Visual Simulation Software Demonstration for Quantum Multi-Drone Reinforcement Learning

Quantum computing (QC) has received a lot of attention according to its light training parameter numbers and computational speeds by qubits. Moreover, various researchers have tried to enable quantum machine learning (QML) using QC, where there are also multifarious efforts to use QC to implement quantum multi-agent reinforcement learning (QMARL). Existing classical multi-agent reinforcement learning (MARL) using neural network features non-stationarity and uncertain properties due to its large number of parameters. Therefore, this paper presents a visual simulation software framework for a novel QMARL algorithm to control autonomous multi-drone systems to take advantage of QC. Our proposed QMARL framework accomplishes reasonable reward convergence and service quality performance with fewer trainable parameters than the classical MARL. Furthermore, QMARL shows more stable training results than existing MARL algorithms. Lastly, our proposed visual simulation software allows us to analyze the agents' training process and results.Comment: 5 pages, 4 figure

Development of Pd Alloy Hydrogen Separation Membranes with Dense/Porous Hybrid Structure for High Hydrogen Perm-Selectivity

For the commercial applications of hydrogen separation membranes, both high hydrogen selectivity and permeability (i.e., perm-selectivity) are required. However, it has been difficult to fabricate thin, dense Pd alloy composite membranes on porous metal support that have a pore-free surface and an open structure at the interface between the Pd alloy films and the metal support in order to obtain the required properties simultaneously. In this study, we fabricated Pd alloy hydrogen separation membranes with dense/porous hybrid structure for high hydrogen perm-selectivity. The hydrogen selectivity of this membrane increased owing to the dense and pore-free microstructure of the membrane surface. The hydrogen permeation flux also was remarkably improved by the formation of an open microstructure with numerous open voids at the interface and by an effective reduction in the membrane thickness as a result of the porous structure formed within the Pd alloy films

Optimal Frequency Intensity of Physical Activity to Reduce the Risk of Hypertension in the Korean Population

PURPOSE: Regular physical activity (PA) is an effective lifestyle modification for preventing hypertension. This study aimed to analyze the optimal frequency of PA required to reduce the incidence of hypertension in the Korean population. Most Korean studies have included only small samples and limited age ranges. METHODS: The present study analyzed 16,299,865 participants aged ≥20 years (44.25±12.74 years) from the 2009 to 2012 Korean National Health Insurance Corporation Survey database. The International Physical Activity Questionnaire was used to assess the frequency and intensity of physical activity. Hazard ratios for incident hypertension were analyzed by physical activity participation, age, and sex using multivariable Cox proportional hazard models, with a non-regular physical activity group as reference. RESULTS: A total of 1,322,674 cases of incident hypertension were identified during the mean follow-up period of over 3 years. Hazard ratios for incident hypertension increased with age, with values of 50.4 and 56.1 for men and women in the older age group, respectively. Hazard ratios for incident hypertension were significantly lower in the regular PA group of middle-aged (4%) and older (7%) adults than in the non-regular PA group. The study revealed that moderate-to-vigorous-intensity PA 3-5 times/week was most effective in reducing the risk of incident hypertension in middle-aged and older adults but not in young adults. We observed no additional lowering of incident hypertension risk in the group undergoing moderate-to-vigorous PA at a frequency of 6-7 days/week compared to the 35 days/week group. CONCLUSIONS: We suggest PA at a frequency of 3-5 times/week for the prevention of incident hypertension in Korean adults

Antioxidant effect of lidocaine and procaine on reactive oxygen species-induced endothelial dysfunction in the rabbit abdominal aorta

Background: Reactive oxygen species (ROS) induce lipid peroxidation and tissue damage in the endothelium. We tested the antioxidant effect of lidocaine and procaine on ROS-induced endothelial damage in the rabbit aorta. Methods: Aortic rings isolated from rabbits were suspended in an organ bath filled with Krebs-Henseleit (K-H) solution bubbled with 5% CO2 and 95% O 2 at 37.5??C. After precontraction with phenylephrine (PE, 10 -6 M), changes in tension were recorded following a cumulative administration of acetylcholine (ACh 3 ?? 10-8 to 10 -6 M). Differences were measured as percentages of ACh-induced relaxation of aortic rings before and after exposure to ROS as generated by electrolysis of the K-H solution. The aortic rings were pretreated with lidocaine or procaine (10-5 M to 3 ?? 10-3 M) to compare their effects, as well as ROS scavengers, catalase, mannitol, sodium salicylate, and deferoxamine, and a catalase inhibitor, 3-amino-1,2,4-triazole (3AT). Results: Lidocaine and procaine dose-dependently maintained endothelium-dependent relaxation induced by ACh despite ROS activity (P < 0.05 vs control value). The 3AT pretreated procaine (3 ?? 10-3 M) group decreased more significantly than the un-pretreated procaine group (P < 0.05). Conclusions: These findings suggest that lidocaine and procaine dose-dependently preserve endothelium-dependent vasorelaxation against ROS attack, potentially via hydrogen peroxide scavenging. Copyright ?? Korean Society of Anesthesiologists, 2010

Visfatin exerts angiogenic effects on human umbilical vein endothelial cells through the mTOR signaling pathway

