Three-dimensional fi nite element analysis of the eff ects of diff erent attachments on molar distal displacement in invisible orthodontics

Objective: The aim of this study was to establish a three-dimensional fi nite element model and use fi nite element analysis to explore the eff ects of diff erent attachments on the distal movement of molars. Methods: Using Mimics, Geomagic Wrap, Soildworks, and Ansys software, a three-dimensional fi nite element model of the mandible was established. According to the diff erences in the attachment attached to the second molar, the model was divided into four groups for ex periment: A-Rectangular attachment(abbreviation:RA); B-Half water drop shaped attachment 1(abbreviation:HWDA1); C-Half water drop shaped attachment 2(abbreviation:HWDA2); D-Double half water drop shaped attachments set(abbreviation:DHWDAS). The distal movement of molar was analyzed by simulating the orthodontic process of invisible appliance with diff erent loads.Results: The displacement patterns of all models were accompanied by diff erent degrees of tilt. From the simulation results alone, the root control eff ect of half water drop attachment 2 was slightly better than that of half water drop attachment 1 and double half water drop attachments set, but both were better than rectangular attachments. In terms of volume, the volume of the double half water drop attachments set was signifi cantly smaller than the other three groups, and the root control eff ect was also better. Conclusion: Comprehensively, when simulating the distal displacement of the second molar with clear aligner, the double half water drop attachments set has more advantages

A facile assembly of polyimide/graphene core-shell structured nanocomposites with both high electrical and thermal conductivities

Polyimide/reduced graphene oxide (PI/r-GO) core-shell structured microspheres were fabricated by in situ reduction of graphene oxide (GO), which was coated on the surface of PI microspheres via hydrogen bonding and pi-pi stacking interaction. The highly ordered 3D core-shell structure of PI/r-GO micro spheres with graphene shell thickness of 3 nm was well characterized by scanning electron microscope (SEM), transmission electron microscopy (TEM) and Raman spectra. The glass transition temperature (T-g) of PI/r-GO microspheres was slightly increased because of the interaction of r-GO and PI matrix while the temperature at 5% weight loss (T-5%) of PI/r-GO microspheres was decreased due to the side effect of reductant hydrazine hydrate. The PI/r-GO nanocomposites exhibited highly electrical conductivity with percolation threshold of 0.15 vol% and ultimate conductivity of 1.4 x 10(-2) S/m. Besides, the thermal conductivity of PI/r-GO nanocomposites with 2% weight content of r-GO could reach up to 0.26 W/m K. (C) 2016 Elsevier Ltd. All rights reserved

Effect of controlling filamentous bulking sludge by Sequencing Batch Reactor Activated Sludge Process

Three groups of SBR reactors A, B and C with different aeration time were set up to culture the activated sludge which has already bulked. The results showed that the settling performance of activated sludge in reactor A changed a little, but reactors B and C had been significantly improved. High-throughput sequencing results showed that the aeration time had a significant inhibitory effect on the growth of Thothrix, and the longer the aeration time was, the more obvious the inhibition was. When the aeration time is more than 6h, the SBR mode can effectively inhibit filamentous sludge bulking, and the longer the aeration time, the better the effect

Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring.

Fetal nicotine exposure increased risk of developing cardiovascular disease later in life. The present study tested the hypothesis that perinatal nicotine-induced programming of heart ischemia-sensitive phenotype is mediated by enhanced reactive oxygen species (ROS) in offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in drinking water. Experiments were conducted in 8 month old age male offspring. Isolated hearts were perfused in a Langendorff preparation. Perinatal nicotine treatment significantly increased ischemia and reperfusion-induced left ventricular injury, and decreased post-ischemic recovery of left ventricular function and coronary flow rate. In addition, nicotine enhanced cardiac ROS production and significantly attenuated protein kinase Cε (PKCε) protein abundance in the heart. Although nicotine had no effect on total cardiac glycogen synthase kinase-3β (GSK3β) protein expression, it significantly increased the phosphorylation of GSK3β at serine 9 residue in the heart. NAC inhibited nicotine-mediated increase in ROS production, recovered PKCε gene expression and abrogated increased phosphorylation of GSK3β. Of importance, NAC blocked perinatal nicotine-induced increase in ischemia and reperfusion injury in the heart. These findings provide novel evidence that increased oxidative stress plays a causal role in perinatal nicotine-induced developmental programming of ischemic sensitive phenotype in the heart, and suggest potential therapeutic targets of anti-oxidative stress in the treatment of ischemic heart disease

Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring.

