Effect of microwave sterilization and water storage on the Vickers hardness of acrylic resin denture teeth

Statement of problem. Acrylic resin denture teeth soften upon immersion in water, and the heating generated during microwave sterilization may enhance this process.Purpose. Six brands of acrylic resin denture teeth were investigated with respect to the effect of microwave sterilization and water immersion on Vickers hardness (VHN).Material and Methods. The acrylic resin denture teeth (Dentron [D], Vipi Dent Plus [V], Postaris [P], Biolux [B], Trilux [T], and Artiplus [A]) were embedded in heat-polymerized acrylic resin within polyvinylchloride tubes. For each brand, the occlusal surfaces of 32 identical acrylic resin denture posterior teeth were ground flat with 1500-grit silicon carbide paper and polished on a wet polishing wheel with a slurry of tin oxide. Hardness tests were performed after polishing (control group, C) after polishing followed by 2 cycles of microwave sterilization at 650 W for 6 minutes (MwS group), after polishing followed by 90-day immersion in water (90-day Wim group), and after polishing followed by 90-day storage in water and 2 cycles of microwave sterilization (90-day Wim + MwS group). For each specimen, 8 hardness measurements were made and the mean was calculated. Data were analyzed with a 2-way analysis of variance followed by the Bonferroni procedure to determine any significance between pairs of mean values (alpha=.01).Results: Mircrowave sterilization of specimens significantly decreased (P <.001) the hardness of the acrylic resin denture tooth specimens P (17.8 to 16.6 VHN, V (18.3 to 15.8 VHN), T (17.4 to 15.3 VHN), B (16.8 to 15.7 VHN), and A (17.3 to 15.7 VHN). For all acrylic resin denture teeth, no significant differences in hardness were found between the groups Mws, 90-day Wim, and 90-day Wim + MwS, with the exception of the 90-day Wim + MwS tooth A specimens (14.4 VHN), which demonstrated significant lower mean values (P <.001) than the 90-day Wim (15.8 VHN) and MwS (15.7 VHN) specimens.Conclusions. For specimens immersed in water for 90 days, 2 cycles of microwave sterilization had no effect on the hardness of most of the acrylic resin denture teeth.

REGULATION OF BOVINE ENDOMETRIAL SECRETION OF PROSTAGLANDINS AND SYNTHESIS OF 2',5'-OLIGOADENYLATE SYNTHETASE BY INTERFERON-ALPHA MOLECULES

Experiments were performed to (1) verify the inhibitory effect of bovine trophoblast protein-1 (bTP-1) on uterine prostaglandin synthesis, (2) evaluate whether other interferon-alpha (IFN-alpha) molecules also inhibit prostaglandin secretion, and (3) test whether the enzyme 2',5'-oligoadenylate synthetase (2-5A synthetase) can be induced in endometrium by interferon-alpha. In experiment 1, all interferon molecules (bTP-1, oTP-1, bIFN-alpha and hIFN-alpha) equally inhibited secretion of PGF and PGE2 from endometrial explant cultures obtained at day 17 of the estrous cycle. In experiment 2, endometrial explants obtained from day 17 of the cycle were cultured with and without bovine serum albumin (BSA; 50-mu-g/ml) and bIFN-alpha (0, 0.84, 4.2, and 42 nM). Addition of BSA to the culture medium greatly enhanced the accumulation of PGF into the medium. The bIFN-alpha inhibited accumulation of PGF and PGE2 in both the presence or absence of BSA by 12 h. All three concentrations of bIFN-alpha were equally effective in inhibiting prostaglandin accumulation. Additionally, all concentrations of bIFN-alpha increased the amounts of 2-5A synthetase in endometrium. In conclusion, these results confirm the inhibitory effect of bTP-1 on PGF release from endometrium and demonstrate that bTP-1 can also inhibit PGE2 secretion. Furthermore, other interferon-alpha molecules, including bIFN-alpha, hIFN-alpha, and oTP-1, also reduced PGF and PGE2 secretion in culture. It is likely, therefore, that conceptus and other interferon-alpha molecules exert similar effects on endometrium in vitro and that the antiluteolytic effects of bIFN-alpha in vivo are mediated in part by changes in endometrial prostaglandin synthesis.

