rivers, including five non-steroidal anti-inflammatory drugs (salicylic acid, ibuprofen, diclofenac, mefenamic acid and naproxen), and two blood lipid regulators (clofibric acid and gemfibrozil). The concentrations for acidic pharmaceuticals in the Yellow River and Liao River were in most cases higher in the dry season than in the wet season, but the concentrations of acidic compounds in the Hai River were generally higher in July than in November. High concentrations of these detected compounds in the Yellow River, Hai River and Liao River were found more frequently at those sites located in metropolitan areas, lower reaches or river confluences. Only diclofenac and ibuprofen were found to have medium to high risks in the three rivers based on the calculated risk quotients.
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A study of the electroencephalographic patterns observed following iv administration of increasing doses of mefenamic acid in acute experiments on curarized cats and rats and the possible modification of these effects by naloxone was carried out. Mefenamic acid produced in both species a progressive and dose-related increase of the voltage of the baseline patterns. With high doses, besides slow waves and fusiform complexes, an irritative activity with spikes and complexes of polyspikes was observed. The recovery of the basal activity was obtained within 15 min, except for the highest dose, under which the effect lasted 30 min after administration. Cats displayed a higher sensitivity than did rats. Naloxone did not modify the EEG effects of mefenamic acid, neigher in rats nor in rats. This fact suggests that the locus of action of these drugs is different. Mefenamic acid appears to act centrally with relatively short-lasting depressant effects at low doses and facilitating or stimulant effects at high doses.
Reactions to human seminal plasma may present as immediate hypersensitivity, cell-mediated hypersensitivity, or fixed eruptions. There are no typical responses to semen. An abnormal skin lesion or systemic response after intercourse may be the only clue to identifying those who are reacting to semen. The use of condoms has proven to be the most consistent preventive modality. However, the use of condoms is unacceptable to some regardless of the relief provided. Although conventional therapy for hypersensitivity reactions to human seminal plasma is suboptimal, one should be aware of MA in the treatment of an atypical cause of human seminal plasma induced reactions.
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A Finnigan MAT TSQ 700 triple quadrupole mass spectrometer equipped with a Harvard 22 syringe pump has been used to investigate the thermal decomposition of three common pharmaceuticals, acetaminophen, indomethacin, and mefenamic acid. In addition, comparative measurements on these same drugs were carried out by HPLC after thermally degrading them at elevated temperatures in order to evaluate the usefulness of the ESI-MS as a rapid means of determining the relative stability and identifying thermal decomposition products. Similar results were obtained between the two techniques (i.e., the relative rates of decomposition were mefenamic acid > indomethacin > acetaminophen), with the advantage that the ESI-MS approach was much quicker to perform.
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The effect of sodium meclofenamate on the binding of [3H]prostaglandin E2 [( 3H]PGE2) to membranes from human myometrium was investigated. Meclofenamate inhibited the binding of [3H]PGE2 to high-affinity (dissociation constant 1.5 nmol/l) sites in a reversible dose-dependent manner (inhibition constant 11 mumol/l). The mechanism of inhibition was mainly competitive, but at high doses of meclofenamate (greater than or equal to 100 mumol/l) there was loss of PGE receptor sites. Of several PG synthesis inhibitors tested, only meclofenamate and, to a lesser extent, mefenamic acid had a significant inhibitory effect. PGE2 stimulated cyclic AMP generation in slices of human myometrium and this was inhibited by meclofenamate in a dose-dependent manner (50% inhibition occurred at 9 mumol/l). Again, this effect was specific for meclofenamate and fitted a competitive mechanism at doses in the range 1-10 mumol/l and a non-competitive mechanism at higher doses. The data show that meclofenamate, in addition to its traditional role as a PG synthesis inhibitor, affects directly PGE receptor binding and activation.
