The Influence Of Job Insecurity On Career Commitment And Attitude In Multinational Corporations

As the perception of lifelong work shifts into lifelong career in the job insecurity market, the career development of employees through professional and competitive career management has become more important than being loyal to a lifelong work. Furthermore, in the case of multinational corporations, such as differentiation from the head office policy, cultural differences in labor relations, and the liquidity of business withdrawal, such a feature has a higher possibility of job insecurity than general companies. Therefore, the purpose of this study is to verify empirically how job insecurity influences career commitment and career attitude through individual, job and career characteristics as intermediation with the members of multinational corporations as objectives. For this purpose, a total of 366 questionnaire data that targeted 27 multinational corporations were collected and analyzed. The result shows that the job insecurity of multinational corporations affects individual characteristic rather than job or career characteristic, and it is confirmed that individual characteristic has an effect on career commitment and career attitude. In the end, multinational corporations, unlike ordinary domestic companies, need active organizational career development program that corresponds to an open corporate culture as well as innovative and open systems and policies that balance both internal and external networking activities in terms of human resource management of corporations

Association between the Risk of Obstructive Sleep Apnea and Lung Function: Korea National Health and Nutrition Examination Survey

Background Obstructive sleep apnea (OSA) is a prevalent sleep disorder associated with various health issues. Although some studies have suggested an association between reduced lung function and OSA, this association remains unclear. Our study aimed to explore this relationship using data from a nationally representative population- based survey. Methods We performed an analysis of data from the 2019 Korea National Health and Nutrition Examination Survey. Our study encompassed 3,675 participants aged 40 years and older. Risk of OSA was assessed using the STOP-Bang (Snoring, Tiredness during daytime, Observed apnea, and high blood Pressure-Body mass index, Age, Neck circumference, Gender) questionnaire and lung function tests were performed using a portable spirometer. Logistic regression analysis was applied to identify the risk factors associated with a high-risk of OSA, defined as a STOP-Bang score of ≥3. Results Of 3,675 participants, 600 (16.3%) were classified into high-risk OSA group. Participants in the high-risk OSA group were older, had a higher body mass index, and a higher proportion of males and ever-smokers. They also reported lower lung function and quality of life index in various domains along with increased respiratory symptoms. Univariate logistic regression analysis indicated a significant association between impaired lung function and a high-risk of OSA. However, in the multivariable analysis, only chronic cough (odds ratio [OR], 2.413; 95% confidence interval [CI], 1.383 to 4.213) and sputum production (OR, 1.868; 95% CI, 1.166 to 2.992) remained significantly associated with a high OSA risk. Conclusion Our study suggested that, rather than baseline lung function, chronic cough, and sputum production are more significantly associated with OSA risk

Modular evolution of glutathione peroxidase genes in association with different biochemical properties of their encoded proteins in invertebrate animals

<p>Abstract</p> <p>Background</p> <p>Phospholipid hydroperoxide glutathione peroxidases (PHGPx), the most abundant isoforms of GPx families, interfere directly with hydroperoxidation of lipids. Biochemical properties of these proteins vary along with their donor organisms, which has complicated the phylogenetic classification of diverse PHGPx-like proteins. Despite efforts for comprehensive analyses, the evolutionary aspects of GPx genes in invertebrates remain largely unknown.</p> <p>Results</p> <p>We isolated GPx homologs via <it>in silico </it>screening of genomic and/or expressed sequence tag databases of eukaryotic organisms including protostomian species. Genes showing strong similarity to the mammalian PHGPx genes were commonly found in all genomes examined. GPx3- and GPx7-like genes were additionally detected from nematodes and platyhelminths, respectively. The overall distribution of the PHGPx-like proteins with different biochemical properties was biased across taxa; selenium- and glutathione (GSH)-dependent proteins were exclusively detected in platyhelminth and deuterostomian species, whereas selenium-independent and thioredoxin (Trx)-dependent enzymes were isolated in the other taxa. In comparison of genomic organization, the GSH-dependent PHGPx genes showed a conserved architectural pattern, while their Trx-dependent counterparts displayed complex exon-intron structures. A codon for the resolving Cys engaged in reductant binding was found to be substituted in a series of genes. Selection pressure to maintain the selenocysteine codon in GSH-dependent genes also appeared to be relaxed during their evolution. With the dichotomized fashion in genomic organizations, a highly polytomic topology of their phylogenetic trees implied that the GPx genes have multiple evolutionary intermediate forms.</p> <p>Conclusion</p> <p>Comparative analysis of invertebrate GPx genes provides informative evidence to support the modular pathways of GPx evolution, which have been accompanied with sporadic expansion/deletion and exon-intron remodeling. The differentiated enzymatic properties might be acquired by the evolutionary relaxation of selection pressure and/or biochemical adaptation to the acting environments. Our present study would be beneficial to get detailed insights into the complex GPx evolution, and to understand the molecular basis of the specialized physiological implications of this antioxidant system in their respective donor organisms.</p

A STUDY ON THE ESTIMATION METHOD OF THE FORM FACTOR FOR A FULL-SCALE SHIP

In this study, a prediction method of the form factor for a full-scale ship is suggested to minimize the power prediction error from a small model ship. Numerical simulations were carried out at various Reynolds numbers from a small model to a full-scale ship. The variation of the form factors was investigated from the results of the numerical simulation according to the Reynolds numbers. In addition, the results from the numerical simulations and experimental data of the geosim models were utilized to drive the correlation line and predict the form factor of a full-scale ship. The correlation line was applied to predict the effective power and the delivered power of a full-scale ship. As a result, the developed prediction method confirmed the possibility of predicting the power reliably from experiments using a small model