Ceramic Primer Heat-Treatment Effect on Resin Cement/Y-TZP Bond Strength

The purpose of this study was to evaluate the effect of different heat-treatment strategies for a ceramic primer on the shear bond strength of a 10-methacryloyloxydecyl-dihydrogen-phosphate (MDP)-based resin cement to a yttrium-stabilized tetragonal zirconia polycrystal (Y-TZP) ceramic. Specimens measuring 4.5 x 3.5 x 4.5 mm(3) were produced from Y-TZP presintered cubes and embedded in polymethyl methacrylate (PMMA). Following finishing, the specimens were cleaned using an ultrasound device and distilled water and randomly divided into 10 experimental groups (n=14) according to the heat treatment of the ceramic primer and aging condition. The strategies used for the experimental groups were: GC (control), without primer; G20, primer application at ambient temperature (20 degrees C); G45, primer application + heat treatment at 45 degrees C; G79, primer application + heat treatment at 79 degrees C; and G100, primer application + heat treatment at 100 degrees C. The specimens from the aging groups were submitted to thermal cycling (6000 cycles, 5 degrees C/55 degrees C, 30 seconds per bath) after 24 hours. A cylinder of MDP-based resin cement (2.4 mm in diameter) was constructed on the ceramic surface of the specimens of each experimental group and stored for 24 hours at 37 degrees C. The specimens were submitted to a shear bond strength test (n=14). Thermal gravimetric analysis was performed on the ceramic primer. The data obtained were statistically analyzed by two-way analysis of variance and the Tukey test (alpha=0.05). The experimental group G79 without aging (7.23 +/- 2.87 MPa) presented a significantly higher mean than the other experimental groups without aging (GC: 2.81 +/- 1.5 MPa; G20: 3.38 +/- 2.21 MPa; G100: 3.96 +/- 1.57 MPa), showing no difference from G45 only (G45: 6 +/- 3.63 MPa). All specimens of the aging groups debonded during thermocycling and were considered to present zero bond strength for the statistical analyses. In conclusion, heat treatment of the metal/zirconia primer improved bond strength under the initial condition but did not promote stable bonding under the aging condition.

The analgesic effect of crotoxin on neuropathic pain is mediated by central muscarinic receptors and 5-lipoxygenase-derived mediators

Crotoxin (CTX). a neurotoxin isolated from the venom of the South American rattlesnake Crotalus durissus terrificus. induces analgesia. In this study, we evaluated the antinociceptive effect of CTX in a model of neuropathic pain induced by rat sciatic nerve transection. Hyperalgesia was detected 2 h after nerve transection and persisted for 64 days. Immersion of proximal and distal nerve stumps in CTX solution (0.01 mM for 10 s), immediately after nerve transection, blocked hyperalgesia. The antinociceptive effect of CTX was long-lasting, since it was detected 2 h after treatment and persisted for 64 days. CTX also delayed, but did not block, neurectomy-induced neuroma formation. The effect of CTX was blocked by zileuton (100 mg/kg, p.o.) and atropine (10 mg/kg. i.p.), and reduced by yohimbine (2 mg/kg, i.p.) and methysergide (5 mg/kg, i.p.). on the other hand. indomethacin (4 mg/kg, i.v.). naloxone (1 mg/kg, i.p.). and N-methyl atropine (30 mg/kg, i.p.) did not interfere with the effect of CTX. These results indicate that CTX induces a long-lasting antinociceptive effect in neuropathic pain, which is mediated by activation of central muscarinic receptors and partially, by activation of alpha-adrenoceptors and 5-HT receptors. Eicosanoids derived from the lipoxygenase pathway modulate the action of crotoxin. (C) 2008 Elsevier B.V. All rights reserved.