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The purpose of this mini review is to discuss the use of physiologically-based drug absorption modeling to guide the formulation development. Following an introduction to drug absorption modeling, this article focuses on the preclinical formulation development. Case studies are presented, where the emphasis is not only the prediction of absolute exposure values, but also their change with altered input values. Sensitivity analysis of technologically relevant parameters, like the drug's particle size, dose and solubility, is presented as the basis to define the clinical formulation strategy. Taking the concept even one step further, the article shows how the entire design space for drug absorption can be constructed. This most accurate prediction level is mainly foreseen once clinical data is available and an example is provided using mefenamic acid as a model drug. Physiologically-based modeling is expected to be more often used by formulators in the future. It has the potential to become an indispensable tool to guide the formulation development of challenging drugs, which will help minimize both risks and costs of formulation development.
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Late proliferative (days 9 to 14) and midsecretory (days 18 to 24) human endometria were maintained in organ culture in the presence of 17 beta-estradiol and/or progesterone or mefenamic acid 17 beta-estradiol (0.1 to 1,000 ng/ml) increased prostaglandin F (PGF) secretion by both proliferative and secretory endometria. Progesterone (1,000 ng/ml) markedly inhibited PGF secretion by proliferative but not secretory endometrium. 17 beta-estradiol and progesterone had no effect on prostaglandin E (PGE) secretion by both types of endometrium. Secretion of both PGF and PGE by proliferative and secretory endometria was inhibited by mefenamic acid ( 1 microgram/ml). This was more apparent with PGF secretion and was detectable within the first 2 hours of culture. These findings indicate that the human endometrium is a rich source of PGF and PGE and that the production of PGF is regulated by gonadal steroids. These results support the concept that one mechanism of action of mefenamic acid in the treatment of dysmenorrhea is inhibition of prostaglandin production.
The X-ray scanning and X-ray exposure under our experimental conditions did not affect the pharmaceutical quality of drug tablets.
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To determine whether an educational package could influence the management of menorrhagia, increase the appropriateness of choice of non-hormonal treatment, and reduce referral rates from primary to secondary care.
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To determine the effectiveness of antifibrinolytics in achieving a reduction in heavy menstrual bleeding.
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Television microscopy was used to observe the responses of in vivo arterioles and venules of the rat cremaster muscle to the topical application of angiotensin II (10(-8) and 10(-6) M). Neither the first- (A1) or second-order arterioles (A2) nor the first- (V1) or second-order venules (V2) constricted significantly to angiotensin II. However, after the inhibition of local prostaglandin synthesis with either mefenamic acid or indomethacin, both A1 and A2, but not the venules, gave a significant constrictor response to angiotensin II (10(-6) M). Arterioles and venules, which were preconstricted with norepinephrine, dilated to their initial baseline diameters after angiotensin II (10(-6) M), a response not observed when the microvessels were pretreated with either an angiotensin antagonist or a prostaglandin synthesis inhibitor. These observations indicate that endogenous prostaglandins exert a significant dilator influence on the larger arterioles, that this dilator influence appears to oppose the constrictor effect of angiotensin II, and that angiotensin II acts on specific receptors to induce synthesis and/or release of dilator prostaglandins in large arterioles. However, prostaglandins cannot account for the absence of a venular constriction to angiotensin.
The current data demonstrate that milk is a promising drug carrier.
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There has been growing awareness that alleviation of wound pain and associated symptoms after obstructive sleep apnea (OSA) surgeries may improve the quality of care. We performed a hospital-based study to compare the effectiveness and safety of two different regimens in the treatment of postoperative pain.
