Evaluation of Color-matching Ability of a Structural Colored Resin Composite.

PURPOSE: The present study evaluated the color-matching ability of a structural colored resin composite to compare it with resin composites employing pigments. METHODS AND MATERIALS: A structural colored resin composite (Omnichroma [OMC]), a supranano-filled resin composite (Estelite ∑ Quick [ELQ]), and a nano-filled resin composite (Filtek Supreme Ultra [FSU]) were used. Each resin composite was packed into a Teflon mold and pressed down with a clear strip under a glass slide. The specimens were light irradiated through the slide with a light-emitting diode curing unit. The thickness of the specimens (n=6) was measured with a digital caliper before being transferred to distilled water and stored at 37°C for 24 hours. The measurements of the optical characteristics of the specimens on a black-and-white background were performed using a spectrophotometer. D65 (CIE D65) was used as a light source for the spectrophotometer. Measurements were repeated three times for each specimen under each color-measurement condition, and average values for three same-shade specimens were calculated. One-way analysis of variance and Tukey post hoc tests were used (α=0.05). To determine its ability to match the color of artificial teeth, each shade of resin composite was placed in a cavity before performing color measurements. Using a spectrophotometer (CMS-35F S/C) with a flexible sensor, L*, a*, and b* values were obtained. RESULTS: The spectral reflectance curve of OMC showed that it reflected light wavelengths from 430-700 nm regardless of the background color and thickness of the specimens. The percentage of reflectance of ELQ decreased near wavelengths of 550-580 nm. Regarding the influence of background color on CIE L*, a*, b* values, the L* level showed significantly higher values for all tested materials with white backgrounds, and OMC was most affected by the difference in background color. However, a* values of ELQ and FSU were significantly higher with a black background than with a white background, and OMC showed a significantly higher value with a white background than with a black background. The b* values were higher with a white background than with a black background and were significantly higher for all three products, and these tendencies were much greater for ELQ and FSU. CONCLUSIONS: The ability of OMC to match the color of artificial teeth showed acceptable color compatibility, regardless of the shade of the artificial teeth and the depth of the cavity. However, ELQ and FSU showed reduced color compatibility, especially for a cavity depth of 3.0 mm. Excellent color matching ability was confirmed for the structural colored resin composite OMC, resulting in reduced color differences and therefore improving the esthetic appearance of the restoration, simplifying shade matching, and compensating for any color mismatch.

Acetyl-CoA carboxylase from Escherichia coli: gene organization and nucleotide sequence of the biotin carboxylase subunit.

Biotin carboxylase [biotin-carboxyl-carrier-protein:carbon-dioxide ligase (ADP-forming), EC 6.3.4.14] is the enzyme mediating the first step of the acetyl-CoA carboxylase [acetyl-CoA:carbon-dioxide ligase (ADP-forming), EC 6.4.1.2] reaction. We screened an Escherichia coli DNA library and a DNA fragment carrying the biotin carboxylase gene fabG, and its flanking regions were cloned. The gene for biotin carboxyl carrier protein was found 13 base pairs upstream of the fabG gene. Nucleotide sequencing of the recombinant plasmids revealed that the fabG codes for a 449-amino acid residue protein with a calculated molecular weight of 49,320, a value in good agreement with that of 51,000 determined by SDS/polyacrylamide gel electrophoresis of the purified enzyme. The deduced amino acid sequence of biotin carboxylase is also consistent with the partial amino acid sequence determined by Edman degradation. The primary structure of this enzyme exhibits a high homology with those of other biotin-dependent enzymes and carbamoyl-phosphate synthetase [carbon-dioxide:L-glutamine amino-ligase (ADP-forming, carbamate-phosphorylating), EC 6.3.5.5]; therefore, all these enzymes probably function through the same mechanism of reaction.

Cytoprotective action of roxatidine acetate HCl.

The cytoprotective action of roxatidine acetate HCl (roxatidine) was investigated. We also studied the involvement of endogenous prostaglandins (PGs) in the cytoprotective action of roxatidine and the effect of roxatidine on SRS content in pleurisy induced by A23187. Simultaneously, these effects of roxatidine were compared with those of other histamine H2-receptor antagonists at the same anti-secretory activity level. Roxatidine prevented formation of the gastric mucosal lesions induced by abs. ethanol, 0.6 N HCl and 0.2 N NaOH, but it failed to prevent 30% NaCl-induced gastric mucosal lesions. Cimetidine, ranitidine and famotidine failed to prevent formation of the gastric mucosal lesions induced by necrotizing agents. The cytoprotective action of roxatidine was not abolished by pretreatment with indomethacin. Roxatidine did not greatly influence SRS production. Consequently, it appears that roxatidine has a cytoprotective action and that this action is not associated with endogenous PGs and SRS.

Histamine H2-receptor antagonistic action of N-(3-[3-(1-piperidinylmethyl)phenoxy]propyl)acetoxyacetamide hydrochloride (TZU-0460).

The antagonism of histamine H2-receptor by N-(3-[3-(1-piperidinylmethyl)phenoxy)propyl)acetoxyacetamide hydrochloride (TZU-0460) was estimated on isolated guinea-pig right atrium and rat uterus in vitro and on gastric acid secretion in dog with Heidenhain pouch. The concentration-response curves for the positive chronotropic effect of histamine and dimaprit (S-[3-(N,N-dimethylamino) propyl]isothiourea) on atrium were displaced to the right in parallel without change in the maximum response by TZU-0460 with pA2 values of 6.56 and 6.74 and also for the relaxant effect on uterus with pA2 values of 6.81 and 6.65, respectively. There was no significant difference between the estimated pA2 values for TZU-0460 on the different tissues against the same agonist, and also between the pA2 values on the same tissue against the different agonists. The slope of the regression line of log (DR-1) against log TZU-0460 concentration on either tissue was not significantly different from unity; 0.98 (95% confidence limits, 0.81-1.14) on atrium, 0.95 (0.56-1.34) on uterus. These results indicate that TZU-0460 is a competitive antagonist of histamine and dimaprit in vitro. In Heidenhain pouch dog, TZU-0460 also competitively antagonized the stimulation of acid secretion by histamine with pA2 of 6.59 and by dimaprit with pA2 of 6.52, calculated on infused rates. These results indicate that TZU-0460 was about 6 times more potent than cimetidine.

