Effects of rehydration on dentin strengthened by heating or UV irradiation.

Type I collagen, the major organic component of human dentin, plays an important role in regulating the mechanical strength of dentin. Collagen in dentin can be strengthened by heating. We hypothesized that UV irradiation could produce similar strengthening effects and might maintain the strength of dentin after rehydration. Beam-shaped dentin specimens from the crowns of human third molars were subjected to flexural testing. Flexural strengths were two and three times greater than those in the control group after 5 minutes' UV irradiation and heating to 140 degrees C, respectively. After 30 days of rehydration, the heated specimens reverted to their original strength, whereas the UV specimens were 69% stronger than the original. Raman spectra of dental collagen were unchanged after heating, whereas several peaks, including a C-C bond in a proline ring, were amplified by UV irradiation. It is concluded that dentin strengthened by UV irradiation retains strength after rehydration because of chemical changes in collagen.

Heat treatment strengthens human dentin.

The flexural strength of Type I collagen, the major organic component of human dentin, increases with heat. We hypothesized that human dentin can be strengthened by heating, which may help prevent fracture of non-vital teeth after restoration. Beam-shaped dentin specimens were obtained from the crowns of human third molars. The dentinal tubular orientations were arranged to run parallel or perpendicular to loading surfaces. The flexural and microtensile strengths of dentin in the parallel specimens were 2- to 2.4-fold greater after being heated between 110 degrees C and 140 degrees C for 1 hr. The stress intensity factors at fracture also increased after specimens were heated. The x-ray diffraction analyses suggested that shrinking of the lateral packing of the collagen triple-helices from 14 A to 11 A was the probable cause of the strengthening of heated dentin. We conclude that heat treatment strengthens human dentin.

Estimation of glycemic and insulinemic responses to short-grain rice (Japonica) and a short-grain rice-mixed meal in healthy young subjects.

We estimated glycemic and insulinemic responses to short-grain rice (Japonica) and a short-grain rice-mixed meal (i.e. short-grain rice and other ingredients) in three healthy male, and five healthy female subjects aged 22-31 years. A 50 g carbohydrate portion of dry rice was used in this study to estimate the glycemic index (GI) of short-grain rice (Experiment 1). The GI of short-grain rice was 68 (white bread = 100). In Eperiment 2, the subjects took three mixed meals (rice-, bread- and cornflakes-mixed) containing 60 g available carbohydrate, 25-29 g fat, 18-22 g protein, 2331-2486 kJ energy, and 67-123 meal GI in order to detemine whether both the amount and source of carbohydrate consumed determined postprandial glycemic and insulinemic responses of mixed meals. Glycemic response after the rice-mixed meal was significantly lower (p<0.05) than that after the cereal-mixed meal. The predicted glycemic and insulinemic responses, based on GI and the amount of carbohydrate, were related to the observed mean plasma glucose responses. These results suggest that short-grain rice (Japonica) grown in Japan should not be classified as a high GI food and that, in a mixed meal, it is a lower glycemic and insulinemic responder compared with bread or cereal mixed meals. Moreover, both the amount and source of carbohydrate consumed determine the glycemic and insulinemic responses after different mixed meals with variable GI.

[Chemotactic activity of human peripheral eosinophils toward leukotriene E4].

We studied the chemotactic activity of isolated human peripheral eosinophils toward leukotriene (LT) E4. We obtained eosinophil suspensions by the method of CD16 negative selection. Eosinophil chemotactic activities toward platelet activating factor (PAF, 10(-6) M) and LTE4 (10(-7) M, 10(-6) M, 10(-5) M) were studied using a modified Boyden Chamber method. Eosinophils migrated significantly toward PAF and LTE4 (10(-7) M, 10(-6) M). The chemotactic activity toward LTE, was most potential at 10(-6) M. These results suggest that LTE4 is an eosinophil chemoattractant.

[Effects of SDZ ISQ 844, a cyclic nucleotide phosphodiesterase isozyme type III/IV inhibitor, on the release of histamine from human peripheral leukocytes].