Unleashing the full potential of Hsp90 inhibitors as cancer therapeutics through simultaneous inactivation of Hsp90, Grp94, and TRAP1

Cancer therapeutics: Extending a drug&apos;s reach A new drug that blocks heat shock proteins (HSPs), helper proteins that are co-opted by cancer cells to promote tumor growth, shows promise for cancer treatment. Several drugs have targeted HSPs, since cancer cells are known to hijack these helper proteins to shield themselves from destruction by the body. However, the drugs have had limited success. Hye-Kyung Park and Byoung Heon Kang at Ulsan National Institutes of Science and Technology in South Korea and coworkers noticed that the drugs were not absorbed into mitochondria, a key cellular compartment, and HSPs in this compartment were therefore not being blocked. They identified a new HSP inhibitor that can reach every cellular compartment and inhibit all HSPs. Testing in mice showed that this inhibitor effectively triggered death of tumor cells, and therefore shows promise for anti-cancer therapy. The Hsp90 family proteins Hsp90, Grp94, and TRAP1 are present in the cell cytoplasm, endoplasmic reticulum, and mitochondria, respectively; all play important roles in tumorigenesis by regulating protein homeostasis in response to stress. Thus, simultaneous inhibition of all Hsp90 paralogs is a reasonable strategy for cancer therapy. However, since the existing pan-Hsp90 inhibitor does not accumulate in mitochondria, the potential anticancer activity of pan-Hsp90 inhibition has not yet been fully examined in vivo. Analysis of The Cancer Genome Atlas database revealed that all Hsp90 paralogs were upregulated in prostate cancer. Inactivation of all Hsp90 paralogs induced mitochondrial dysfunction, increased cytosolic calcium, and activated calcineurin. Active calcineurin blocked prosurvival heat shock responses upon Hsp90 inhibition by preventing nuclear translocation of HSF1. The purine scaffold derivative DN401 inhibited all Hsp90 paralogs simultaneously and showed stronger anticancer activity than other Hsp90 inhibitors. Pan-Hsp90 inhibition increased cytotoxicity and suppressed mechanisms that protect cancer cells, suggesting that it is a feasible strategy for the development of potent anticancer drugs. The mitochondria-permeable drug DN401 is a newly identified in vivo pan-Hsp90 inhibitor with potent anticancer activity

Measurement of epigenetic alterations from patient’s tissues in myoma, adenomyoma and endometriosis

Background: Myoma, adenomyoma, and endometriosis are estrogen-dependent gynecologic diseases and result in reproductive dysfunction and pelvic pain in women. However, these gynecologic diseases have a complex and poorly understood etiology, involving both genetic and environmental factors. Epigenetic alterations, heritable changes that can modify gene expression without affecting genetic sequence, are associated with the development and progression of numerous pathological states and diseases. Therefore, there is great potential for the use of epigenetics as biomarkers to better understand the early-stage biological responses and molecular mechanisms of gynecologic diesases. We aimed to examine levels of global DNA and gene-specific methylation, which are epigenetic alterations that could be associated with development of gynecologic diseases, including myoma, adenomyoma, and endometriosis. Methods: We measured global DNA methylation (LINE-1) as well as disease relevant gene-specific methylation (i.e. ER, PR, and aromatase) using pyrosequencing assay. For this measurement, gene-specific primers for the selected genes were designed using the Pyro-Mark assay design software. Genomic DNAs from each tissue were extracted, and underwent bisulfite modification to convert unmethylated cytosine residues to uracil. A Pyromark Q96 MD was used for all subsequent pyrosequencing. Samples were processed in duplicates on plates with water controls. Percent methylation of a sample was calculated by averaging all of the interrogated CpG sites. Results: Different methylation levels of selected genes were measured from myoma, adenomyoma, and endometriosis tissues. Our obtained results suggest that epigenetic changes are involved in development of different types of gynecologic diseases

Role of Neuronal NADPH Oxidase 1 in the Peri-Infarct Regions after Stroke

The molecular mechanism underlying the selective vulnerability of neurons to oxidative damage caused by ischemia-reperfusion (I/R) injury remains unknown. We sought to determine the role of NADPH oxidase 1 (Nox1) in cerebral I/R-induced brain injury and survival of newborn cells in the ischemic injured region. Male Wistar rats were subjected to 90 min middle cerebral artery occlusion (MCAO) followed by reperfusion. After reperfusion, infarction size, level of superoxide and 8-hydroxy-20-deoxyguanosine (8-oxo-2dG), and Nox1 immunoreactivity were determined. RNAi-mediated knockdown of Nox1 was used to investigate the role of Nox1 in I/R-induced oxidative damage, neuronal death, motor function recovery, and ischemic neurogenesis. After I/R, Nox1 expression and 8-oxo-2dG immunoreactivity was increased in cortical neurons of the peri-infarct regions. Both infarction size and neuronal death in I/R injury were significantly reduced by adeno-associated virus (AAV)-mediated transduction of Nox1 short hairpin RNA (shRNA). AAV-mediated Nox1 knockdown enhanced functional recovery after MCAO. The level of survival and differentiation of newborn cells in the peri-infarct regions were increased by Nox1 inhibition. Our data suggest that Nox-1 may be responsible for oxidative damage to DNA, subsequent cortical neuronal degeneration, functional recovery, and regulation of ischemic neurogenesis in the peri-infarct regions after stroke