41 research outputs found

    How Can Companies Harness a Learning Organization to Lead the Collaborative Culture?

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    Employees in multinational companies tend to become departmentalized by business processes, and are increasingly losing touch with their organizationsā€™ goals and strategies. Learning Organization is a concept that focuses on the interconnectedness among employees in the same organizations by collaborating interdepartmentally and maintaining knowledge on new strategies, products, services, industries, and their macro-environment in order to give their organizations the competitive advantages over competitors. Our research investigated the best practices and made conclusions on how to implement the mentioned cross-functional concept

    Nepmucin, a novel HEV sialomucin, mediates L-selectinā€“dependent lymphocyte rolling and promotes lymphocyte adhesion under flow

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    Lymphocyte trafficking to lymph nodes (LNs) is initiated by the interaction between lymphocyte L-selectin and certain sialomucins, collectively termed peripheral node addressin (PNAd), carrying specific carbohydrates expressed by LN high endothelial venules (HEVs). Here, we identified a novel HEV-associated sialomucin, nepmucin (mucin not expressed in Peyer's patches [PPs]), that is expressed in LN HEVs but not detectable in PP HEVs at the protein level. Unlike conventional sialomucins, nepmucin contains a single V-type immunoglobulin (Ig) domain and a mucin-like domain. Using materials affinity-purified from LN lysates with soluble L-selectin, we found that two higher molecular weight species of nepmucin (75 and 95 kD) were decorated with oligosaccharides that bind L-selectin as well as an HEV-specific MECA-79 monoclonal antibody. Electron microscopic analysis showed that nepmucin accumulates in the extended luminal microvillus processes of LN HEVs. Upon appropriate glycosylation, nepmucin supported lymphocyte rolling via its mucin-like domain under physiological flow conditions. Furthermore, unlike most other sialomucins, nepmucin bound lymphocytes via its Ig domain, apparently independently of lymphocyte functionā€“associated antigen 1 and very late antigen 4, and promoted shear-resistant lymphocyte binding in combination with intercellular adhesion molecule 1. Collectively, these results suggest that nepmucin may serve as a dual-functioning PNAd in LN HEVs, mediating both lymphocyte rolling and binding via different functional domains

    Donepezil Regulates LPS and AĪ²-Stimulated Neuroinflammation through MAPK/NLRP3 Inflammasome/STAT3 Signaling

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    The acetylcholinesterase inhibitors donepezil and rivastigmine have been used as therapeutic drugs for Alzheimerā€™s disease (AD), but their effects on LPS-and AĪ²-induced neuroinflam-matory responses and the underlying molecular pathways have not been studied in detail in vitro and in vivo. In the present study, we found that 10 or 50 Ī¼M donepezil significantly decreased the LPS-induced increases in the mRNA levels of a number of proinflammatory cytokines in BV2 mi-croglial cells, whereas 50 Ī¼M rivastigmine significantly diminished only LPS-stimulated IL-6 mRNA levels. In subsequent experiments in primary astrocytes, donepezil suppressed only LPS-stimulated iNOS mRNA levels. To identify the molecular mechanisms by which donepezil regulates LPS-induced neuroinflammation, we examined whether donepezil alters LPS-stimulated proin-flammatory responses by modulating LPS-induced downstream signaling and the NLRP3 inflam-masome. Importantly, we found that donepezil suppressed LPS-induced AKT/MAPK signaling, the NLRP3 inflammasome, and transcription factor NF-kB/STAT3 phosphorylation to reduce neuroin-flammatory responses. In LPS-treated wild-type mice, a model of neuroinflammatory disease, donepezil significantly attenuated LPS-induced microglial activation, microglial density/morphol-ogy, and proinflammatory cytokine COX-2 and IL-6 levels. In a mouse model of AD (5xFAD mice), donepezil significantly reduced AĪ²-induced microglial and astrocytic activation, density, and mor-phology. Taken together, our findings indicate that donepezil significantly downregulates LPS-and AĪ²-evoked neuroinflammatory responses in vitro and in vivo and may be a therapeutic agent for neuroinflammation-associated diseases such as AD. Ā© 2021 by the authors. Licensee MDPI, Basel, Switzerland.1

    Assessing the Effects of Higher-Education Factors on the Job Satisfaction of Engineering Graduates in Korea