We studied the effects of SDZ ISQ 844, a cyclic nucleotide phosphodiesterase (PDE) isozyme type III/IV inhibitor, and salbutamol on the release of histamine from activated human peripheral leukocytes. We stimulated the leukocyte suspensions with calcium ionophore A23187 (Ca-I, 10(-6 M) accompanied with SDZ ISQ 844 (10(-7) M, 10(-6) M, 10(-5) M), salbutamol (10(-7) M, 10(-6) M, 10(-5) M) and combination of SDZ ISQ 844 and salbutamol (10(-7) M, 10(-6) M, 10(-5) M), and measured the levels of histamine in the supernatant fluid and total cyclic AMP levels in the leukocyte suspensions. The increase of histamine levels induced by Ca-I was significantly inhibited by SDZ ISQ 844 (10(-6) M, 10(-5) M) in a dose-dependent manner (p < 0.05, p < 0.01). Salbutamol at the concentration until 10(-5) M did not inhibit the increase of histamine levels. Combination of SDZ ISQ 844 and salbutamol significantly inhibited the increase of histamine levels (10(-6) M, 10(-5) M) in a dose-dependent manner (p < 0.05, p < 0.01). The inhibition of the histamine release by SDZ ISQ 844 (10(-5) M was enhanced significantly by salbutamol (10(-5) M) (p < 0.05). Total cyclic AMP levels in the leukocytes suspensions increased significantly by SDZ ISQ 844 (10(-5) M) and combination of SDZ ISQ 844 and salbutamol (10(-6) M, 10(-5) M) in a dose-dependent manner (p < 0.05, p < 0.01). The increase of cyclic AMP levels by SDZ ISQ 844 (10(-5) M) was enhanced by salbutamol significantly (p < 0.01). These results suggest that selective inhibition of PDE isozyme type III/IV protects the release of histamine from human activated leukocytes in connection with intracellular cyclic AMP levels and the protection is enhanced by beta-agonist.

[Effects of theophylline and doxofylline on airway responsiveness in beagles].

We examined the effects of doxofylline, which is a new methylxanthine analog, on heart rate, respiratory rate, respiratory resistance and airway responsiveness in five beagles, and compared with those effects of theophylline. Airway responsiveness to inhaled methacholine was determined by modified Astograph (7Hz oscillation method). Theophylline (10 mg/kg, 20 mg/kg, 40 mg/kg) was orally administered one hour prior to the determination of airway responsiveness and doxofylline (20 mg/kg, 40 mg/kg, 80 mg/kg) was orally administered thirty minutes prior to determination of airway responsiveness at intervals of about one week. Heart rate increased significantly by all dose of theophylline in a dose-dependent manner and by 80 mg/kg of doxofylline. Respiratory rate increased significantly only by 40 mg/ kg of theophylline. Respiratory resistance decreased significantly after administration of 40 mg/kg of theophylline. Airway responsiveness decreased significantly by 40 mg/kg of theophylline and 40 mg/kg, 80 mg/kg of doxofylline in a dose-dependent manner. These results suggest that doxofylline decreased airway responsiveness at the dosage which dose not affect the heart rate and respiratory rate compared with theophylline.

[Relation of platelet activating factor induced airway hyperresponsiveness to thromboxane A2 and neutrophil in dogs].

We studied the relation of the airway hyperresponsiveness induced by platelet activating factor (PAF) inhalation to thromboxane (Tx)A2 and neutrophil in ten dogs. Airway responsiveness to inhaled methacholine was determined by Astograph (7 Hz oscillation method), PAF (1000 micrograms/ml) was delivered as an aerosol generated from a Devilbiss 646 nebulizer for ten minutes. After determination of airway responsiveness, we carried out bronchoalveolar lavage and measured the TxB2 levels and the number of neutrophils in bronchoalveolar lavage fluid (BALF). Airway responsiveness developed significantly (p < 0.01), and the levels of TxB2 and the number of neutrophils in BALF were increased (p < 0.01) 3 hr after PAF inhalation. The change in airway responsiveness correlated significantly with the percent change of TxB2 levels (r = 0.746, p < 0.05). However no significant correlation was recognized between the increase in TxB2 levels and the increase in the number of neutrophils, nor between the change in airway responsiveness and the increase in the number of neutrophils. These results suggest that the increase in airway responsiveness induced by PAF inhalation is involved in the hyperproduction of TxA2 but that TxA2 is not released from neutrophils infiltrating into the airway; furthermore neutrophils may not induce airway hyperresponsiveness in dogs.

[Effects of a cyclic nucleotide phosphodiesterase isoenzyme type III inhibitor, SDZ MKS 492 on airway responsiveness in beagles].