All NSAIDs with different acidic functional groups were classified as highly permeable based on their Caco-2 cell permeability. Only ketorolac appeared to have a potential for interaction with cellular efflux pumps. Solubility classification was based on comparison of equilibrium solubility at pH 1.2, 5.0. and 7.4 relative to marketed dose strengths in 250 ml. The pKa values for the acidic NSAIDs studied were between 3.5 and 5.1. and, as expected, their solubility increased dramatically at pH 7.4 compared to pH 1.2. Only three NSAIDs, ketorolac, ketoprofen. and acetyl salicylic acid, meet the current criteria for high solubility over the entire pH range. However, with the exception of ibuprofen, oxaprozin, and mefenamic acid, the remaining compounds can be classified as Class I drugs (high solubility-high permeability) relative to solubility at pH 7.4. The use of bio-relevant media simulating gastric and intestinal milieu for solubility measurements or increasing the dose volume to 500 ml did not provide for a better boundary for solubility classification.
Tranexamic acid, a synthetic derivative of the amino acid lysine, is an antifibrinolytic agent that acts by binding to plasminogen and blocking the interaction of plasmin(ogen) with fibrin, thereby preventing dissolution of the fibrin clot. Tranexamic acid (Transamin®) is indicated in Japan for use in certain conditions with abnormal bleeding or bleeding tendencies in which local or systemic hyperfibrinolysis is considered to be involved. This article reviews the efficacy and tolerability of tranexamic acid in conditions amenable to antifibrinolytic therapy and briefly overviews the pharmacological properties of the drug. In large, randomized controlled trials, tranexamic acid generally significantly reduced perioperative blood loss compared with placebo in a variety of surgical procedures, including cardiac surgery with or without cardiopulmonary bypass, total hip and knee replacement and prostatectomy. In many instances, tranexamic acid also reduced transfusion requirements associated with surgery. It also reduced blood loss in gynaecological bleeding disorders, such as heavy menstrual bleeding, postpartum haemorrhage and bleeding irregularities caused by contraceptive implants. Tranexamic acid significantly reduced all-cause mortality and death due to bleeding in trauma patients with significant bleeding, particularly when administered early after injury. It was also effective in traumatic hyphaema, gastrointestinal bleeding and hereditary angioneurotic oedema. While it reduces rebleeding in subarachnoid haemorrhage, it may increase ischaemic complications. Pharmacoeconomic analyses predicted that tranexamic acid use in surgery and trauma would be very cost effective and potentially life saving. In direct comparisons with other marketed agents, tranexamic acid was at least as effective as ε-aminocaproic acid and more effective than desmopressin in surgical procedures. It was more effective than desmopressin, etamsylate, flurbiprofen, mefenamic acid and norethisterone, but less effective than the levonorgestrel-releasing intra-uterine device in heavy menstrual bleeding and was as effective as prednisolone in traumatic hyphaema. Tranexamic acid was generally well tolerated. Most adverse events in clinical trials were of mild or moderate severity; severe or serious events were rare. Therefore, while high-quality published evidence is limited for some approved indications, tranexamic acid is an effective and well tolerated antifibrinolytic agent.
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The present study investigates the effects of several nonsteroidal anti-inflammatory drugs on mouse palatal fusion in vivo and in vitro. Five different nonsteroidal anti-inflammatory agents were injected into pregnant mice of the AKR-strain on day 13.5 of gestation. Paired palatal processes from 13.5- and 14.5-day-old mouse embryos were organ-cultured for 72 hours in control and anti-inflammatory drug-containing media. Each experimental group of animals and explants received one of the following drugs: naproxen, sulindac, indomethacin, diclofenac, and mefenamic acid. Drug treatment induced different frequencies of cleft palate in the offspring. The most teratogenic drug was sulindac, and indomethacin was almost ineffective. In vitro each drug prevented fusion of the palatine processes in treated explants, and the degree of inhibition was dependent on the stage of development at the time of explanation. In both the in vivo and in vitro experiments, the drugs prevented medial epithelial cell breakdown that normally occurs in the medial secondary palatal epithelium. The results obtained in the present study suggest that prostaglandins may play an important role in normal differentiation of the developing palatine region.
