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Overwork-related disorders and recent improvement of national policy in South Korea
Objectives: Recently, overwork-related disorders have become a major public health concern in Korea. This study investigated the current trends of working hours, causes of death in the working population, and compensation rates.
Methods: We reviewed the current trends of working hours, cause of death statistics in the working population, industrial accident compensation insurance (IACI) statistics, issues of compensation and prevention of work-related cerebro-cardio vascular diseases (CCVDs), mental disorders, and suicide.
Results: Although weekly working hours and the proportion of long working days have decreased, workers in small companies with fewer than five employees and those in the service sector continue to work long hours. The age standardized mortality due to CCVD and suicide was highest among those with managerial roles. In total, 589 CCVD cases and 104 mental disorder or suicide cases were compensated as occupational diseases in 2017. Between 2016 and 2017, 61% of 59 compensated suicides were related to overwork, specifically: long working hours, increased responsibility, or increased workload. The Korean government has introduced various policies to reduce working hours and to increase compensation approval rate for overwork-related CCVDs. Stakeholders have called for the introduction of independent laws to prevent overwork-related disorders, change organizational culture, and address the blind spots of the IACI Act and Labor Standard Act.
Conclusions: Prevention and compensation policies have improved working conditions in Korea, but there remains much to be done. This review significantly contributes to the understanding of the overall policies and research to prevent overwork-related disorders in Korea
Analysis of Tourism Technology Trends in Korea and the U.S. Using Patent Information: Based on Topic Modeling
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Most studies on the technology trends in the field of tourism have mainly focused on the cases that are currently used by the tourism industry. The purpose of this paper is to quantitatively measure and evaluate technology trends in the tourism field in Korea and the U.S. based on tourism-related patents. For this purpose, this study attempts to derive the detailed techniques used in the field of tourism using the latent Dirichlet allocation (LDA) model of topic modeling and to understand the growing and declining technologies that are currently being used in both countries. As a result of this analysis, eight technologies were identified: (1) tourism information providing systems based on location information; (2) improvements in travel bag function and design; (3) business methods related to the hospitality industry; (4) tourism information provision and experience systems based on augmented and virtual reality; (5) terminal devices and software related to tourism information provision systems; (6) improvements in the function and design of travel equipment (excluding travel bags); (7) travel recommendation and reservation systems; and (8) travel information sharing and travel record collection systems. Three of these technologies are growing in Korea (tourism information and experience systems based on augmented reality and virtual reality, travel recommendation and reservation systems, and travel information sharing and travel record collection systems) and two are declining (business methods related to the hospitality industry and terminal devices and software related to tourism information provision systems). Data for the initial research on the tourism-related technology analysis and information about the technologies to be applied in tourism in the future is provided
Characteristics of lower-hybrid surface waves
We have derived the dispersion relation for the lower-hybrid surface waves propagating perpendicularly to the magnetic field in the semi-bounded warm plasma. The mirror reflection boundary condition is adopted to obtain the surface mode of lower-hybrid plasma waves. The effects of magnetic-field strength and the finite ion temperature on the propagation of the lower-hybrid surface wave are investigated. The increase of ion temperature significantly increases the wave frequency, but an interesting hump of the group velocity appears in the region where the wavelength of the lower-hybrid surface wave is much larger than the electron Debye length. For cold ions, the surface wave is resonant near the lower-hybrid frequency as the wave number goes to infinity. Copyright (C) EPLA, 2019Two of the authors (MJL and Y-DJ) acknowledge Prof. H. J. Lee for useful discussions on surface plasma waves. One of the authors (Y-DJ) gratefully acknowledges Dr. M. Rosenberg for useful discussions and warm hospitality while visiting the Department of Electrical and Computer Engineering at the University of California, San Diego. The work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean Government (MISP) (No. 2019R1A2C1003363)
CRISPR-mediated upregulation of DR5 and downregulation of cFLIP synergistically sensitize HeLa cells to TRAIL-mediated apoptosis
