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At 8 weeks after surgery, gastroduodenal reflux induced esophageal erosions and ulcer formation as well as marked thickening of the esophageal wall. Histological study showed an increase of thickness of the esophageal mucosa, hyperplasia of the epidermis and basal cells, ulcer formation, and marked infiltration of inflammatory cells. The macroscopic ulcer score and histological ulcer length were significantly reduced by treatment with rabeprazole or CMM but not by nizatidine or ecabet sodium, compared with each control. Rabeprazole, nizatidine, or ecabet sodium did not affect the severity of mucosal hyperplastic scores or histological parameters in esophagitis. In contrast, the CMM group showed a significant decrease in the mucosal hyperplastic and inflammatory scores. The enhanced expression of CINC-1, COX-2, and iNOS mRNA in the control group was also markedly inhibited in the CMM-treated group. ONO-1714 or meloxicam treatment significantly reduced the macroscopic scores of ulcer and hyperplasia. The trypsin activity in the esophageal lumen was significantly increased in the control diet group, and this increase was significantly inhibited in the CMM-treated group. The expression of PAR-1 and -2 mRNA was confirmed in rat esophageal epithelium.
The NSAIDs Indo, Ibu, Ke, Ket, P and Te yielded an antrum ulcer area: 5-29% and intestinal erosion, 101-395 mm2, similar to Indo (p > 0.50). In contrast there were neither ulcers nor intestinal erosions with Mac, A, Di, E and Nap (p > 0.50). While there were absence of ulcers with Ace, Me, Na, Ni and Pa and slight intestinal erosion (0-23 mm2; p < 0.01). II. There were differences in the following oral (NAIDs: Ace, Me, NA, Ni and Pa, yielding 0-5% fundic erosion and 0-22 mm2 intestinal erosion (p < 0.001). The other NSADs yielded 33-90% fundic erosion and 116-550 mm2 intestinal erosion, similarly to Indo (p > 0.50).
mobic medication guide
We have evaluated the selectivity in vitro of various conventional nonsteroidal anti-inflammatory drugs (NSAIDs) and new anti-inflammatory compounds (NS-398, L-745,337 and SC58125) in inhibiting the cyclooxygenase activity of platelet prostaglandin endoperoxide synthase (PGHS)-1 and monocyte PGHS-2 in a human whole blood assay. The effects of the compounds towards the cyclooxygenase activity of monocyte PGHS-2 induced in response to lipopolysaccharide (LPS) was evaluated by measuring the levels of PGE2 produced in plasma. The effects of the same inhibitors on platelet PGHS-1 activity were assessed by allowing 1-ml whole blood samples to clot at 37 degrees C for 1 h in the presence of the compounds and measuring immunoreactive TXB2 levels in serum. Under these experimental conditions, most compounds resulted equipotent towards the two isozymes. Differently, meloxicam, nimesulide and diclofenac were approximately 10- to 20-fold more potent in inhibiting the cyclooxygenase activity of monocyte PGHS-2 than platelet PGHS-1. L-745,337, NS-398 and SC58125 achieved selective inhibition of monocyte PGHS-2 (IC50, PGHS-1/IC50, PGHS-2: < 100) and may provide adequate tools to test the contribution of this novel pathway of arachidonate metabolism to human inflammatory disease and to verify the hypothesis that the common side-effects of NSAIDs are due primarily to their ability to affect the activity of PGHS-1.
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The involvement of the nitric oxide-cyclic GMP pathway in the antinociceptive action of the cyclooxygenase-2 preferential inhibitor meloxicam was assessed in the rat formalin test. Rats received local pretreatment with saline or meloxicam and then 50 microl of dilute formalin (1%). Local administration of meloxicam produced a dose-dependent antinociception in the second phase of the formalin test. The antinociception produced by meloxicam was due to a local action as its administration in the contralateral paw was ineffective. Local pretreatment of the paws with saline or N(G)-D-nitro-arginine methyl ester (D-NAME) did not affect the antinociception produced by meloxicam. However, N(G)-L-nitro-arginine methyl ester (L-NAME, a NO synthesis inhibitor) or 1H-(1,2,4)-oxadiazolo(4,2-a)quinoxalin-1-one (ODQ, a soluble guanylyl cyclase inhibitor) blocked in a dose-dependent way the effect of meloxicam. It is concluded that the peripheral antinociceptive effect of meloxicam involves a local NO-cyclic GMP pathway.
L-carnitine and meloxicam alleviated oxidative stress, probably by decreasing lipid peroxidation and enforcing antioxidant defense system. Acute renal inflammatory injury can be prevented much more effectively by combination therapy rather than by conventional therapy alone.
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Duhuo Jisheng decoction (DJD) is considered beneficial for controlling knee osteoarthritis (KOA)-related symptoms in some Asian countries. This review compiles the evidence from randomised clinical trials and quantifies the effects of DJD on KOA.
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The results suggest that niosomes may be promising vehicles for transdermal delivery of MX.
The optimal treatment of cancer cachexia remains unknown. In this study, we compared the efficacy of three different treatment modalities in the management of cancer cachexia.
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Cervical periradicular injection of meloxicam reduced CBP by 81% at 90-day follow-up and also improved functional recovery.