Certain nonsteroidal anti-inflammatory drugs (NSAID) of the fenamate chemical class are known to cause diarrhea in clinical use. Paradoxically, this action is shared by prostaglandins, against whose syntheses are inhibited by NSAID. This study was done to investigate the laxative potential of 5 NSAID (meclofenamate, flufenamate, mefenamate, indomethacin and aspirin). The ability to produce a laxative response was assessed by determining effects on fluid absorption in vitro in hamster everted sacs and by the enteropooling assay in hamster small intestine. In addition, the lytic action of these drugs on the erythrocyte membrane was determined to arrive at a possible mechanism of action. All of the NSAID, except aspirin, produced dose-related inhibition of fluid transport, similar to prostaglandin E1 and E2. The order of inhibition was flufenamate greater than meclofenamate greater than mefenamate greater than indomethacin. Like results were obtained when enteropooling was measured in vivo. Flufenamate and meclofenamate produced lumenal fluid accumulation comparable to two laxatives, dioctyl sodium sulfosuccinate and ricinoleic acid. Finally, the effects of these NSAID on fluid movement paralleled their lytic action on the erythrocyte membrane model, suggesting that NSAID may produce diarrhea in a manner similar to certain laxatives, by increasing mucosal permeability through membrane damage.
The asymmetric unit of the title compound, C22H21N3O2, consists of two independent mol-ecules (A and B) having differing conformations. The differences mainly concern the dihedral angles which the hy-droxy-phenyl and di-methyl-phenyl rings subtend to the central phenyl-ene ring, these being 30.16 (6) and 58.60 (6)° in mol-ecule A and 13.42 (7) and 60.31 (7)° in B. With the exception of the dimethyphenyl substituent, the conformations of the rest of each mol-ecule are largely determined by intra-molecular O-H⋯N and N-H⋯O hydrogen bonds. In the crystal, N-H⋯O hydrogen bonds link the mol-ecules into chains extending parallel to the a axis in which the types of mol-ecules alternate in an …A…B…A…B… fashion.
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Gastric infection with Helicobacter pylori was excluded in all patients. Of the 16 patients on NSAIDs, four had gastritis, four had erosions or ulceration and eight had a normal examination. Endoscopy was normal in all patients in the control group. The LI% (mean +/- S.E.M.) in the entire NSAID group was 4.09 +/- 0.29 and in the control group 3.57 +/- 0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 +/- 0.61 and 3.07 +/- 0.32, respectively. There was no significant difference in LI% between the endoscopic subgroups of patients on NSAIDs or between patients on NSAIDs who had normal endoscopy and the control patients.
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885 women consulting their general practitioner with menorrhagia over four years.
The activities of HL-PST and HL-CST were measured with 4 microM 4-nitrophenol and 60 microM dopamine (the sulfate acceptors) and 0.4 microM 3'-phosphoadenosine-5'-phosphosulfate [35S] (the sulfate donor). Samples of liver were obtained from five patients, aged 55-79 years, undergoing clinically indicated hepatectomy. The inhibition curves were constructed with at least five concentrations of the inhibitor.
Pharmaceutical and personal care products (PPCPs) enter aquatic environments via sewage treatment facilities and their potentially toxic effects on biota, particularly aquatic organisms, are of considerable concern. In this study, we investigated the acute toxicity of selected PPCPs on a freshwater crustacean (Thamnocephalus platyurus) and a fish species (Oryzias latipes). The 24-hr median lethal concentration (LC(50)) values of ibuprofen, mefenamic acid, indometacin, carbamazepine, propranolol, ifenprodil, clarithromycin and triclosan for T. platyurus were estimated to be 19.59, 3.95, 16.14, > 100, 10.31, 4.43, 94.23 and 0.47 mg/l respectively. Conversely, the 96-hr LC(50) values for these PPCPs were estimated at > 100, 8.04, 81.92, 45.87, 11.40, 8.71, > 100 and 0.60 mg/l for O. latipes, respectively. The toxic sensitivity of T. platyurus to these PPCPs, except for carbamazepine, was therefore higher than for O. latipes. No acute toxicity effects were associated with PPCPs, such as atenolol, disopyramide, famotidine, fluconazole, erythromycin and levofloxacin, in the two aquatic organisms at the concentrations tested in this study (> 100 mg/l). These findings may help us to understand the potential biological effects and risks associated with PPCP exposure in aquatic organisms. Further long-term studies are required to fully assess the growth and reproduction of these compounds on aquatic biota.