To elucidate the effects of cyclic nucleotide phosphodiesterase (PDE) isoenzyme inhibition on airway responsiveness, we studied the effects of a selective PDE isoenzyme type III inhibitor, SDZ MKS 492, on airway responsiveness to inhaled methacholine (Mch) in 6 beagles. Base-line respiratory resistance and airway responsiveness to Mch were determined by modified Astograph (7 Hz oscillation method). SDZ MKS 492 (1.0 mg/kg, 0.3 mg/kg or 0.1 mg/kg) was orally administered 1 hr prior to the determination of airway responsiveness at intervals of one week. Base-line respiratory resistance was decreased in a dose-dependent manner by SDZ MKS 492. SDZ MKS 492 significantly decreased airway responsiveness to Mch (log D min) in a dose-dependent manner, and the airway responsiveness (log PD2.0 Mch) was significantly decreased by 1.0 mg/kg of SDZ MKS 492. These results indicate that selective inhibition of PDE isoenzyme type III results in a decrease in respiratory resistance and airway responsiveness.

[Role of thromboxane A2 and prostaglandin I2 in the increase of airway responsiveness in dogs after ozone exposure].

To investigate the role of thromboxane (Tx) A2 and prostaglandin (PG) I2 in the development of airway responsiveness after ozone exposure, we measured the airway responsiveness to inhaled methacholine (Mch), TxB2 and 6-keto-PGF1 alpha levels in bronchoalveolar lavage fluid (BALF) in 18 dogs after ozone exposure. Airway responsiveness to Mch was determined by Astograph (7 Hz oscillation method), and ozone exposure was carried out for 2 hr at an ozone level of 3.01 +/- 0.05 ppm (mean +/- SEM). Airway responsiveness to Mch increased significantly after ozone exposure (p less than 0.001). TxB2 levels in BALF were not affected by ozone exposure, but the levels of 6-keto-PGF1 alpha decreased significantly after ozone exposure (p less than 0.001). The ratio of TxB2/6-keto-PGF1 alpha increased significantly after ozone exposure, and the change in this ratio correlated significantly with the change of airway responsiveness to Mch (p less than 0.01, r = 0.654). These results suggest that airway hyperresponsiveness after ozone exposure is induced by the relative increase of TxA2 due to the decrease of PGI2.

[Inhibitory effect of S-1452, a specific thromboxane A2 receptor antagonist on the increase of airway responsiveness in dogs after ozone exposure].

We evaluated the inhibitory effect of S-1452, a specific thromboxane (Tx) A2 receptor antagonist on the increase of airway responsiveness in 7 dogs after ozone exposure. Airway responsiveness to inhaled methacholine (Mch) was determined by Astograph (7 Hz oscillation technique), and at the same time TxB2, 6-keto-prostaglandin (PG) F1 alpha, PGE2 levels and total cell counts in the bronchoalveolar lavage fluid (BALF) were measured. Ozone exposure was carried out for 2 hr at an ozone level of 3.04 +/- 0.02 ppm (mean +/- SEM). Airway responsiveness to Mch increased significantly after ozone exposure (p less than 0.01), and this hyperresponsiveness was inhibited significantly by pretreatment with S-1452 (p less than 0.02). TxB2 and PGE2 levels in BALF did not change after ozone exposure, but the levels of 6-keto-PGF1 alpha decreased significantly after ozone exposure (p less than 0.05). Total cell counts in BALF increased significantly after ozone exposure (p less than 0.02). The decrease of 6-keto-PGF1 alpha levels and the increase of total cell counts were not affected by pretreatment with S-1452. These results suggest that S-1452 is protective against the increase of airway responsiveness induced by ozone exposure, and that TxA2 plays an important role in the hyperresponsiveness. But hyperresponsiveness may not be induced by hyperproduction of TxA2, but by the relative increase of TxA2 to PGI2.

[Inhibitory effect of prostaglandin I2 on the increase of airway responsiveness induced by inhaled thromboxane A2 mimetic U-46619 in dogs].

To investigate the effect of prostaglandin I2 (PGI2) on the increase of airway responsiveness induced by inhaled thromboxane A2 (TxA2), we measured the airway responsiveness to inhaled methacholine (Mch) after inhalation of TxA2 mimetic U-46619 alone and after inhalation of U-46619 in combination with PGI2 (U-46619/PGI2) in six dogs. Airway responsiveness to Mch was determined by Astograph (7Hz oscillation method). Inhalation of U-46619 was carried out for five minutes at a half of minimum threshold concentration, and the concentration of PGI2 was double that of U-46619. Inhaled U-46619 significantly increased airway responsiveness to Mch (p less than 0.01). However the airway responsiveness to Mch did not increase following inhalation of U-46619/PGI2, and the increase of airway responsiveness to Mch induced by inhaled U-46619 was inhibited significantly by PGI2 (p less than 0.01). PGI2 inhalation alone did not affect the basal airway responsiveness to Mch. These results indicate that PGI2 protects the hyperresponsiveness induced by TxA2 inhalation in dogs.