Fiber Post Cementation Strategies: Effect of Mechanical Cycling on Push-out Bond Strength and Cement Polymerization Stress

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Inhibitory effect of PGE(2) on the killing of Paracoccidioides brasiliensis by human monocytes can be reversed by cellular activation with cytokines

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

13,14-Dihydro-15-Keto Prostaglandin F-2 alpha Release in Response to Oxytocin Challenge Early Post-Partum in Anoestrous Nelore Cows Submitted to Temporary Calf Removal and Progesterone Priming

The study evaluated, in early post-partum anoestrous Nelore cows, if the increase in plasma oestradiol (E2) concentrations in the pre-ovulatory period and/or progesterone priming (P4 priming) preceding ovulation, induced by hormonal treatment, reduces the endogenous release of prostaglandin PGF(2)alpha and prevents premature lysis of the corpus luteum (CL). Nelore cows were subjected to temporary calf removal for 48 h and divided into two groups: GPE/eCG group (n = 10) and GPG/eCG group (n = 10). Animals of the GPE/eCG group were treated with a GnRH agonist. Seven days later, they received 400 ID of eCG, immediately after PGF(2)alpha treatment, and on day 0, 1.0 mg of oestradiol benzoate (EB). Cows of the GPG/eCG group were similarly treated as those of the GPE/eCG group, except that EB was replaced with a second dose of GnRH. All animals were challenged with oxytocin (OT) 9, 12, 15 and 18 days after EB or GnRH administration and blood samples were collected before and 30 min after OT. Irrespective of the treatments, a decline in P4 concentration on day 18 was observed for cows without P4 priming. However, animals exposed to P4 priming, treated with EB maintained high P4 concentrations (8.8 +/- 1.2 ng/ml), whereas there was a decline in P4 on day 18 (2.1 +/- 1.0 ng/ml) for cows that received GnRH to induce ovulation (p < 0.01). Production of 13,14-dihydro-15-keto prostaglandin F-2 alpha (PGFM) in response to OT increased between days 9 and 18 (p < 0.01), and this increase tended to be more evident in animals not exposed to P4 priming (p < 0.06). In conclusion, the increase in E2 during the pre-ovulatory period was not effective in inhibiting PGFM release, which was lower in P4-primed than in non-primed animals. Treatment with EB promoted the maintenance of elevated P4 concentrations 18 days after ovulation in P4-primed animals, indicating a possible beneficial effect of hormone protocols containing EB in animals with P4 priming.

Effect of adrenergic stimulation of the amygdaloid complex on water intake

The effect of noradrenaline, isoproterenol, phentolamine and propranolol, injected into the basolateral nuclei of the amygdala on water intake, was investigated in male Holtzman rats. The injection of noradrenaline (40 nmol) into the amygdaloid complex (AC) of satiated rats produced no change in water intake (0.05 ± 0.03 ml/1 hour). The injection of isoproterenol (40 nmol) produced an increase in water intake in sedated rats (1.93 ± 0.23 ml/1 hour). Noradrenaline injected into the AC produced a decrease in water intake in deprived rats (0.40 ± 0.19 ml/1 hour). The injection of isoproterenol into the AC of deprived rats produced no change in water intake in comparison with control (11.65 ± 1.02 and 10.92 ± 0.88 ml/1 hour, respectively). When compared with control values, phentolamine injected prior to noradrenaline blocked the inhibitory effect of noradrenaline on water intake in deprived rats (10.40 ± 1.31 ml/1 hour). Propranolol blocked the effect of isoproterenol in satiated rats (0.85 ± 0.49 ml/1 hour) and also blocked the water intake induced by deprivation (0.53 ± 0.38 ml/1 hour). In satiated and deprived animals the injection of phentolamine before hexamethonium blocked the inhibitory effect of hexamethonium on water intake. In satiated animals, when hexamethonium was injected alone, water intake was 0.39 ± 0.25 ml/1 hour and when hexamethonium was injected with phentolamine, water intake was 1.04 ± 0.3 ml/1 hour. In deprived animals, hexamethonium alone blocked water intake (0.40 ± 0.17 ml/1 hour) and when injected with phentolamine it elicited an intake of 9.7 ± 1.8 ml/1 hour. these results clearly demonstrate the participation of catecholaminergic receptors of the AC in the regulation of water intake.