AbstractThe biologically active factors known as adipocytokines are secreted primarily by adipose tissues and can act as modulators of angiogenesis. Visfatin, an adipocytokine that has recently been reported to have angiogenic properties, is upregulated in diabetes, cancer, and inflammatory diseases. Because maintenance of an angiogenic balance is critically important in the management of these diseases, understanding the molecular mechanism by which visfatin promotes angiogenesis is very important. In this report, we describe our findings demonstrating that visfatin stimulates the mammalian target of the rapamycin (mTOR) pathway, which plays important roles in angiogenesis. Visfatin induced the expression of hypoxia-inducible factor 1α (HIF1α) and vascular endothelial growth factor (VEGF) in human endothelial cells. Inhibition of the mTOR pathway by rapamycin eliminated the angiogenic and proliferative effects of visfatin. The visfatin-induced increase in VEGF expression was also eliminated by RNA interference-mediated knockdown of the 70-kDa ribosomal protein S6 kinase (p70S6K), a downstream target of mTOR. Visfatin inactivated glycogen synthase kinase 3β (GSK3β) by phosphorylating it at Ser-9, leading to the nuclear translocation of β-catenin. Both rapamycin co-treatment and p70S6K knockdown inhibited visfatin-induced GSK3β phosphorylation at Ser-9 and nuclear translocation of β-catenin. Taken together, these results indicate that mTOR signaling is involved in visfatin-induced angiogenesis, and that this signaling leads to visfatin-induced VEGF expression and nuclear translocation of β-catenin

PKCε-mediated ERK1/2 activation involved in radiation-induced cell death in NIH3T3 cells

AbstractProtein kinase C (PKC) isoforms play distinct roles in cellular functions. We have previously shown that ionizing radiation activates PKC isoforms (α, δ, ε, and ζ), however, isoform-specific sensitivities to radiation and its exact mechanisms in radiation mediated signal transduction are not fully understood. In this study, we showed that overexpression of PKC isoforms (α, δ, ε, and ζ) increased radiation-induced cell death in NIH3T3 cells and PKCε overexpression was predominantly responsible. In addition, PKCε overexpression increased ERK1/2 activation without altering other MAP-kinases such as p38 MAPK or JNK. Co-transfection of dominant negative PKCε (PKCε-KR) blocked both PKCε-mediated ERK1/2 activation and radiation-induced cell death, while catalytically active PKCε construction augmented these phenomena. When the PKCε overexpressed cells were pretreated with PD98059, MEK inhibitor, radiation-induced cell death was inhibited. Co-transfection of the cells with a mutant of ERK1 or -2 (ERK1-KR or ERK2-KR) also blocked these phenomena, and co-transfection with dominant negative Ras or Raf cDNA revealed that PKCε-mediated ERK1/2 activation was Ras–Raf-dependent. In conclusion, PKCε-mediated ERK1/2 activation was responsible for the radiation-induced cell death

Arrhythmia surgery for atrial fibrillation associated with atrial septal defect: Right-sided maze versus biatrial maze

BackgroundAlthough it has been inferred that a biatrial maze procedure for atrial fibrillation in left-sided heart lesions may lead to better outcomes compared with a limited left atrial lesion set, it remains controversial whether the biatrial maze procedure is superior to the right atrial maze procedure in right-sided heart lesions.MethodsA retrospective review was performed for 56 adults who underwent surgical closure of atrial septal defect and various maze procedures for atrial fibrillation between June 1998 and February 2011. The median age at operation was 59 years (range, 34-79 years). Clinical manifestations of atrial fibrillation were paroxysmal in 8 patients, persistent in 15 patients, and long-standing persistent in 33 patients. A right atrial maze procedure was performed in 23 patients (group 1), and a biatrial maze procedure was performed in 33 patients (group 2). Treatment failure was defined as atrial fibrillation recurrence, development of atrial flutter or other types of atrial tachyarrhythmia, or implantation of a permanent pacemaker. The Cox proportional hazards model was used to identify risk factors for decreased time to treatment failure.ResultsDuring the median follow-up period of 49 months (range, 5-149 months), there was no early death and 1 late noncardiac death. On Cox survival model, group 1 showed a significantly decreased time to treatment failure in comparison with group 2 (hazard ratio, 5.11; 95% confidence interval, 1.59-16.44; P = .006). Maintenance of normal sinus rhythm without any episode of atrial fibrillation recurrence at 2 and 5 years postoperatively was 57% and 45% in group 1, respectively, and 82% and 69% in group 2, respectively.ConclusionsLeft-sided ablation in addition to a right atrial maze procedure leads to better electrophysiologic outcome in atrial fibrillation associated with atrial septal defect

Tetraarsenic Hexoxide Induces Beclin-1-Induced Autophagic Cell Death as well as Caspase-Dependent Apoptosis in U937 Human Leukemic Cells

Tetraarsenic hexaoxide (As4O6) has been used in Korean folk remedy for the treatment of cancer since the late 1980s, and arsenic trioxide (As2O3) is currently used as a chemotherapeutic agent. However, evidence suggests that As4O6-induced cell death pathway was different from that of As2O3. Besides, the anticancer effects and mechanisms of As4O6 are not fully understood. Therefore, we investigated the anticancer activities of As4O6 on apoptosis and autophagy in U937 human leukemic cells. The growth of U937 cells was inhibited by As4O6 treatment in a dose- and a time-dependent manner, and IC50 for As4O6 was less than 2 μM. As4O6 induced caspase-dependent apoptosis and Beclin-1-induced autophagy, both of which were significantly attenuated by Bcl-2 augmentation and N-acetylcysteine (NAC) treatment. This study suggests that As4O6 should induce Beclin-1-induced autophagic cell death as well as caspase-dependent apoptosis and that it might be a promising agent for the treatment of leukemia