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    This paper investigates the relationship between the influential factors related to higher education and job satisfaction of engineering graduates in Korea. The education factors considered in this study can be categorized into three groups: those related to personal information, satisfaction with higher-education quality, and participation in career development programs. The Graduates Occupational Mobility Survey data collected in 2016 and provided by the Korea Employment Information Service were used to evaluate the job satisfaction of Korean engineering graduates, which was in turn analyzed using the hierarchical multiple regression approach. The verification of the statistical analysis results indicates the importance of school location and high satisfaction with overall school quality in determining the job satisfaction of engineering graduates in Korea. It also reveals that internship is more efficient in enhancing job satisfaction than relatively short-term programs such as interviews, resume coaching, and job camps

    Alleviation of Irritable Bowel Syndrome-Like Symptoms and Control of Gut and Brain Responses with Oral Administration of Dolichos lablab L. in a Mouse Model

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    Irritable bowel syndrome (IBS) is a common gastrointestinal disorder manifesting as unexplained abdominal pain and bowel habit changes. The pathogenesis of post-infectious IBS is associated with gut–brain axis dysfunction, including low-grade colonic inflammation and anxiety-related long-term brain changes. This study analyzed the efficacy of a standardized extract of Dolichos lablab L. extract (DL), a bean species, in an IBS mouse model resembling post-infectious, diarrhea-dominant IBS. Using a zymosan-induced animal IBS model, we found that oral administration of DL significantly attenuated zymosan-induced increases in colonic macroscopic scores and minimized weight loss without affecting food intake. In the DL-treated mice, the mast cell count and tumor necrosis factor-α level in the colon markedly decreased, similar to results in sulfasalazine-treated mice and in mice with lipopolysaccharide-stimulated bone marrow-derived mast cells. The number of visceral pain-related behaviors was much lower in the DL-treated mice. Anxiety-like behaviors significantly improved, comparable to that after treatment with amitriptyline. The c-Fos expression level in the prefrontal cortex was significantly reduced. Our data suggest that DL could be beneficial for treating IBS by acting on the gut and brain

    Single Trace Side Channel Analysis on NTRU Implementation

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    As researches on the quantum computer have progressed immensely, interests in post-quantum cryptography have greatly increased. NTRU is one of the well-known algorithms due to its practical key sizes and fast performance along with the resistance against the quantum adversary. Although NTRU has withstood various algebraic attacks, its side-channel resistance must also be considered for secure implementation. In this paper, we proposed the first single trace attack on NTRU. Previous side-channel attacks on NTRU used numerous power traces, which increase the attack complexity and limit the target algorithm. There are two versions of NTRU implementation published in succession. We demonstrated our attack on both implementations using a single power consumption trace obtained in the decryption phase. Furthermore, we propose a countermeasure to prevent the proposed attacks. Our countermeasure does not degrade in terms of performance

    Bone metastasis and skeletal-related events in patients with solid cancer: A Korean nationwide health insurance database study.

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    Bone is one of the most common sites of metastasis from advanced solid tumors. Bone metastasis is a leading cause of pain and increases the risk of skeletal-related events (SREs) in cancer patients. In addition to affecting the quality of life, it also increases the medical costs and mortality risk. We aimed to examine the occurrence of bone metastasis and SREs in Korean cancer patients using a nationwide health database. Using claims data from the National Health Insurance Service-National Sample Cohort (2002-2013), we extracted the data of bone metastasis patients diagnosed with any of the seven major cancers in Korea from January 2002 to December 2010. Selected SREs included pathologic fracture, spinal cord compression, radiation therapy, and palliative bone surgery. We used time-to-event analysis to estimate patient survival after bone metastasis. A total of 21,562 newly diagnosed cancer patients were identified; bone metastases developed in 1,849 patients (breast cancer, 18.8%; prostate cancer, 17.5%; lung cancer, 13.7%). The median time from primary cancer diagnosis to bone metastasis was 18.9 months. The cumulative incidence of SREs was 45.1% in all bone metastasis patients. The most common cancer type was lung cancer (53.4%), followed by liver (50.9%), prostate (45.9%), breast (43.6%), and colorectal (40.2%) cancers. Almost all SREs developed 1 month after bone metastasis, except in patients with breast and prostate cancers (median: 5.9 months in breast cancer and 4.7 months in prostate cancer). Survival duration after the development of bone metastasis was 1 year after the occurrence of SREs. This study reveals the epidemiology of bone metastasis and SREs in Korean cancer patients, and the findings can be used to assess the actual bone health status of cancer patients

    Thymosin Beta-4 Suppresses Osteoclastic Differentiation and Inflammatory Responses in Human Periodontal Ligament Cells.

