966 resultados para prostaglandin E1
Resumo:
The authors tested the T clasp of Roach in three differents proportions among width and thickness: E1-1.7; E2-2.0 and E3-2.3, with a constant length of 15 mm. These clasps were casted with three cobalt-chromium alloys (L1-Biosil; L2-Steldent and L3-Duracrom), through two casting techniques (F1-oxygen-gas and F2-oxygen-acetylene). The fatigue of the clasps were verified by using and assay machine, that through movements, simulate the insertion and removal of the clasps for a pattern which were obtained from a premolar, prepared in a surveyor. This machine detect the fatigue of the clasps and count the number of cycles of insertion and removal realized. The obtained results of the interaction between the analysed factors, were submitted to the statistic analysis and the authors concluded that: a) the interaction of factors, Alloy x Thickness, Alloy x Casting Technique and Thickness x Casting Technique did not change the order of effects that the factors showed separately but gave rise to effects of different magnitude for any observed sense; b) the simultaneous interaction of the factors Alloy x Thickness x Casting Technique confirmed the superiority of the L3 alloy, the thickness E3 and the F2 casting technique.
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Norepinephrine (NE) and clonidine produce a phasic, dose-dependent contraction of the isolated guinea-pig terminal ileum. The effect of NE was blocked by prazosin which produced a parallel rightward shift of the concentration-effect curve to NE, with a significant depression of maximum effects. Yohimbine and indomethacin noncompetitively blocked, whereas practolol potentiated, the contractile effect of NE. The contractile effect of clonidine was not antagonized by indomethacin or atropine. These results suggest that the isolated guinea-pig terminal ileum has excitatory receptors sensitive to clonidine stimulation and excitatory alpha receptors sensitive to blockade by prazosin, and that the activation of the latter may be related to the activation of endogenous prostaglandin synthesis.
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The present studies were conducted to determine the role of prostaglandins in the etiology of a rise of body temperature observed in rats after electrolytic lesion made on the dorsal mesencephalic areas. This hyperthermia was abolished by intraperitoneal administration of indomethacin, an inhibitor of prostaglandins synthesis. These results strengthen the suggestion of a similar mechanism for both neurogenic hyperthermia and the fevers produced by pyrogens. However, until further experiments are carried out, the possibility of lesion in producing hyperthermia by different mechanisms cannot be ruled out.
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Fourteen complexes in the series [RuCl2(CO)(L)(PPh3)2] (where L = N-heterocycles) have been prepared and characterized by IR and NMR spectroscopies, and cyclic voltammetry. A good correlation is found between observed and calculated electrochemical potentials; E1/2 vs pKa or (Gp, σm for a series of similar ligands. It is now reported that the carbonyl stretching frequency, νCO, and the 13C and 31P NMR signals do not correlate well with any of the physico-chemical parameters used (E1/2, Taft's and Hammett's parameters). This behaviour is probably due to the characteristics of the Ru(II) species, which does not transmit the steric and electron donor/acceptor properties of the ligands to the carbonyl group, or because the measurements are not able to detect the effect induced by the changes in the ligand L. Indeed, good correlations are obtained when the measurements directly involve the metal centre, as is the case in the E1/2 measurements. Crystals of o[RuCl2(CO)(4-pic)(PPh3)2] are monoclinic, space group P21/n, a = 12.019(2), b = 13.825(3) and c = 22.253(3) . The structure was solved by the Patterson method and was refined by full-matrix least-squares procedure to R = 0.054 and Rw = 0.055, for 2114 reflections with I > 3σ(I). For L = 2-acetylpyridine and 2-methylimidazole, complexes with formulae [RuCl2(CO)(L)(PPh3)] · L and [RuCl2(CO)(L)2 (PPh3)], respectively, were obtained. © 1998 Elsevier Science Ltd. All rights reserved.
