• Safety and Health at Work
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• 제13권4호
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• pp.415-420
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• 2022

Background: Healthcare workers perform an emotionally exhausting daily work activity, making them prone to occupational hazards, namely psychosocial ones. This study aims to assess the impact of psychosocial risk factors on healthcare workers' mental health. Methods: A cross-sectional study was developed between May and June of 2021 with 479 healthcare workers from Portuguese hospitals. The Depression, Anxiety and Stress Scale was used to assess mental health, and psychosocial risks were assessed through the Health and Work Survey - INSAT. Statistical analysis was performed to identify the psychosocial risk factors related to anxiety, depression, and stress. Subsequently, a multiple linear regression was performed to identify the models that better explained psychosocial risk factors' relationship with anxiety, depression, and stress. Results: Data showed a strong exposure to psychosocial risks. Work pace and intensity, work relationships, and emotional demands stood out with higher global average percentages for yes answers to "exposure and discomfort." The analysis of the b values and p-values from the multiple linear regression shows that some cross-sectional psychosocial risks are predictors of anxiety and stress dimensions, and other psychosocial risks differ in the two mental health dimensions. However, it is important to highlight that healthcare workers still showed great joy and pleasure in performing their work activities. Conclusion: Support network development in the work environment is needed to prevent healthcare workers' emotional stress and promote their psychological well-being. Therefore, new research is essential to understand the psychosocial risks that affect healthcare workers and assess the less visible effects of work-health relationships.

• Journal of Ginseng Research
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• 제47권4호
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• pp.524-533
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• 2023

Background: Obesity is a risk factor for aging and many diseases, and the disorder of lipid metabolism makes it prominent. This study aims to investigate the effect of ginsenoside Rg1 on aging, lipid metabolism and stress resistance Methods: Rg1 was administered to Caenorhabditis elegans (C. elegans) cultured in NGM or GNGM. The lifespan, locomotory activity, lipid accumulation, cold and heat stress resistance and related mRNA expression of the worms were examined. Gene knockout mutants were used to clarify the effect on lipid metabolism of Rg1. GFP-binding mutants were used to observe the changes in protein expression Results: We reported that Rg1 reduced lipid accumulation and improved stress resistance in C. elegans. Rg1 significantly reduced the expression of fatty acid synthesis-related genes and lipid metabolism-related genes in C. elegans. However, Rg1 did not affect the fat storage in fat-5/fat-6 double mutant or nhr-49 mutant. Combined with network pharmacology, we clarified the possible pathways and targets of Rg1 in lipid metabolism. In addition, Rg1-treated C. elegans showed a higher expression of anti-oxidative genes and heat shock proteins, which might contribute to stress resistance Conclusion: Rg1 reduced fat accumulation by regulating lipid metabolism via nhr-49 and enhanced stress resistance by its antioxidant effect in C. elegans.

• 수완나부미
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• 제8권1호
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• pp.17-53
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• 2016

Debates continue to multiply on the definition and rationale of Southeast Asia as a region and on the utility of the multidisciplinary field of area studies. However, we have now entered a post-colonialist, post-Orientalist, post-structuralist stage of reflection and re-orientation in the era of globalization, and a strong tendency on the part of insiders to pose these issues in terms of an insider-outsider dichotomy. On the one hand, the study of Southeast Asia for researchers from outside the region has become fragmented. This is for very obvious reasons: the strengthening and re-energizing of academic disciplines, the increasing popularity of other non-regional multidisciplinary studies, and the entry of globalization studies into our field of vision. On the other hand, how has the local Southeast Asian academy addressed these major issues of change in conceptualizing the region from an insider perspective? In filling in and giving substance to an outsider, primarily Euro-American-Australian-centric definition and vision of Southeast Asia, some local academics have recently been inclined to construct Southeast Asia in terms of the Association of Southeast Asian Nations (ASEAN): a nation-state-based, institutional definition of what a region comprises. Others continue to operate at a localized level exploring small-scale communities and territories, while a modest number focus on sub-regional issues (the Malay-Indonesian world or the Mekong sub-region are examples). However, further reflections suggest that the Euro-American-Australian hegemony is a thing of the past and the ground has shifted to a much greater emphasis on academic activity within the region. Southeast Asia-based academics are also finding it much more important to network within the region and to capture, understand, and analyze what Chinese, Japanese, and Korean scholars are saying about Southeast Asia, its present circumstances and trajectories, and their increasingly close involvement with the region within a greater Asia-Pacific rim. The paper argues that the insider-outsider dichotomy requires considerable qualification. It is a neat way of dramatizing the aftermath of colonialism and Orientalism and of reasserting local priorities, agendas, and interests. But there might be a way forward in resolving at least some of these apparently opposed positions with recourse to the concepts of culture and identity in order to address Southeast Asian diversities, movements, encounters, hybridization, and hierarchies.