In the control group, there were more positive cells of Wnt, GSK-3β and Axin, which were intensively distributed, deeply colored, and strongly positive; In the model group, there were less positive cells of Wnt, GSK-3β and Axin, which were sparsely distributed and weakly positive. The expression of Wnt, GSK-3β, Axin and P-β-catenin in the model group was less than that in the control group (all P < 0.05); expression of Wnt, GSK-3β, Axin and P-β-catenin in the EA group and medication group was higher than that in the model group (all P < 0.05); expression of Wnt, GSK-3β, Axin and P-β-catenin was not significantly different between EA group and medication group (all P > 0.05).
mobic inflammatory medicine
To determine the lowest efficacious dose of oral meloxicam for relieving pain in cats with a sodium urate (SU)-induced acute inflammatory synovitis.
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The trend towards increased incidence of no follicular rupture when Melox was combined with LNG suggests that the addition of a cox-2 inhibitor has the potential to improve the contraceptive efficacy of LNG by a pre-fertilization effect.
Overall rUO rates were 10.94% (21/192 cats) at 24 hours and 23.57% (37/157 cats) at 30 days after IUC. At 24 hours and 30 days after IUC, rUO developed in 10 of 140 (7.14%) and 20 of 110 (18.18%) prazosin-treated cats, respectively, compared with 10 of 46 (21.74%) and 16 of 41 (39.02%) phenoxybenzamine-treated cats, respectively. Reobstruction developed following use of a 5F or 3.5F urinary catheter in 11 of 58 (18.97%) and 7 of 105 (6.67%) cats, respectively, through 24 hours. There was no association between rUO and duration of urinary catheterization, administration of antimicrobials or meloxicam, or consistent administration of pain medication during IUC.
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Although further assessment is needed, these data have suggested that IV administration of meloxicam may be a useful alternative to flunixin meglumine for postoperative treatment of horses with colic.
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Sixty-six client owned cats with degenerative joint disease and owner-reported impairments in mobility were screened and enrolled into a double-masked, placebo-controlled, randomized clinical trial. Following a run-in baseline period, cats were given either placebo or meloxicam for 21 days, then in a masked washout, cats were all given placebo for 21 days. Subsequently, cats were given the opposite treatment, placebo or meloxicam, for 21 days. Cats wore activity monitors throughout the study, owners completed clinical metrology instruments following each period.
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NSAIDs (nonsteroidal anti-inflammatory drugs) are a class of drugs with analgesic, anti-inflammatory, and antipyretic effects. Diclofenac sodium is one of the world's most widely-prescribed NSAIDs. Meloxicam is another NSAID that was approved in the last several years. Treatment with NSAIDs may result in renal damage. Relatively, little is known about comparative nephrotoxicity of NSAIDs. Therefore, the present study was designed to compare the adverse effects of diclofenac sodium and meloxicam on renal tissue in rats. Forty eight Wistar male rats were randomly assigned into 3 groups of 16 animals each. Group C served as normal control and received normal saline. Group D and M received diclofenac sodium (2.3 mg/kg/day) and meloxicam (2.3 mg/kg/day), respectively. After 17 days, all rats were scarified. Their kidneys were then harvested and processed for histological examination. In addition to cellular details, renal tubular count and diameter were assessed with the light microscope. The data were analyzed using SPSS software. We found that the mean number of renal tubules was significantly lower in group D, than in group C. Moreover, the mean renal tubular diameter was significantly higher in group D than in group C. The present study showed that a considerable degree of nephrotoxicity resulted from diclofenac sodium, compared to meloxicam. We suggest that diclofenac sodium can be replaced with meloxicam.
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Between January 2005 and February 2006 we performed single-blind oral challenge tests with meloxicam in NSAID-intolerant patients, exposing them first to placebo and then, after 30 minutes, to the first dose of meloxicam (7.5 mg). After 30 minutes, if no response appeared, the last dose of meloxicam (15 mg) was given, for a total accumulated dose of 22.5 mg. The test was considered positive if urticaria, erythema. and/or angioedema appeared.
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A single 15 mg dose of generic or branded meloxicam tablets was administered to 24 healthy male volunteers in a crossover fashion. Plasma samples, collected for 24 hours after dosing, were assayed for meloxicam concentration by a validated highperformance liquid chromatography method.
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Rosuvastatin treatment after lung contusion attenuated several features of ALI. The enhanced activity of iNOS, COX-2, and HO-1 in the lung may reflect the advent of protective processes that took place in the contused lung. To our knowledge, this is the first demonstration that prostaglandin pathways play an essential role in the effects of statins in lung injury.
mobic medication interactions
Cyclooxygenase-2 (COX-2) inhibitors reduce prostaglandin synthesis and disrupt essential reproductive processes. Ultrasound studies in women demonstrated that oral COX-2 inhibitors can delay or prevent follicle collapse associated with ovulation. The goal of this study was to determine if oral administration of a COX-2 inhibitor can inhibit reproductive function with sufficient efficacy to prevent pregnancy in primates.
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The list of all drugs purchased by the Health Ministry of Guatemala in 2004 was quantitatively and qualitatively analyzed both according to the number of units and value. All NSAIDs bought during that period were analyzed in order to find potential intervention areas which could be addressed to improve drug selection.
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MEDLINE and LILACS databases and Food and Drug Administration (FDA) and National Agency for Sanitary Vigilance (ANVISA - Agência Nacional de Vigilância Sanitária) websites. The most important articles were selected and preference was given to articles published within the last 5 years.