Resumo:
Background and Objectives. The analgesic actions of nonsteroidal anti-inflammatory drugs (NSAID) result from the inhibition of the peripheral synthesis of prostaglandins. In spite of the emphasis on the peripheral action, several studies have shown the potential central action of such drugs. In rats, NSAID doses insufficient to block pain when systemically administered were effective when intrathecally injected. This effect could be mediated by interaction with descending serotoninergic ways together with neurotransmission modulation of glycine or N-methyl-D-aspartate receptors. Our goal was to study the effect of different tenoxican doses in the histology of dogs spinal cord and meninges. Methods. Thirty two dogs (7 to 17 kg) were randomly distributed in four groups: G1 - Control with distilled water (DW); G2 - 2 mg tenoxican diluted in DW; G3 - 4 mg tenoxican diluted in DW; G4 - 10 mg tenoxican diluted in DW in a constant volume of 1 ml. Anesthesia was induced with etomidate and fentanyl and dural puncture was performed with a 25G spinal needle in interspace L6-7. Animals were observed for 72 hours and subsequently euthanized by electrocution. Lumbar and sacral spinal cord segments were removed for further histologic examination. Results. All animals were clinically normal during the observation period and there has been no histologic alteration of the nervous system and meninges. Conclusions. In our experimental model intrathecal tenoxican doses up to 10 mg have not triggered nervous tissue or meningeal injuries in dogs.
Resumo:
The effects of several doses of progesterone on FSH and LH concentrations were used to study the role of the gonadotropins on deviation in growth rates of the two largest follicles during the establishment of follicle dominance. Progesterone was given to pony mares at a daily dose rate of 0 mg (controls), 30 mg (low dose), 100 mg (intermediate dose), and 300 mg (high dose). All follicles ≥ 6 mm were ablated at Day 10 (Day 0 = ovulation) to initiate a new follicular wave; prostaglandin F(2α) was given to induce luteolysis, and progesterone was given from Days 10 to 24. The low dose did not significantly alter any of the ovarian or gonadotropin end points. The high dose reduced (P < 0.05) the ablation-induced FSH concentrations on Day 11. Maximum diameter of the largest follicle (17.2 ± 0.6 mm) and the second- largest follicle (15.5 ± 0.9 mm) in the high-dose group was less (P < 0.04) than the diameter of the second-largest follicle in the controls (20.0 ± 1.0 mm) at the beginning of deviation (Day 16.7 ± 0.4). Thus, the growth of the two largest follicles was reduced by the high dose, presumably through depression of FSH, so that the follicles did not attain a diameter characteristic of deviation in the controls. The intermediate dose did not affect FSH concentrations. However, the LH concentrations increased in the control, low, and intermediate groups, but then decreased (P < 0.05) in the intermediate group to pretreatment levels. The LH decrease in the intermediate group occurred 2 days before deviation in the controls. The maximum diameter of the largest follicle was less (P < 0.0001) in the intermediate group (27.3 ± 1.8 mm) than in the controls (38.9 ± 1.5 mm), but the maximum diameter of the second-largest follicle was not different between the two groups (19.0 ± 1.1 vs. 20.3 ± 1.0 mm). Thus, the onset of deviation, as assessed by the second-largest follicle, was not delayed by the decrease in LH. Diameter of the largest follicle by Day 18 in the intermediate group (23.1 ± 1.6 mm) was less (P < 0.05) than in the controls (28.0 ± 1.0 mm). These results suggest that circulating LH was not involved in the initiation of dominance (inhibition of other follicles by the largest follicle) but was required for the continued growth of the largest follicle after or concurrently with its initial expression of dominance.
Resumo:
The effect of altered LH concentrations on the deviation in growth rates between the 2 largest follicles was studied in pony mares. The progestational phase was shortened by administration of PGF2α on Day 10 (Day 0=ovulation; n=9) or lengthened by daily administration of 100 mg of progesterone on Days 10 to 30 (n=11; controls, n=10). All follicles ≥5 mm were ablated on Day 10 in all groups to initiate a new follicular wave. The interovulatory interval was not altered by the PGF2α treatment despite a 4-day earlier decrease in progesterone concentrations. Time required for growth of the follicles of the new wave apparently delayed the interval to ovulation after luteolysis. The FSH concentrations of the first post-ablation FSH surge were not different among groups. A second FSH surge with an associated follicular wave began by Day 22 in 7 of 11 mares in the progesterone group and in 0 of 19 mares in the other groups, indicating reduced functional competence of the largest follicle. A prolonged elevation in LH concentrations began on the mean day of wave emergence (Day 11) in the prostaglandin group (19.2 ± 2.2 vs 9.0 ± 0.7 ng/mL in controls; P<0.05), an average of 4 d before an increase in the controls. Concentrations of LH in the progesterone group initially increased until Day 14 and then decreased so that by Day 18 the concentrations were lower (P<0.05) than in the control group (12.9 ± 1.6 vs 20.2 ± 2.6 ng/mL). Neither the early and prolonged increase nor the early decrease in LH concentrations altered the growth profile of the second-largest follicle, suggesting that LH was not involved in the initiation of deviation. However, the early decrease in LH concentrations in the progesterone group was followed by a smaller (P<0.05) diameter of the largest follicle by Day 20 (26.9 ± 1.7 mm) than the controls (30.3 ± 1.7 mm), suggesting that LH was necessary for continued growth of the largest follicle after deviation. (C) 2000 by Elsevier B.V.