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has received attention as an anticancer therapy because it mediates apoptosis of several cancer cell types but not normal human cell types. In this study, we implemented genome editing techniques to upregulate DR5 and downregulate cFLIP in HeLa cells to stimulate TRAIL-induced apoptosis. We designed and validated sgRNAs to enrich the endogenous level of DRS by dead Cas9 (dCas9). Similarly, we designed two sgRNAs to disrupt the cFLIP gene by CRISPR/Cas9. We analyzed the effect of TRAIL on tumor cells by co-transfecting HeLa cells with the best combinations of sgRNAs regulating DR5 and cFLIP genes. TRAIL-induced apoptosis in HeLa cells was evaluated by the gamma H2AX foci formation assay to check for double-strand break and propidium iodide and Annexin V staining to quantify apoptotic cells. Viable cells were identified by CCK-8 assay, and cleaved-PARP level was evaluated by Western blot. This is the first study to demonstrate that genome editing techniques can be used as an effective combinatorial treatment strategy to induce apoptosis of cancer cells. In particular, enhancement of DR5 expression and inhibition of cFLIP expression by genome editing had a synergistic effect of inhibiting proliferation and inducing apoptosis in TRAIL-resistant HeLa cells. These results suggest that combinatorial treatment strategies mediated by the CRISPR/Cas9 system may be effective for design of other human TRAIL-resistant cell types. (C) 2019 Elsevier Inc. All rights reserved.This study was supported by a grant from the National Research Foundation of Korea (2017M3A9C6061361) and Medical Research Center (2017R1A5A2015395), funded by the National Research Foundation of Korea (NRF) of the Ministry of Science, ICT and Future Planning, Republic of Korea
CRISPR-mediated upregulation of DR5 and downregulation of cFLIP synergistically sensitize HeLa cells to TRAIL-mediated apoptosis
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has received attention as an anticancer therapy because it mediates apoptosis of several cancer cell types but not normal human cell types. In this study, we implemented genome editing techniques to upregulate DR5 and downregulate cFLIP in HeLa cells to stimulate TRAIL-induced apoptosis. We designed and validated sgRNAs to enrich the endogenous level of DRS by dead Cas9 (dCas9). Similarly, we designed two sgRNAs to disrupt the cFLIP gene by CRISPR/Cas9. We analyzed the effect of TRAIL on tumor cells by co-transfecting HeLa cells with the best combinations of sgRNAs regulating DR5 and cFLIP genes. TRAIL-induced apoptosis in HeLa cells was evaluated by the gamma H2AX foci formation assay to check for double-strand break and propidium iodide and Annexin V staining to quantify apoptotic cells. Viable cells were identified by CCK-8 assay, and cleaved-PARP level was evaluated by Western blot. This is the first study to demonstrate that genome editing techniques can be used as an effective combinatorial treatment strategy to induce apoptosis of cancer cells. In particular, enhancement of DR5 expression and inhibition of cFLIP expression by genome editing had a synergistic effect of inhibiting proliferation and inducing apoptosis in TRAIL-resistant HeLa cells. These results suggest that combinatorial treatment strategies mediated by the CRISPR/Cas9 system may be effective for design of other human TRAIL-resistant cell types. (C) 2019 Elsevier Inc. All rights reserved.This study was supported by a grant from the National Research Foundation of Korea (2017M3A9C6061361) and Medical Research Center (2017R1A5A2015395), funded by the National Research Foundation of Korea (NRF) of the Ministry of Science, ICT and Future Planning, Republic of Korea
Role of MicroRNA-34a in Anti-Apoptotic Effects of Granulocyte-Colony Stimulating Factor in Diabetic Cardiomyopathy
Background: Recent studies have shown that microRNAs (miRNAs) are involved in the process of cardiomyocyte apoptosis. We have previously reported that granulocyte-colony stimulating factor (G-CSF) ameliorated diastolic dysfunction and attenuated cardiomyocyte apoptosis in a rat model of diabetic cardiomyopathy. In this study, we hypothesized a regulatory role of cardiac miRNAs in the mechanism of the anti-apoptotic effect of G-CSF in a diabetic cardiomyopathy rat model.
Methods: Rats were given a high-fat diet and low-dose streptozotocin injection and then randomly allocated to receive treatment with either G-CSF or saline. H9c2 rat cardiomyocytes were cultured under a high glucose (HG) condition to induce diabetic cardiomyopathy in vitro. We examined the extent of apoptosis, miRNA expression, and miRNA target genes in the myocardium and H9c2 cells.
Results: G-CSF treatment significantly decreased apoptosis and reduced miR-34a expression in diabetic myocardium and H9c2 cells under the HG condition. G-CSF treatment also significantly increased B-cell lymphoma 2 (Bcl-2) protein expression as a target for miR-34a. In addition, transfection with an miR-34a mimic significantly increased apoptosis and decreased Bcl-2 luciferase activity in H9c2 cells.
Conclusion: Our results indicate that G-CSF might have an anti-apoptotic effect through down-regulation of miR-34a in a diabetic cardiomyopathy rat model.This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2015R1D1A1-A02062008 and 2016R1D1A1B03931479)
Ultrathin electronic synapse having high temporal/spatial uniformity and an Al2O3/graphene quantum dots/Al2O3 sandwich structure for neuromorphic computing
An electronic synapse (e-synapse) based on memristive switching is a promising electronic element that emulates a biological synapse to realize neuromorphic computing. However, the complex resistive switching process it relies on hampers the reproducibility of its performance. Thus, achievement of a reproducible electronic synapse with a high rate of finished products has become a significant challenge in the development of an artificial intelligent circuit. Here, we demonstrate an ultrathin e-synapse having high yield (��95%), minimal performance variation, and extremely low power consumption based on an Al2O3/graphene quantum dots/Al2O3 sandwich structure that was fabricated using atomic layer deposition. The e-synapse showed both high device-to-device and cycle-to-cycle reproducibility with high stability, endurance, and switching uniformity, because the essential synaptic behaviors could be observed. This implementation of an e-synapse with an Al2O3/graphene quantum dots/Al2O3 structure should intensify motivation for engineering e-synapses for neuromorphic computing.This work was supported by the National Key Research and Development Program of China (2016YFB0401305), the National Natural Science Foundation of China (U1605244), the Natural Science Foundation of Fujian Province (2016J01296), and the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2016R1A2A1A05005502)