Effect of microwave treatment on the shear bond strength of different types of commercial teeth to acrylic resin

doi:10.1111/j.1741‐2358.2009.00333.x
Effect of microwave treatment on the shear bond strength of different types of commercial teeth to acrylic resin Objective: The purpose of this study was to verify the effect of microwave treatment on the shear bond strength of commercial types of teeth to acrylic resin, when the glossy ridge laps were unmodified (groups 1 and 5), bur abraded (groups 2 and 6), bur grooved (groups 3 and 7) or etched by monomer (groups 4 and 8). Background: Controversial findings have shown that mechanical or chemical changes in ridge‐lap surface of the tooth increase or decrease the bond strength between tooth and acrylic resin, and the microwave disinfection may cause different changes on this bond strength. Materials and methods: Eighty specimens (n = 10) were made with the acrylic resin bonded to tooth glossy ridge lap, polymerised in water at 74°C for 9 h, and deflasked after flask cooling. Specimens of the groups 5, 6, 7 and 8 were individually immersed in 150 ml of water and submitted to microwave treatment in an oven at 650 W for 3 min. Control specimens (groups 1, 2, 3 and 4) were not microwave treated. Shear bond strength test was performed in an Instron machine with a cross‐speed of 1 mm/min. Collected data were submitted to anova and Tukey’s test (α = 0.05). Results: Microwave treatment decreased the shear bond strength values of the tooth/resin bond. In the microwaved and non‐microwaved procedures, mechanical retention improved the shear bond strength when compared with the control and monomer treatments. Conclusion: Shear bond strength of the tooth/resin bond was influenced by the microwave treatment and different commercial teeth association, and was lower for the Biotone tooth.     

Differential effects of cAMP and cGMP on in vitro epidermal cell growth.

Primary keratinocyte cultures free of dermal fibroblasts were used to investigate the effect of varying cyclic AMP (cAMP) concentrations on epidermal cell function. Addition of 10^?3, 10^?4 or 10^?5 M dibutyryl cAMP to plated cells (day 1) results by day 5 in a dose dependent increase of [³H]TdR incorporation into DNA as determined by increases in both the labeling index and incorporation of ³H label into an isolated DNA fraction. 8-Bromo cAMP, another cAMP analogue, likewise induced keratinocyte proliferation. The proliferative response was dose and time dependent, and 5- to 6-fold increases in ³H label incorporated into DNA were seen at day 6, 8 and up until day 15 of culture. Moreover, elevation of cellular cAMP by addition of cholera toxin, an irreversible stimulator of adenylate cyclase, also demonstrated a time dependent stimulation of [³H]TdR uptake into DNA and increased the labeling index. Specific histochemical staining for keratinaceous protein (Kreyberg technique) demonstrated that elevated cAMP levels also enhance the production of specialized (differentiated) epidermal cells. Determination of the level of cAMP and cyclic GMP (cGMP) by RIA of partially purified fractions of the cultures revealed that addition of 8-bromo cAMP or cholera toxin to the cultures increased the levels of cAMP but not of cGMP. Addition of 8-bromo cGMP to the keratinocytes on day 1 at concentrations of 10^?6, 10^?7 or 10^?8 M had no effect on culture proliferation on days 4, 6 and 8, although qualitative changes in the electron microscopic pattern of the culture stratification and specialization were observed. The results indicate (1) both large and moderate increases in cellular cAMP levels induce keratinocyte culture proliferation and specialization in the absence of fibroblasts or dermal influences, (2) the quantitative enhancement of keratinocyte growth and specialization occurs without apparent participation of cGMP, (3) cGMP may be a qualitative effector of epidermal cell differentiation.     

Choricotyle anisotremi n. sp. (Monogenea: Diclidophoridae) parasitic on Anisotremus scapularis (Tschudi) from the northern Chilean coast

Choricotyle anisotremi n. sp. is described from the gills and on the inner surface of the operculum of Anisotremus scapularis (Pomadasyidae) from the Chilean coast. Distinct characteristics of the new species are: presence of an oval accessory sclerite on the inner quadrant of the clamp adjacent to the accessory sucker; 12 genital hooks; short and stout peduncles, the last pair of which are closely apposed; a lobed seminal receptacle; and a fan-like posthaptor without a terminal lappet.     

Chemically induced Parkinson's disease: intermediates in the oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to the 1-methyl-4-phenyl-pyridinium ion

Various unstable intermediate oxidation states have been postulated in the metabolic activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to the 1-methyl-4-phenyl pyridinium ion. We now report the first direct observation of these free radical intermediates by pulse radiolysis and flash photolysis. Studies are described of various reactions of such species, in particular with dopamine whose autoxidation to dopamine quinone is reported to be potentiated by 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine.     

Multistage carcinogenesis induced by ras and myc oncogenes in a reconstituted organ

ras and myc oncogenes were able to induce distinct phenotypic alterations, resembling different types of premalignant lesions, when introduced into approximately 0.1% of the cells used to reconstitute the mouse prostate gland. While ras induced dysplasia in combination with angiogenesis, myc induced a hyperplasia of the otherwise normally developed organ. ras and myc together induced primarily carcinomas. However, tumor progression was also associated with additional genetic alterations involving gene amplification. Our data indicate that specific types of benign premalignant lesions may reflect the activation of different single oncogenes, and that the consecutive activation of multiple oncogenes could be a causal event in the step-like progression of tumorigenesis.     

Hydrocortisone regulates arylsulfatase A (cerebroside-3-sulfate-3-sulfohydrolase) by decreasing the quantity of the enzyme in cultures of cells dissociated from embryonic mouse cerebra

Previous work from our laboratory (Biochem. J. 219:689–697 (1984) had shown that hydrocortisone stimulated the net accumulation of the myelin-specific sulfolipid in cultures of cells dissociated from embryonic mouse cerebra. This accumulation caused by hydrocortisone was shown to be due to a decrease of sulfolipid degradation by arylsulfatase A (ASA) and not due to a stimulation of its synthesis by a sulfotransferase. Both ASA activity and the turnover of sulfolipid were decreased by hydrocortisone to 60–62% of untreated cells. In current work the same decrease in enzyme activity was obtained and enzyme linked immunosorbent assays demonstrate that hydrocortisone decreased the number of ASA protein molecules to 61% of untreated cells [(-)hydrocorcortisone 0.31±0.06 ng ASA/g protein; (+)hydrocortisone: 0.18±0.04 ng ASA/g protein]. This decrease in the number of ASA molecules correlates well with the decrease in both the enzyme activity and the sulfolipid turnover, which suggests that the major mode of inhibition of ASA activity by hydrocortisone involves a decrease in the concentration of ASA in the cells rather than some other mechanism of inhibition.The material in this paper has been included in a dissertation submitted by A.J.M. in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Temple University.