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The purpose of this study was to evaluate the effect of an intramuscular injection of prostaglandin, within the first hour post partum, on the incidence of retained fetal membranes in cows, at 8 and 12 hours post-partum. Eighty-two cows were used as controls and 82 were treated with 25mg of prostaglandin (LUTALYSE®, 5ml), in two different farms. Cows treated with PGF 2α released the placenta faster (P < 0.10) than cows in the control group (7.72±0.84 vs. 10.07±1.09h). The incidence of retained placenta with more than 8h post partum was 30.5% in the control group and 17.1% in the treated group (P < 0.05), and with more than 12h was 19.5% in the control group and 12.2% in the treated group (P < 0.10). Farm, body condition score and parity showed influence on retained placenta rates, whereas sex of calf and help during calving did not have influence. These data showed that prostaglandin treatment within the first hour post-partum is capable of reduce the incidence of retained placenta and may work as a preventive treatment.
Resumo:
The aim of this study was to evaluate the effect of delaying ovulation subsequent to superstimulation of follicular growth in beef cows (Bos indicus) on embryo recovery rates and the capacity of embryos to establish pregnancies. Ovulation was delayed by three treatments using either progesterone (CIDR-B®) or a GnRH agonist (deslorelin). Multiparous Nelore cows (n = 24) received three of four superstimulation treatments in an incomplete block design (n = 18 per group). Cows in Groups CTRL, P48 and P60 were treated with a CIDR-B device plus estradiol benzoate (EB, 4 mg, i.m.) on Day-5, while cows in Group D60 were implanted with deslorelin on Day-7. Cows were superstimulated with FSH (Folltropin-V® 200 mg), from Day 0 to 3, using twice daily injections in decreasing amounts. All cows were treated with a luteolytic dose of prostaglandin on Day 2 (08:00 h). CIDR-B devices were removed as follows: Group CTRL, Day 2 (20:00 h); Group P48, Day 4 (08:00 h); Group P60, Day 4 (20:00 h). Cows in Group CTRL were inseminated at 10, 20 and 30 h after first detected estrus. Ovulation was induced for cows in Group P48 (Day 4, 08:00 h) and Groups P60 and D60 (Day 4, 20:00 h) by injection of LH (Lutropin®, 25 mg, i.m.), and these cows were inseminated 10 and 20 h after treatment with LH. Embryos were recovered on Days 11 or 12, graded and transferred to synchronized recipients. Pregnancies were determined by ultrasonography around Day 100. Data were analyzed by mixed procedure, Kruskal-Wallis and Chi-square tests. The number of ova/embryos, transferable embryos (mean ± S.E.M.) and pregnancy rates (%) were as follows, respectively: Group CTRL (10.8 ± 1.8, 6.1 ± 1.3, 51.5), P48 (12.6 ± 1.9, 7.1 ± 1.0, 52.3), P60 (10.5 ± 1.6, 5.7 ± 1.3, 40.0) and D60 (10.3 ± 1.7, 5.0 ± 1.2, 50.0). There were no significant differences among the groups (P > 0.05). It was concluded that fixed time AI in association with induced ovulation did not influence embryo recovery. Furthermore, pregnancy rates in embryos recovered from cows with delayed ovulation were similar to those in embryos obtained from cows treated with a conventional superstimulation protocol. © 2002 Elsevier B.V. All rights reserved.
