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PURPOSE: This study investigated the impact of reducing the oxygen concentration via nitrogen injection during the postcuring process of 3D-printed dental materials. MATERIALS AND METHODS: Resin specimens for dental crown and bridge (15-mm diameter, both 1-mm and 2-mm heights) were 3D-printed and rinsed. Subsequently, the postcuring process was conducted on nine groups categorized according to atmospheric conditions within the curing device (20% [control], 10%, and 5% oxygen) and curing times (10, 15, and 20 minutes). Surface roughness was measured using a gloss meter. Surface polymerization was confirmed through Fourier-transform infrared spectroscopy (FT-IR) analysis, and the flexural strength and elastic modulus of the specimens were measured using a universal testing machine. Water absorption and solubility were determined according to Inernational Organization for Standardization (ISO) standards. All evaluation criteria were statistically analyzed using one-way ANOVA and Tukey's post hoc test based on oxygen concentration. RESULTS: The elastic modulus did not show statistically significant differences in all groups. However, compared to the control group, the flexural strength, degree of conversion, and gloss significantly increased in the groups with decreased oxygen concentrations. Conversely, water solubility and water absorption significantly decreased in a few groups with reduced oxygen concentration. CONCLUSIONS: Reducing oxygen concentration through nitrogen injection during the postcuring process of 3D printing enhances the suitability of the dental prosthetic materials. The significant increase in flexural strength can particularly enhance the utility of these materials in dental prosthetics.

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Synthetic cannabinoids (CBs) such as the JWH series have caused social problems concerning their abuse liability. Because the JWH series produces euphoric and hallucinogenic effects, they have been distributed illegally under street names such as "Spice" and "Smoke". Many countries including Korea have started to schedule some of the JWH series compounds as controlled substances, but there are a number of JWH series chemicals that remain uncontrolled by law. In this study, three synthetic CBs with different binding affinities to the CB1 receptor (JWH-073, 081, and 210) and Δ(9)-tetrahydrocannabinol (Δ(9)-THC) were evaluated for their potential for psychological dependence. The conditioned place preference test (unbiased method) and self-administration test (fixed ratio of 1) using rodents were conducted. Ki values of the three synthetic cannabinoids were calculated as supplementary data using a receptor binding assay and overexpressed CB1 protein membranes to compare dependence potential with CB1 receptor binding affinity. All mice administered JWH-073, 081, or 210 showed significantly increased time spent at unpreferred space in a dose-dependence manner in the conditioned place preference test. In contrast, all tested substances except Δ(9)-THC showed aversion phenomenon at high doses in the conditioned place preference test. The order of affinity to the CB1 receptor in the receptor binding assay was JWH-210 > JWH-081 >> JWH-073, which was in agreement with the results from the conditioned place preference test. However, no change in self-administration was observed. These findings suggest the possibility to predict dependence potential of synthetic CBs through a receptor binding assay at the screening level.

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Quetiapine is an atypical or second-generation antipsychotic agent and has been a subject of a series of case report and suggested to have the potential for misuse or abuse. However, it is not a controlled substance and is not generally considered addictive. In this study, we examined quetiapine's dependence potential and abuse liability through animal behavioral tests using rodents to study the mechanism of quetiapine. Molecular biology techniques were also used to find out the action mechanisms of the drug. In the animal behavioral tests, quetiapine did not show any positive effect on the experimental animals in the climbing, jumping, and conditioned place preference tests. However, in the head twitch and self-administration tests, the experimental animals showed significant positive responses. In addition, the action mechanism of quetiapine was found being related to dopamine and serotonin release. These results demonstrate that quetiapine affects the neurological systems related to abuse liability and has the potential to lead psychological dependence, as well.

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Nortriptyline, a second-generation tricyclic antidepressant, is an active metabolite of amitriptyline. Amitriptyline induces QT prolongation and torsades de pointes (TdP), which causes sudden death. We studied the cardiovascular safety of nortriptyline, including QT prolongation risk. We examined the effects of nortriptyline on the cardiovascular system in vivo and in vitro in accordance with the ICH-S7B guideline. We tested its effect on QT interval in conscious telemetered dogs. We also performed in vitro electrophysiological studies on hERG tail currents using stably transfected human embryonic kidney 293 (HEK293) cells. Action potential parameters were studied in isolated rabbit purkinje fibers. Nortriptyline dose-dependently blocked hERG current, with a tail IC(50) value of 2.20 ± 0.09 µM (n = 4). In the APD assay, total amplitude, Vmax, and resting membrane potential were not significantly changed by 1 µM nortriptyline, but nortriptyline at 0.3 and 1 µM shortened APD(50) and APD(90). Nortriptyline did not affect QTcV at 2 or 6 mg/kg, but slightly increased QTcV at 20 mg/kg. In conclusion, it is unlikely that nortriptyline affects the ventricular repolarization process at therapeutic dosages.

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The immunosuppressive compound FK506 has been successfully used in kidney and liver transplant recipients. However, the compound can induce significant side effects on kidney function. Taurine is a potent free radical scavenger that attenuates a variety of renal diseases that are the consequence of excessive oxygen free radical damage. The purpose of this study was to investigate FK506-mediated death of Madin Darby canine kidney (MDCK) cells, in relation to reactive oxygen species (ROS) production. We determined the calcium (Ca(2+)) and magnesium (Mg(2+)) concentration in cultured MDCK cells by microfluorescence techniques and the level of activation of c-Jun-N-terminal kinase (JNK), extracellular signal regulated kinases (ERK), Bcl-2 and Bax proteins by Western blot. Treatment with 10 muM FK506 induced apoptosis in MDCK cells by increasing the level of intracellular ROS and Ca(2+) and by decreaseing the level of intracellular Mg(2+). This increase in intracellular ROS promoted JNK and Bax activation, which increased FK506-induced MDCK cell death. Taurine reduced the FK506-induced generation of ROS and activation of JNK and Bax. The results indicate that taurine can prevent FK506-induced kidney toxicity.