Effects of N-(3-[3-(1-piperidinylmethyl)phenoxy]propyl)-acetoxyacetamide hydrochloride (TZU-0460), a histamine H2-receptor antagonist, on gastric acid secretion and ulcer formation.

N-(3-[3-(1-Piperidinylmethyl)phenoxy]propyl)-acetoxyacetamide++ + hydrochloride (TZU-0460) was compared with cimetidine for the effects on gastric acid secretion in dog and rat and on ulcer formation in rat. TZU-0460 as well as cimetidine, given i.v. or p.o., produced a dose-dependent inhibition of acid secretion stimulated by histamine, pentagastrin or carbachol in Heidenhain gastric pouch dogs and gastric lumen-perfused rats. In dog, the relative potencies of TZU-0460 to cimetidine, given p.o. and i.v., were 6.2 and 5.1, respectively, in acid secretion stimulated by histamine, and those gained by i.v. route were 3.5 by pentagastrin and 4.2 by carbachol. In rat, however, relative potencies of TZU-0460 to cimetidine, given i.v., were 2.8, 2.2 and 1.6 in acid secretion stimulated by histamine, pentagastrin and carbachol, respectively. TZU-0460, given p.o., prevented the formation of gastric ulcers induced by exposure to stress, pylorus-ligation, both pylorus-ligation and acetylsalicyclic acid, indometacin or reserpine in rats. TZU-0460 was about twice as active as cimetidine on these experimental models of gastric ulcers. TZU-0460, given p.o., prevented the formation of duodenal ulcer induced by cysteamine in rats, whereas cimetidine failed to prevent it significantly.

Role of beta 2-adrenoceptor blockade and circulating adrenaline level for the pressor responses to beta-adrenoceptor blocking drugs in rats.

The present experiments were designed to elucidate what mechanism(s) would be responsible for beta-adrenoceptor blocking drugs (beta-blockers)-induced pressor responses in rats. In urethane-anaesthetized rats, 6 beta-blockers at i.v. doses ranging from 0.3 to 300 micrograms/kg evoked the pressor response in a dose-dependent manner. The relative potency in causing the pressor action was correlated not to their beta 1-blocking activities (r = 0.374, P greater than 0.05) but to their beta 2-blocking ones (r = 0.856, P less than 0.05). In pithed or adrenalectomized rats with low levels of plasma catecholamines, however, propranolol failed to exert its sustained pressor action. Propranolol (300 micrograms/kg i.v.) distinctly potentiated the pressor responses not to noradrenaline but to adrenaline and to electrical stimulation of the sympathetic outflow (E.S.) in pithed rats. On the contrary, there was not any potentiation of pressor response to E.S. in pithed, adrenalectomized rats treated with propranolol (300 micrograms/kg i.v.). In rats treated with phenoxybenzamine (5 mg/kg i.v.), adrenaline was shown to have much more potent vasodilating action resulting from beta 2-stimulation than noradrenaline, the dose difference for causing the diastolic blood pressure decrease by a 25 mm Hg being almost 80 times. In pithed rats, infusion of adrenaline at the rate of 0.02 micrograms/min caused a significant increase in plasma adrenaline level from 0.02 +/- 0.01 to 0.45 +/- 0.048 ng/ml, being close to basal level obtained in urethane-anaesthetized rats. Under this situation, propranolol (1-100 micrograms/kg i.v.) showed a distinct pressor response in a dose-dependent fashion as observed in adrenal intact rats anaesthetized with urethane.(ABSTRACT TRUNCATED AT 250 WORDS)

[Antihypertensive action of adrenergic beta-receptor blockers and its effect on the entire sympathetic outflow in spontaneously hypertensive rats].

Three kinds of beta-adrenoceptor blocking agents were orally administered to spontaneously hypertensive rats (SH rats) from 5 to 13 weeks of age, and their effects on the development of hypertension and on peripheral sympathetic nervous system were investigated. In SH rats treated with the vehicle (2% Tween 80) for 8 weeks, systolic blood pressure increased from 132 +/- 1.3 to 179 +/- 2.7 mmHg (n = 10). Treatment with propranolol (2 X 50 mg/kg/day p.o., n = 8), pindolol (2 X 15 mg/kg/day p.o., n = 8) and D-32 (2 X 15 or 2 X 50 mg/kg/day p.o., n = 9) for 8 weeks slightly but definitely depressed the aforesaid development of hypertension, and their average reduction in systolic blood pressure was approximately 15 mmHg. In the pressor response to electrical stimulation of pre-ganglionic sympathetic nerves, there was not any difference between SH rats treated with vehicle and beta-adrenoceptor blocking agents (propranolol and D-32). P.o. administration of guanethidine or phentolamine, however, caused a slight hypotension and produced a significant reduction in the pressor response to electrical stimulation. SH rats treated with propranolol showed a leftward shift of the pressor response curve not to norepinephrine but to angiotensin II as compared with that obtained from vehicle treated SH rats. This phenomenon is probably due to the decreased renin release by the prolonged-treatment with drug. On the basis of these results, we could not obtain any clear evidence that the antihypertensive action exerted by beta-adrenoceptor blocking agents resulted from some interference with the function of the peripheral sympathetic nervous system.