Fetal nicotine exposure increased risk of developing cardiovascular disease later in life. The present study tested the hypothesis that perinatal nicotine-induced programming of heart ischemia-sensitive phenotype is mediated by enhanced reactive oxygen species (ROS) in offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in drinking water. Experiments were conducted in 8 month old age male offspring. Isolated hearts were perfused in a Langendorff preparation. Perinatal nicotine treatment significantly increased ischemia and reperfusion-induced left ventricular injury, and decreased post-ischemic recovery of left ventricular function and coronary flow rate. In addition, nicotine enhanced cardiac ROS production and significantly attenuated protein kinase Cε (PKCε) protein abundance in the heart. Although nicotine had no effect on total cardiac glycogen synthase kinase-3β (GSK3β) protein expression, it significantly increased the phosphorylation of GSK3β at serine 9 residue in the heart. NAC inhibited nicotine-mediated increase in ROS production, recovered PKCε gene expression and abrogated increased phosphorylation of GSK3β. Of importance, NAC blocked perinatal nicotine-induced increase in ischemia and reperfusion injury in the heart. These findings provide novel evidence that increased oxidative stress plays a causal role in perinatal nicotine-induced developmental programming of ischemic sensitive phenotype in the heart, and suggest potential therapeutic targets of anti-oxidative stress in the treatment of ischemic heart disease

Antenatal Antioxidant Prevents Nicotine-Mediated Hypertensive Response in Rat Adult Offspring.

Previous studies demonstrated that perinatal nicotine exposure increased blood pressure (BP) in adult offspring. However, the underlying mechanisms were unclear. The present study tested the hypothesis that perinatal nicotine-induced programming of hypertensive response is mediated by enhanced reactive oxygen species (ROS) in the vasculature. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from Day 4 of gestation to Day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in the drinking water. Experiments were conducted in 8-mo-old male offspring. Perinatal nicotine treatment resulted in a significant increase in arterial ROS productions in offspring, which was abrogated by NAC. Angiotensin II (Ang II)-induced BP responses were significantly higher in nicotine-treated group than in saline control group, and NAC treatment blocked the nicotine-induced increase in BP response. In consistence, the nicotine treatment significantly increased both Ang II- and phorbol [12, 13]-dibutyrate (PDBu, a Prkc activator)-induced arterial contractions in adult offspring, which were blocked by NAC treatment. In addition, perinatal nicotine treatment significantly attenuated acetylcholine-induced arterial relaxation in offspring, which was also inhibited by NAC treatment. The results demonstrate that inhibition of ROS blocks the nicotine-induced increase in arterial reactivity and BP response to vasoconstrictors in adult offspring, suggesting a key role of increased oxidative stress in nicotine-induced developmental programming of hypertensive phenotype in male offspring

Antenatal Antioxidant Prevents Nicotine-Mediated Hypertensive Response in Rat Adult Offspring.

Previous studies demonstrated that perinatal nicotine exposure increased blood pressure (BP) in adult offspring. However, the underlying mechanisms were unclear. The present study tested the hypothesis that perinatal nicotine-induced programming of hypertensive response is mediated by enhanced reactive oxygen species (ROS) in the vasculature. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from Day 4 of gestation to Day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in the drinking water. Experiments were conducted in 8-mo-old male offspring. Perinatal nicotine treatment resulted in a significant increase in arterial ROS productions in offspring, which was abrogated by NAC. Angiotensin II (Ang II)-induced BP responses were significantly higher in nicotine-treated group than in saline control group, and NAC treatment blocked the nicotine-induced increase in BP response. In consistence, the nicotine treatment significantly increased both Ang II- and phorbol [12, 13]-dibutyrate (PDBu, a Prkc activator)-induced arterial contractions in adult offspring, which were blocked by NAC treatment. In addition, perinatal nicotine treatment significantly attenuated acetylcholine-induced arterial relaxation in offspring, which was also inhibited by NAC treatment. The results demonstrate that inhibition of ROS blocks the nicotine-induced increase in arterial reactivity and BP response to vasoconstrictors in adult offspring, suggesting a key role of increased oxidative stress in nicotine-induced developmental programming of hypertensive phenotype in male offspring

Amination of Nitroazoles — A Comparative Study of Structural and Energetic Properties