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Lipopolysaccharide (LPS) can cause damage to the epithelia of the respiratory tract. However, taurine can protect the lung tissue from such oxidant-induced inflammation. This study examined the effects of a LPS treatment on the intracellular calcium levels ([Ca(2+)]i) as well as the specific mechanisms of LPS-induced cell death in pneumocytes. In addition, the effects of taurine on the LPS-induced increase in the accumulation of reactive oxygen species (ROS) in pneumocytes were investigated. The [Ca(2+)]i in cultured pneumocytes was determined using microfluorescence techniques. The level of activation of the mitogen-activated protein kinases (MAPKs) and Bax protein were measured by Western blotting. LPS at 10 and 100 ng/ml induced cell death and decreased the viability of MRC-5 cells. Moreover, the intracellular Ca(2+) and ROS levels were increased by LPS. The LPS treatment led to the phosphorylation of ERK1/2, JNK and the activation of Bax. A pretreatment with 20 mM taurine reduced the LPS-induced production of ROS and MARK activity. These results show that a LPS treatment induces cell death in MRC-5 cells by increasing the intracellular ROS and Ca(2+) levels. The increase in the intracellular level of ROS promotes MAPKs activation and Bax translocation. Overall, LPS induces lung cell death by activating MAPKs. Furthermore, taurine decreased the LPS-induced generation of ROS and activation of MAPK and Bax.

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AIMS: Previous studies reported that FK506 influences bone mineralizing and hypomagnesemia, and also has immune modifying properties. This study examined whether or not the function of Mg2+ in bone metabolism plays a role in the loss of bone volume caused by immunosuppressants. MAIN METHODS: The effects of the FK506 treatment on the intracellular magnesium and lactate dehydrogenase (LDH) activity were examined in cultured human osteoblasts (HOB) cells. The magnesium concentration was determined using microfluorescence techniques and atomic absorption spectrophotometry. Western blotting was used to measure the level of extracellular signal-regulated kinases 1/2 (ERK 1/2) activation. KEY FINDINGS: FK506 (0.1 microM) did not affect cell death in HOB cells after a 24 hour treatment but decreased the level of ERK 1/2 activation. In HOB cells, the mean [Mg2+]i after exposure to a 1 mM extracellular Mg2+ ([Mg2+]o) buffer was 0.53+/-0.01 mM (n=25). Exposure to 100 nM FK506 produced a significant decrease in [Mg2+]i (0.41+/-0.01 mM). The ERK inhibitor (PD98059) and FK506 produced similar effects but they were not cumulative. SIGNIFICANCE: This study examined the role of ERK1/2 activation on the regulation of magnesium in HOB. These results suggest that the inhibition of ERK phosphorylation is an essential intermediate in the effects of FK506 on magnesium. Overall, FK506 causes bone disorders partly by decreasing [Mg2+]i accompanied by the inhibition of ERK 1/2.

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Bee venom (BV) has been used in Oriental medicine to treat inflammatory diseases, such as tendonitis, bursitis, and rheumatoid arthritis, despite the sensitivity of the victims and toxicity of the venom. This study examined the mechanisms for the effects of BV on the cardiovascular system in rats. The arterial pressure and heart rate (HR) were measured in anesthetized rats. In addition, the left ventricular development pressure (LVDP) and total magnesium efflux ([Mg]e) in isolated perfused hearts, the vascular tonic responses in the isolated aorta, and the blood ionic and biochemical changes were determined simultaneously. In the anesthetized rats, the mean arterial pressure, systolic pressure, and pulse pressure were reduced by BV in a dose-dependent manner, even though the HR was increased. BV had no effects on the relaxation of phenylephrine- or KCl-induced contraction of the aortic rings. In the isolated hearts, BV generated a reversible decrease in the LVDP and velocity with changes in pressure, which were accompanied by increases in the HR and [Mg]e. BV increased the plasma ionized and total magnesium concentrations, and decreased the total magnesium level in the red blood cells. The ratio of ionized calcium/ionized magnesium was also decreased by the BV treatment. BV caused a detectable increase in blood creatine kinase, glutamic oxaloacetic transaminase, and lactic dehydrogenase, as well as a decrease in the blood total protein albumin and globulin levels. These results suggest that BV induces cardiovascular depression by decreasing the cardiac pressure and increasing the ionized magnesium concentration in the blood.

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Taurine has been reported to influence bone metabolism, and its specific transport system, the taurine transporter, is expressed in osteoblasts. The mean [Mg2+]i was 0.51+/-0.01 mM in normal culture media. Taurine caused an increase in [Mg(2+)]i by 0.72+/-0.04 mM in human osteoblast (HOB) cells. This increment in [Mg2+]i was inhibited significantly by PD98059, nifedipine, lidocaine, and imipramine. Taurine was also shown to stimulate the activation of ERK 1/2. This taurine-stimulated ERK 1/2 activation was inhibited by PD98059. In the present study, taurine was shown to increase cell proliferation and generate an increase in [Mg2+]i accompanied by ERK 1/2 activation in HOB cells.

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