• IMMUNE NETWORK
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• 제23권6호
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• pp.46.1-46.16
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• 2023

Autoimmune hepatitis (AIH) affects all age group and occurs mainly in women. Pyroptosis is a novel programmed cell death featured with cell bursting and release of proinflammatory cytokines. A deeper understanding of AIH pathogenesis will contribute to novel therapy for AIH patients. Here, we aimed to investigate the role of IL-17 in immune-mediated liver injury. The levels of cytokines were measured by ELISA, and mRNA levels of STAT3 and IFN gamma-inducible protein 16 (IFI16) were detected by PCR. Expressions of STAT3, IFI16, gasdermin D and cleaved caspase-1 were measured by western-blotting. Immunohistochemical staining and transmission electron microscopy were applied to evaluate liver histopathological changes of the treated mice. Our results showed that the levels of IFI16 was increased in hepatocytes treated with IL-17 protein, and further elevated after STAT3-overexpressed (STAT3-OE) lentivirus treatment. The levels of IFI16 were reduced in hepatocytes treated with IL-17 neutralizing Ab (nAb), but were significantly increased after STAT3-OE treatment. Pyroptosis was observed in hepatocytes treated with IL-17 protein, and further cell damage was observed after STAT3-OE lentivirus treatment. Liver damage was alleviated in mice treated with IL-17 nAb, however sever damage was experienced after STAT3-OE lentivirus treatment. A binding interaction between IFI16 and STAT3 was detected in IL-17 treated hepatocytes. Glutathione transaminase activity was enhanced in concanavalin A-induced AIH mice compared to the control group (p<0.01). IL-17 plays an important role in activating STAT3 and up-regulating IFI16, which may promote the pyroptosis in AIH-related liver injury through STAT3-IFI16 axis.

• IMMUNE NETWORK
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• 제23권5호
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• pp.37.1-37.11
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• 2023

Forkhead box P3-positive (Foxp3⁺)-inducible Tregs (iTregs) are readily generated by TGF-β1 at low TCR signaling intensity. TGF-β1-mediated Foxp3 expression is further enhanced by retinoic acid (RA) and lactoferrin (LF). However, the intensity of TCR signaling required for induction of Foxp3 expression by TGF-β1 in combination with RA and LF is unknown. Here, we found that either RA or LF alone decreased TGF-β1-mediated Foxp3 expression at low TCR signaling intensity. In contrast, at high TCR signaling intensity, the addition of either RA or LF strongly increased TGF-β1-mediated Foxp3 expression. Moreover, decreased CD28 stimulation was more favorable for TGF-β1/LF-mediated Foxp3 expression. Lastly, we found that at high signaling intensities of both TCR and CD28, combined treatment with TGF-β1, RA, and LF induced robust expression of Foxp3, in parallel with powerful suppressive activity against responder T cell proliferation. Our findings that TGFβ/RA/LF strongly generate high affinity Ag-specific iTreg population would be useful for the control of unwanted hypersensitive immune reactions such as various autoimmune diseases.