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    Recent reports suggest that thymosin beta-4 (TĪ²4) is a key regulator for wound healing and anti-inflammation. However, the role of TĪ²4 in osteoclast differentiation remains unclear.The purpose of this study was to evaluate TĪ²4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of TĪ²4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.Reverse transcription-polymerase chain reactions and Western blot analyses were used to measure mRNA and protein levels, respectively. Osteoclastic differentiation was assessed in mouse bone marrow-derived macrophages (BMMs) using conditioned medium (CM) from H2O2-treated PDLCs.TĪ²4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. TĪ²4 activation with a TĪ²4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-Ī±, IL-1Ī², IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. TĪ²4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-ĪŗB in PDLCs. Furthermore, TĪ²4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-ĪŗB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of TĪ²4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.In conclusion, this study demonstrated, for the first time, that TĪ²4 was down-regulated in ROS-stimulated PDLCs as well as TĪ²4 activation exhibited anti-inflammatory effects and anti-osteoclastogenesis in vitro. Thus, TĪ²4 activation might be a therapeutic target for inflammatory osteolytic disease, such as periodontitis

    Dynamic changes in endothelial cell adhesion molecule nepmucin/CD300LG expression under physiological and pathological conditions.

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    Vascular endothelial cells often change their phenotype to adapt to their local microenvironment. Here we report that the vascular endothelial adhesion molecule nepmucin/CD300LG, which is implicated in lymphocyte binding and transmigration, shows unique expression patterns in the microvascular endothelial cells of different tissues. Under physiological conditions, nepmucin/CD300LG was constitutively and selectively expressed at the luminal surface of the small arterioles, venules, and capillaries of most tissues, but it was only weakly expressed in the microvessels of the splenic red pulp and thymic medulla. Furthermore, it was barely detectable in immunologically privileged sites such as the brain, testis, and uterus. The nepmucin/CD300LG expression rapidly decreased in lymph nodes receiving acute inflammatory signals, and this loss was mediated at least in part by TNF-Ī±. It was also down-regulated in tumors and tumor-draining lymph nodes, indicating that nepmucin/CD300LG expression is negatively regulated by locally produced signals under these circumstances. In contrast, nepmucin/CD300LG was induced in the high endothelial venule-like blood vessels of chronically inflamed pancreatic islets in an animal model of non-obese diabetes. Interestingly, the activated CD4(+) T cells infiltrating the inflamed pancreas expressed high levels of the nepmucin/CD300LG ligand(s), supporting the idea that nepmucin/CD300LG and its ligand interactions are locally involved in pathological T cell trafficking. Taken together, these observations indicate that the nepmucin/CD300LG expression in microvascular endothelial cells is influenced by factor(s) that are locally produced in tissues, and that its expression is closely correlated with the level of leukocyte infiltration in certain tissues

    Anti-Inflammatory Activity and Mechanism of Isookanin, Isolated by Bioassay-Guided Fractionation from <i>Bidens pilosa</i> L.

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    Bidens pilosa L. (Asteraceae) has been used historically in traditional Asian medicine and is known to have a variety of biological effects. However, the specific active compounds responsible for the individual pharmacological effects of Bidens pilosa L. (B. pilosa) extract have not yet been made clear. This study aimed to investigate the anti-inflammatory phytochemicals obtained from B. pilosa. We isolated a flavonoids-type phytochemical, isookanin, from B. pilosa through bioassay-guided fractionation based on its capacity to inhibit inflammation. Some of isookaninā€™s biological properties have been reported; however, the anti-inflammatory mechanism of isookanin has not yet been studied. In the present study, we evaluated the anti-inflammatory activities of isookanin using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We have shown that isookanin reduces the production of proinflammatory mediators (nitric oxide, prostaglandin E2) by inhibiting the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated macrophages. Isookanin also inhibited the expression of activator protein 1 (AP-1) and downregulated the LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-jun NH2-terminal kinase (JNK) in the MAPK signaling pathway. Additionally, isookanin inhibited proinflammatory cytokines (tumor necrosis factor-a (TNF-Ī±), interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-1Ī² (IL-1Ī²)) in LPS-induced THP-1 cells. These results demonstrate that isookanin could be a potential therapeutic candidate for inflammatory disease
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