Effects of 10% carbamide peroxide bleaching materials on enamel microhardness

Purpose: To evaluate the microhardness of enamel treated with two different 10% carbamide peroxide bleaching materials at different time intervals. Materials and Methods: Two bleaching agents were analyzed: Opalescence (OPA) and Rembrandt (REM). The control group (CON) consisted of dental fragments maintained in artificial saliva. Bleaching was accomplished for 8 hrs per day and stored during the remaining time in an individual recipient with artificial saliva. Enamel microhardness testing was performed before the initial exposure to the treatments and after 1, 7, 14, 21, 28, 35 and 42 days. Results: the ANOVA, followed by the Bartlet and Tukey tests, showed significant differences for treatments (P < 0.00001) from day 7-day 42. From the 7th to the 14th day, OPA presented an increase of enamel microhardness over time while REM presented a decrease of microhardness. Statistical differences were not found between REM and the control group (OPA > CON = REM). From the 21st-35th day, enamel fragments bleached with OPA and REM presented a decrease of microhardness. Statistical differences of microhardness were verified among all the treatments (OPA > CON > REM). on the day 42, statistical differences were not found between OPA and the control group, but they were found between REM and the control group (OPA = CON > REM). The polynomial regression showed an increase of microhardness for OPA until the 21st day, followed by a decrease of microhardness up to the 42nd day. A decrease of microhardness for REM was verified. There were alterations in enamel microhardness as a function of bleaching time when using the two different 10% carbamide peroxide whiteners. Over a 42-day treatment time, bleaching with REM agent caused a decrease in enamel microhardness. The OPA agent initially increased the microhardness, then returned to the control level. Different bleaching materials with the same concentration of carbamide peroxide have different effects on the enamel.

Inhibition of hydrogen peroxide, nitric oxide and TNF-alpha production in peritoneal macrophages by ethyl acetate fraction from Alchornea glandulosa

The effects of Alchornea glandulosa ethyl acetate fraction (AGF) on hydrogen peroxide (H2O2), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) production in peritoneal macrophages activated with lipopolysaccharide (LPS) or phorbol myristate acetate (PMA) were investigated. Analysis by thin layer chromatography (TLC) of AGF showed several constituents, including flavonoids, which may have anti-inflammatory activity. Inhibitory effects of the fraction in H2O2 and NO production ranged from 8.59 +/- 7.84% to 70.56 +/- 4.16% and from 16.06 +/- 3.65% to 38.73 +/- 3.90%, respectively. The TNF-alpha production was only partially inhibited in the tested concentrations (12.21 +/- 6.23%-15.16 +/- 0.96%). According to these results, it is suggested that AGF has anti-inflammatory activity. This medicinal plant may have therapeutic potential in the control of inflammatory disorders.

Release of intermediate reactive hydrogen peroxide by macrophage cells activated by natural products

By determining the hydrogen peroxide (H2O2) released in cultures of peritoneal macrophage cells from Swiss mice, we evaluated the action of 27 vegetable compounds (pristimerin, tingenone, jatrophone, palustric acid, lupeol, cladrastin, ocoteine, boldine, tomatine, yohimbine, reserpine, escopoletin, esculine, plumericin, diosgenin, deoxyschizandrin, p-arbutin, mangiferin, and others) using a 2 mg/ml solution of each compound (100 mug/well). Macrophages are cells responsible for the development of the immunological response reaction, liberating more than one hundred compounds into the extracellular environment. Among these are the various cytokines and the intermediate compounds of nitrogen (NO) and oxygen (H2O2). This coordinated sequence of biochemical reactions is known as the oxidative burst. When we compared the results with those obtained with zymosan (an important stimulator of H2O2) we observed that the compounds showing the highest activity were substances 2 (tingenone), 16 (reserpine) and 20. Other substances such as compounds 1, 4, 5, 6, 8, 12, 13, 14, 15, 17, 19, 23, 24, 26, and 27 also showed a certain activity, but with less intensity than the aforementioned ones. Compounds 3, 7, 9, 10, 11, 18, 21, 22 and 25 presented no activity. These results suggest that natural products (mainly tingenone and reserpine and others) with different chemical structures are strong immunological modulators. However, further tests are needed to determine the 'oxidative burst' in future studies.

Barrier penetration for supersymmetric shape-invariant potentials

Exact reflection and transmission coefficients for supersymmetric shape-invariant potentials barriers are calculated by an analytical continuation of the asymptotic wavefunctions obtained via the introduction of new generalized ladder operators. The general form of the wavefunction is obtained by the use of the F(-infinity, +infinity)-matrix formalism of Froman and Froman which is related to the evolution of asymptotic wavefunction coefficients.

Tuning the acidic properties of aluminas via sol-gel synthesis: New findings on the active site of alumina-catalyzed epoxidation with hydrogen peroxide

This study answers several pending questions about alumina-catalyzed epoxidation with aqueous 70 wt% H2O2. To evaluate the effect of the water-to-aluminum tri-sec-butoxide molar ratio, this was systematically changed from 1 to 24. The xerogels were calcined at 450 degrees C and gave different gamma-Al2O3's with distinct textural and acidic properties. A combination of Al-27 MAS NMR and TPD-NH3 results of calcined aluminas allowed us to assign the type la. Al-OH sites as the catalytic sites for epoxidation. The type Ib Al-OH sites have no function in catalytic epoxidation, because ethyl acetate poisons these sites. The strong acid sites of types IIa, IIb, and III Al-OH groups are responsible for the undesired H2O2 decomposition and decreased oxidant selectivity. (c) 2006 Elsevier B.V. All rights reserved.