• 한국의상디자인학회지
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• 제25권4호
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• pp.77-92
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• 2023

The purpose of this study is to investigate the public perception of Gorpcore through Big Aata analytics. The study was conducted based on the collection of Big Data on the word 'Gorpcore' through Textom from July 24, 2017 to March 31, 2023. As a result, 63,386 words were collected from a total of 18,879 posts, and the top 50 words were determined based on frequency of appearance. Based on the collected words, centrality measures and CONCOR algorithm were performed in Ucinet 6. The research results are as follows. 1) The frequency of appearance was high in the order of 'Gorpcore look', 'fashion', 'coordination', 'clothes', 'outdoor', 'Musinsa', 'look', 'trend', 'brand' and 'ahjussi (middle-aged old man in Korean)'. These words had high TF-IDF scores, which leads to the conclusion that these are key words that are recognized as important. 2) Network centrality shows that 'Gorpcore look', 'fashion', 'outdoor', 'coordination', 'clothes', 'trend', 'look' and 'style' have a high correlation with other words. Through this, it was found that the public thinks it is important to create a variety of fashions by styling high-performance outdoor wear and casual wear, and that they are highly interested in clothes and in brands leading the Gorpcore trend. 3) As a result of the CONCOR algorithm, four significant groups were formed. The words that appear in each group are as follows. Group 1 - 'outdoor', 'Gorp', 'Normcore', 'hiking', 'functionality', 'new', 'sports', 'casual wear', 'activity', 'generation', 'collaboration'. Group 2 - 'fashion', 'trend', 'look', 'brand', 'style', 'shoes', 'ugly', 'item', 'trend', 'product', 'Salomon', 'padded jacket', 'stylishness', 'utilization', 'Winter', 'street', 'design', 'retro', 'popular', 'styling'. Group 3 - 'Gorpcore look', 'coordination', 'Musinsa', 'windbreaker', 'recommendation', 'Arcteryx', 'pants', 'man'. Group 4 - 'clothes' 'ahjussi', 'jacket', 'launching', 'spring', 'The North Face', 'collection', 'utility', 'jumper'. As a result, it can be seen that the Gorpcore is also regarded as a part of outdoor, fashion, coordination, and casual wear.

• IMMUNE NETWORK
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• 제22권4호
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• pp.33.1-33.17
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• 2022

Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages. Treatment of THP1 monocytic cells with dexamethasone (Dex) induced ROS generation and M2 polarization promoting IL-10 and TGF-β production, while suppressing IL-1β, TNF-α and IL-6 production. SOCS3 over-expression reduced, whereas SOCS3 ablation enhanced IL-10 and TGF-β induction with concomitant regulation of ROS. As a mediator of M2 differentiation, glucocorticoid-induced leucine zipper (GILZ) was down-regulated by SOCS3 and up-regulated by shSOCS3. The induction of GILZ and IL-10 by Dex was dependent on ROS and p38 MAPK activity. Importantly, GILZ ablation led to the inhibition of ROS generation and anti-inflammatory cytokine induction by Dex. Moreover, GILZ knock-down negated the up-regulation of IL-10 production induced by shSOCS3 transduction. Our data suggest that SOCS3 targets ROS- and p38-dependent GILZ expression to suppress Dex-induced M2 polarization.

• IMMUNE NETWORK
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• 제20권5호
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• pp.38.1-38.12
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• 2020