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Osteoblast-derived IL-6 functions in coupled bone turnover by supporting osteoclastogenesis favoring bone resorption instead of bone deposition. Gene regulation of IL-6 is complex occurring both at transcription and post-transcription levels. The focus of this paper is at the level of mRNA stability, which is important in IL-6 gene regulation. Using the MC3T3-E1 as an osteoblastic model, IL-6 secretion was dose dependently decreased by SB203580, a p38 MAPK inhibitor. Steady state IL-6 mRNA was decreased with SB203580 (2 μM) ca. 85% when stimulated by IL-1β (1-5 ng/ ml). These effects require de novo protein synthesis as they were inhibited by cycloheximide. p38 MAPK had minor effects on proximal IL-6 promoter activity in reporter gene assays. A more significant effect on IL-6 mRNA stability was observed in the presence of SB203580. Western blot analysis confirmed that SB203580 inhibited p38 MAP kinase, in response to IL-1β in a dose dependent manner in MC3T3-E1 cells. Stably transfected MC3T3-E1 reporter cell lines (MC6) containing green fluorescent protein (GFP) with the 3′untranslated region of IL-6 were constructed. Results indicated that IL-1β, TNFα, LPS but not parathyroid hormone (PTH) could increase GFP expression of these reporter cell lines. Endogenous IL-6 and reporter gene eGFP-IL-6 3′UTR mRNA was regulated by p38 in MC6 cells. In addition, transient transfection of IL-6 3′UTR reporter cells with immediate upstream MAP kinase kinase-3 and -6 increased GFP expression compared to mock transfected controls. These results indicate that p38 MAPK regulates IL-1β-stimulated IL-6 at a post transcriptional mechanism and one of the primary targets of IL-6 gene regulation is the 3′UTR of IL-6.
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Proteinase-activated receptor-2 (PAR2) is a G-protein-coupled receptor that mediates cellular responses to extracellular proteinases. Since PAR2 is expressed by oral epithelial cells, osteoblasts, and gingival fibroblasts, where its activation releases interleukin-8, we hypothesized that PAR2 activation may participate in periodontal disease in vivo. We investigated the role of PAR2 activation in periodontal disease in rats. Radiographic and enzymatic (myeloperoxidase) analysis revealed that topical application of PAR2 agonist causes periodontitis but also exacerbates existing periodontitis, leading to significant alveolar bone loss and gingival granulocyte infiltration. Inhibition of matrix metalloproteinase (MMP) and cyclo-oxygenase (COX) decreased PAR2 agonist-induced periodontitis. More specifically, the overexpression of COX-1, COX-2, MMP-2, and MMP-9 in gingival tissues suggests that they are involved in PAR 2-induced periodontitis. In conclusion, PAR2 agonist causes periodontitis in rats through a mechanism involving prostaglandin release and MMP activation. Inhibition of PAR2 may represent a novel approach to modulate host response in periodontitis.
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Human monocytes lack fungicidal activity against high virulent strains of Paracoccidioides brasiliensis, the etiological agent of paracoccidioidomycosis, even after IFN-γ activation. However, monocytes treated with indomethacin (INDO) or INDO plus IFN-γ effectively killed this fungus, suggesting an inhibitory role of prostaglandins in this process. Thus, the purpose of this work was to test if this regulatory effect of prostaglandin was associated with alterations on H2O2 production and/or on modulatory cytokines levels, such as TNF-α, IL-10, and IL-6. Peripheral blood monocytes obtained from 10 healthy donors were incubated for 18 hours in the presence or absence of IFN-γ, INDO, or IFN-γ plus INDO, and further challenged with a high virulent strain of P. brasiliensis (Pb18) for 4 hours. Then, the monocytes cultures were evaluated for H2O2 release and fungicidal activity calculated by counting the colony forming units after plating. Moreover, on supernatants of the same cultures, TNF-α, IL-10, IL-6, and PGE2 concentrations were evaluated by ELISA. Monocytes treated with INDO or INDO plus IFN-γ presented higher fungicidal activity associated with the release of higher levels of H2O2 and TNF-α, but lesser levels of PGE2, when compared to nontreated cells. However, the levels of IL-10 and IL-6 were similar between treated and nontreated cells. The results suggest that human monocytes when challenged with high virulent strains of P. brasiliensis produce prostaglandins that inhibit the fungicidal activity of these cells by reducing H2O2 and TNF-α levels.