Effect of α-tocopherol, taurine and selenium on the attenuation of ischemia/reperfusion injury of splanchnic organs

Background: Splanchnic artery occlusion shock is caused by increased capillary permeability and cellular injury precipitated by oxygen derived free radicals following ischemia and reperfusion of splanchnic organs. The purpose of this study was to assess the role of several well-known oxygen- derived free radical scavengers in ameliorating or preventing this syndrome. Study design: Anesthetized rats were subjected to periods of occlusion of the visceral arteries and reperfusion. Tocopherol, taurine, selenium or a 'cocktail' of these three agents was injected subcutaneously for 4 consecutive days prior to operation. Mean arterial blood pressure was measured throughout the experimental period. Fluorometry and technetium-99m pyrophosphate counting of the visceral organs were performed as well as a histologic grading system for intestinal viability. Results: Final mean arterial blood pressure associated with the 'cocktail' and selenium groups was 79.1 ± 27.4 mmHg and 83.6 ± 17.8 mmHg, respectively. These values were significantly higher than the control group, 40.8 ± 11.4 mmHg (P < 0.05). Similar patterns of the benefit of selenium in contrast with the other groups were obtained with fluorescein perfusion, radioisotopic activity and histologic analysis. Conclusion: Pretreatment with selenium of splanchnic ischemia and reperfusion in the rat improves mean arterial blood pressure and microcirculatory visceral perfusion. Further analysis of the precise protective mechanism of selenium for reperfusion injury will enable visceral organs to withstand the consequences of increased capillary leakage and oxidant injury.

Characterization of the antinociceptive and sedative effect of amitraz in horses

Amitraz, an acaricide used to control ectoparasites in animals has a complex pharmacological activity, including α2-adrenergic agonist action. The purpose of this research was to investigate the possible antinociceptive and/or sedative effect of amitraz in horses. The sedative effect of the intravenous (i.v.) injection of dimethylformamide (DMF, 5 mL, control) or amitraz (0.05, 0.10, 0.15 mg/kg), was investigated on the head ptosis test. The participation of α2-adrenergic receptors in the sedative effect provoked by amitraz was studied by dosing yohimbine (0.12 mg/kg, i.v.). To measure the antinociception, xylazine hydrochloride (1 mg/kg, i.v., positive control) and the same doses of amitraz and DMF were used. A focused radiant light/heat directed onto the fetlock and withers of a horse were used as a noxious stimulus to measure the hoof withdrawal reflex latency (HWRL) and the skin twitch reflex latency (STRL). The three doses of amitraz used (0.05, 0.10 and 0.15 mg/kg) provoked a dose-dependent relaxation of the cervical muscles. The experiments with amitraz and xylazine on the HWRL showed that after i.v. administration of all doses of amitraz there was a significant increase of HWRL up to 150 min after the injections. Additionally, there was a significant difference between control (DMF) and positive control (xylazine) values up to 30 min after drug injection. On the other hand, the experiments on the STRL show that after administration of amitraz at the dose of 0.15 mg/kg, a significant increase in STRL was observed when compared with the control group. This effect lasted up to 120 min after injection. However, no significant antinociceptive effect was observed with the 0.05 and 0.10 mg/kg doses of amitraz or at the 1.0 mg/kg dose of xylazine.

Effects of the alpha antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by angiotensin II injection into the subfornical organ

The subfornical organ (SFO) and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANG II) on water and salt regulation. Several anatomical findings have demonstrated neural connections between the SFO and the LH. The present experiments were conducted to investigate the role of the α-adrenergic antagonists and agonists injected into the LH on the water and salt intake elicited by injections of ANG II into the SFO. Prazosin (an α1-adrenergic antagonist) injected into the LH increased the salt ingestion, whereas yohimbine (an α2-adrenergic antagonist) and propranolol (a β-adrenergic antagonist) antagonized the salt ingestion induced by administration of ANG II into the SFO. Previous administration of clonidine (an α2-adrenergic agonist) or noradrenaline into the LH increased, whereas pretreatment with phenylephrine decreased the sodium intake induced by injection of ANG II into the SFO. Previous treatment with prazosin and propranolol reduced the water intake induced by ANG II. Phenylephrine increased the dipsogenic responses produced by ANG II, whereas previous treatment with clonidine injected into the LH reduced the water intake induced by ANG II administration into the SFO. The LH involvement with SFO on the excitatory and inhibitory mechanisms related to water and sodium intake is suggested.