In this work, 3-nitro-1H-1,2,4-triazole (1) and 3,5-dinitro-1H-pyrazole (2) were C-aminated and N-aminated using different amination agents, yielding their respective C-amino and N-amino products. All compounds were fully characterized by NMR (1H, 13C, 15N), IR spectroscopy, differential scanning calorimetry (DSC). X-ray crystallographic measurements were performed and delivered insight into structural characteristics as well as inter- and intramolecular interactions of the products. Their impact sensitivities were measured by using standard BAM fallhammer techniques and their explosive performances were computed using the EXPLO 5.05 program. A comparative study on the influence of those different amino substituents on the structural and energetic properties (such as density, stability, heat of formation, detonation performance) is presented. The results showed that the incorporation of an N-amino group into a nitroazole ring can improve nitrogen content, heat of formation and impact sensitivity, while the introduction of a C-amino group can enhance density, detonation velocity and pressure. The potential of N-amino and C-amino moieties for the design of next generation energetic materials is explored

Role of DNA methylation in perinatal nicotine-induced development of heart ischemia-sensitive phenotype in rat offspring.

Background and purposeMaternal cigarette smoking increases the risk of cardiovascular disease in offspring. Recently, we have demonstrated that perinatal nicotine exposure alters heart development and increases heart susceptibility to ischemia/reperfusion (I/R) injury in rat offspring. The present study tested the hypothesis that DNA methylation plays a key role in the nicotine-induced development of heart ischemia-sensitive phenotype in offspring.Experimental approachNicotine was administered to pregnant rats via subcutaneous osmotic minipumps from gestational day 4 until postnatal day 10. After birth, the postnatal offspring were treated with the DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza) or saline from postnatal day 3 to day 10. Experiments were conducted in 1 month old offspring.Key resultsPerinatal nicotine increased I/R-induced left ventricular (LV) injury, and decreased post-ischemic recovery of the LV function and coronary flow rate in both male and female offspring. Nicotine differentially increased DNMT3a expression and global DNA methylation levels in LV tissues. Treatment with 5-Aza inhibited nicotine-induced an increase in DNMT3a and global DNA methylation, and blocked the nicotine-induced increase in I/R injury and dysfunction in the heart. In addition, nicotine attenuated protein kinases Cε and large-conductance Ca(2+)-activated K(+) (BKca) channel β1 subunit protein abundances in the heart, which were reversed by 5-Aza treatment.Conclusions and implicationsThe present findings provide novel evidence that the increased DNA methylation plays a causal role in nicotine-induced development of heart ischemic sensitive phenotype, and suggest a potential therapeutic target of DNA demethylation for the fetal programming of heart ischemic disease later in life

Role of DNA methylation in perinatal nicotine-induced development of heart ischemia-sensitive phenotype in rat offspring.

Background and purposeMaternal cigarette smoking increases the risk of cardiovascular disease in offspring. Recently, we have demonstrated that perinatal nicotine exposure alters heart development and increases heart susceptibility to ischemia/reperfusion (I/R) injury in rat offspring. The present study tested the hypothesis that DNA methylation plays a key role in the nicotine-induced development of heart ischemia-sensitive phenotype in offspring.Experimental approachNicotine was administered to pregnant rats via subcutaneous osmotic minipumps from gestational day 4 until postnatal day 10. After birth, the postnatal offspring were treated with the DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza) or saline from postnatal day 3 to day 10. Experiments were conducted in 1 month old offspring.Key resultsPerinatal nicotine increased I/R-induced left ventricular (LV) injury, and decreased post-ischemic recovery of the LV function and coronary flow rate in both male and female offspring. Nicotine differentially increased DNMT3a expression and global DNA methylation levels in LV tissues. Treatment with 5-Aza inhibited nicotine-induced an increase in DNMT3a and global DNA methylation, and blocked the nicotine-induced increase in I/R injury and dysfunction in the heart. In addition, nicotine attenuated protein kinases Cε and large-conductance Ca(2+)-activated K(+) (BKca) channel β1 subunit protein abundances in the heart, which were reversed by 5-Aza treatment.Conclusions and implicationsThe present findings provide novel evidence that the increased DNA methylation plays a causal role in nicotine-induced development of heart ischemic sensitive phenotype, and suggest a potential therapeutic target of DNA demethylation for the fetal programming of heart ischemic disease later in life