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Indomethacin is an inhibitor of prostaglandin synthesis and has several uses, including the ability to encourage closure of a patent ductus in premature neonates. A rapid, accurate, and sensitive high-performance liquid chromatographic (HPLC) method is described for measuring plasma concentrations of indomethacin. An acidic buffer (citrate, pH 3.0) was employed to alter the pH of the aqueous phase prior to extraction to minimise interference interference from endogenous compounds. Extraction of indomethacin from plasma was optimally achieved with petroleum ether (boiling fraction of 40-60 degrees C):dichloromethane (50:50). However, separation of indomethacin from plasma proteins was attempted unsuccessfully using acetonitrile precipitation; severe band broadening occurred due to injected sample solvent problems. The absolute recoveries for indomethacin and internal standard (mefenamic acid) were over 90% (n = 3). Precision was expressed as the coefficient of variation (n = 4), which was less than or equal to 8% at each of six indomethacin concentrations in the range 50-2,000 ng/ml. The limit of quantitation of indomethacin in plasma was 50 ng/ml (0.5 ml of plasma injected). We report an HPLC method for the quantitation of indomethacin in plasma that may have widespread applicability for routine drug assay laboratories.
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The present study investigated the applicability of a laccase based bioprocess for the treatment of a mixture containing 13 selected pharmaceuticals. To do so, laccase was immobilized as cross-linked enzyme aggregates (MAC-CLEAs) on amine functionalized magnetic nanoparticles using chitosan/1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide hydrochloride (EDAC) as the cross-linking system. The activity recovery of laccase reached 61.4% under the optimal conditions of MAC-CLEAs formation. The latter exhibited enhanced storage stability over one year at 4°C and showed better temperature resistance compared to its soluble counterpart. The biocatalysts were properly recycled and the catalytic activity recovery was good even after a hundred and fifty batch reactions. Complete removal of pharmaceuticals like acetaminophen, diclofenac, mefenamic acid, atenolol and epoxy carbamazepine and partial removal of fenofibrate, diazepam, trimethoprim, and ketoprofen by laccase was achieved within 12h of incubation, whereas efficient removal of indometacin required the presence of mediator.
Agents used to color, flavor, preserve or identify medication frequently used in the treatment of allergic diseases may in themselves produce severe allergic or toxic reactions. Some cross-react with Aspirin. Aminopyrine, Indomethacin (indocin), Mefensmic Acid (ponstel) to which an allergic patient may be sensitive. Three case reports are presented.
Electronic searches for relevant randomised controlled trials of the Cochrane Menstrual Disorders and Subfertility Group Specialised Register of controlled trials, MEDLINE, EMBASE, Current Contents, the Cochrane Library and CINAHL were performed. Attempts were also made to identify trials from citation lists of review articles and drug companies were approached for unpublished data. In most cases, the first author of each included trial was contacted for additional information. An updated search was performed in September and October 2001 but no new eligible trials were identified.
34 women with recurrent primary dysmenorrhea were given prescriptions for mefenamic acid and told to use it as needed for pain and cramps. 85% felt the dysmenorrhea had improved and 15 of the women said it was completely controlled. Virtually all felt it more effective than aspirin and 13 of 18 who could make a comparison considered it more effective than propoxyphene. There were 3instances of nausea or vomiting and 1 of sleepiness. A double-blind study is now underway.
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.