Effect of α-tocopherol on superoxide radical and toxicity of cadmium exposure

Contamination with cadmium compounds poses high potential risk for the health of populations and for this reason the treatment of their toxic effects should urgently be established. The present study was carried out to determine whether α-tocopherol intake can protect tissues against damage induced by cadmium, and to clarify the contribution of superoxide radicals (O 2 -) in this process. Cadmium chloride was tested for tissue damage by a single intraperitoneal injection of Cd 2+ ions (2 mg Kg -1). To determine the potential therapeutic effect of vitamin E, a group of Cd 2+-treated rats received a drinking solution of α-tocopherol (40 mg l -1) for 15 days. Cadmium induced increased serum creatinine and total lactate dehydrogenase, reflecting renal and cardiac damage. The increased lipoperoxide and decreased Cu-Zn superoxide dismutase levels indicated the generation of superoxide radicals in cadmium-treated rats. Tocopherol induced increased serum high-density lipoprotein and depressed the toxic effects of Ca 2+ alone, since creatinine and lactate dehydrogenase determinations were recovered to the control values. Tocopherol decreased lipoperoxide and led the superoxide dismutase activities to approach those of the control values. We concluded that superoxide radicals are produced as mediators of cadmium toxicity. Tocopherol possesses a significant anti-radical activity and inhibits the cadmium effect on superoxide dismutase activity. Tocopherol also protected tissues from the toxic effects of cadmium by a direct antioxidant action which decreased lipoperoxide formation.

Effect of nωnla, an inhibitor of No-synthase, on the release of tissue-plasminogem activator from rat aorta

Alterations in the synthesis or enhanced inactivation of nitric oxide (NO) and increase in fibrin deposition in the vascular bed lead to an imbalance that can induced intravascular coagulation. NO is produced through L-arginine pathway by constitutive and inducible nitric oxide synthase (NOS). The inducible isoform can be activated by cytokines such as tumor necrosis factor alfa. We evaluated NO-induced tissue-plasminogen activator (t-PA) release from isolated aortic segments of Wistar rats measuring the fibrinolytic activity in the fibrin plate. Inhibition of NO biossynthesis with Nω-nitro-L-arginine (NωNLA) significantly attenuated the fibrinolytic activity (FA) evoked by aortic segments of this group (GII) compared to the saline group (GI). The administration of L-arginine produced restoration of FA in this group (GIII) treated with NωNLA suggesting that t-PA arising from segments of rat aorta is influenced by NO.

Effect of dietary supplementation with vitamin E and stocking density on macrophage recruitment and giant cell formation in the teleost fish, Piaractus mesopotamicus

The effect of dietary supplementation with 0, 100 and 450 mg of vitamin E (DL-α tocopheryl acetate)/kg of a dry diet on the kinetics of macrophage recruitment and giant cell formation in the pacu, maintained at different stocking densities (5 kg/m3 and 20 kg/m3), was investigated by insertion of round glass coverslips into the subcutaneous connective tissue. After a feeding period of 18 weeks, the coverslips were implanted and later removed for examination at 2, 7 and 15 days post-implantation. Fish fed diets supplemented with 450 mg of vitamin E showed an increase (P<0.05) in the accumulation of macrophages, foreign body giant cells and Langhans type cells. The kinetics of macrophage recruitment and giant cell formation on the glass coverslips appeared to be strongly influenced by vitamin E supplementation, since fish fed a basal diet and held at high stocking densities showed low numbers of adhering cells on the coverslips, and high concentrations of plasma corticosteroids. On the other hand, fish given a diet supplemented with 450 mg of vitamin E did not show a similar difference in plasma cortisol concentrations related to stocking density. The effect of cortisol concentrations on carbohydrate metabolism, analysed by assessment of plasma glycaemia, was not clear. Blood glucose concentrations did not vary substantially with the different treatments examined. These results suggest that vitamin E may contribute to the efficiency of the fish's inflammatory response by increasing macrophage recruitment and giant cell formation in the foreign body granulomatous reaction. Vitamin E appeared to act on the stress response of pacus by preventing a stress-related immunosuppression. © 2005 Elsevier Ltd. All rights reserved.