Dendritic cells (DCs) are professional antigen-presenting cells (APCs) that initiate both T-cell responses and tolerance. Tolerogenic DCs (tDCs) are regulatory DCs that suppress immune responses through the induction of T-cell anergy and Tregs. Because lactoferrin (LF) was demonstrated to induce functional Tregs and has a protective effect against inflammatory bowel disease, we explored the tolerogenic effects of LF on mouse bone marrow-derived DCs (BMDCs). The expression of CD80/86 and MHC class II was diminished in LF-treated BMDCs (LF-BMDCs). LF facilitated BMDCs to suppress proliferation and elevate Foxp3⁺ induced Treg (iTreg) differentiation in ovalbumin-specific CD4⁺ T-cell culture. Foxp3 expression was further increased by blockade of the B7 molecule using CTLA4-Ig but was diminished by additional CD28 stimulation using anti-CD28 Ab. On the other hand, the levels of arginase-1 and indoleamine 2,3-dioxygenase-1 (known as key T-cell suppressive molecules) were increased in LF-BMDCs. Consistently, the suppressive activity of LF-BMDCs was partially restored by inhibitors of these molecules. Collectively, these results suggest that LF effectively causes DCs to be tolerogenic by both the suppression of T-cell proliferation and enhancement of iTreg differentiation. This tolerogenic effect of LF is due to the reduction of costimulatory molecules and enhancement of suppressive molecules.

• IMMUNE NETWORK
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• 제20권3호
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• pp.25.1-25.13
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• 2020

Acinetobacter baumannii is known for its multidrug antibiotic resistance. New approaches to treating drug-resistant bacterial infections are urgently required. Cathelicidin-related antimicrobial peptide (CRAMP) is a murine antimicrobial peptide that exerts diverse immune functions, including both direct bacterial cell killing and immunomodulatory effects. In this study, we sought to identify the role of CRAMP in the host immune response to multidrug-resistant Acinetobacter baumannii. Wild-type (WT) and CRAMP knockout mice were infected intranasally with the bacteria. CRAMP^-/- mice exhibited increased bacterial colony-forming units (CFUs) in bronchoalveolar lavage (BAL) fluid after A. baumannii infection compared to WT mice. The loss of CRAMP expression resulted in a significant decrease in the recruitment of immune cells, primarily neutrophils. The levels of IL-6 and CXCL1 were lower, whereas the levels of IL-10 were significantly higher in the BAL fluid of CRAMP^-/- mice compared to WT mice 1 day after infection. In an in vitro assay using thioglycollate-induced peritoneal neutrophils, the ability of bacterial phagocytosis and killing was impaired in CRAMP^-/- neutrophils compared to the WT cells. CRAMP was also essential for the production of cytokines and chemokines in response to A. baumannii in neutrophils. In addition, the A. baumannii-induced inhibitor of κB-α degradation and phosphorylation of p38 MAPK were impaired in CRAMP^-/- neutrophils, whereas ERK and JNK phosphorylation was upregulated. Our results indicate that CRAMP plays an important role in the host defense against pulmonary infection with A. baumannii by promoting the antibacterial activity of neutrophils and regulating the innate immune responses.

• IMMUNE NETWORK
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• 제20권3호
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• pp.26.1-26.9
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• 2020

Cereblon (CRBN), a negative modulator of AMP-activated protein kinase (AMPK), is highly expressed in the retina. We confirmed the expression of CRBN in ARPE-19 human retinal cells by Western blotting. We also demonstrated that CRBN knock-down (KD) could effectively downregulate IL-6 and MCP-1 protein and gene expression in LPS-stimulated ARPE-19 cells. Additionally, CRBN KD increased the phosphorylation of AMPK/acetylcoenzyme A carboxylase (ACC) and the expression of heme oxygenase-1 (HO-1) in ARPE-19 cells. Furthermore, CRBN KD significantly reduced LPS-induced nuclear translocation of NF-κB p65 and activation of NF-κB promoter activity. However, these processes could be inactivated by compound C (inhibitor of AMPK) and zinc protoporphyrin-1 (ZnPP-1; inhibitor of HO-1). In conclusion, compound C and ZnPP-1 can rescue LPS-induced levels of proinflammatory cytokines (IL-6 and MCP-1) in CRBN KD ARPE-19 cells. Our data demonstrate that CRBN deficiency negatively regulates proinflammatory cytokines via the activation of AMPK/HO-1 in the retina.