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Purpose: The purpose of this study is to identify latent classes of work values that influence the career choices of Korean workers through a person-centred approach. Because work values may be diverse in individuals, investigating the various combinations of those values will help understand individual's decisions to take, maintain and leave a job. Design/methodology/approach: The authors used a total of 15,103 datasets collected at the national level in South Korea. Data were analyzed by using latent class analysis (LCA); a three-step approach was employed to address classification. Findings: As the results of this study, Class 3, "seeking balanced work values rather than income," presented the highest level of job satisfaction, whereas Class 1, "seeking job security and income," exhibited the lowest. Originality/value: Employing an assessment tool to identify the distinct combinations of work values that individuals possess and then providing them with appropriate training and development programs and customized Human Resource (HR) policies aligned with the classes will be essential tasks for HRD (Human Resource Development)/HRM (Human Resource Management) practitioners.

Purpose: The purpose of this study is to develop a reliable and valid measurement of employee learning agility for use in human resources development. Design/methodology/approach: This paper analyzed a total of 365 cases collected from Korean organizations. This paper conducted exploratory factor analysis, confirmatory factor analysis and Rasch analysis to validate the measurement. This paper conducted a measurement invariance (MI) test to confirm the generalizability of the measurement and used Harman's single factor test to assess the common method variance (CMV). Findings: This paper derived a learning agility measurement with six subfactors (Cronbach's [alpha] = 0.893). This paper verified that it could be applied equally to supervisors and subordinates using an MI test. Factor analysis confirmed the feasibility of CMV. Based on I-ADAPT theory, the learning agility measurement can be applied to assess not only leader competency but also general employee competency. Research limitations/implications: Practitioners may use this model of learning agility for developing competency-based training programs and evaluations. This study is meaningful because it extends the concept of learning agility. In particular, the MI test indicated that there are no differences between supervisors and employees regarding the utility of the concept. Originality/value: This study is meaningful because it extends the concept of learning agility. In particular, the MI test indicated that there are no differences between supervisors and employees regarding the utility of the concept. The concept in this paper is distinguished from other studies by applying the Rasch model from an item response theory perspective.

Background: Psoriasis is an inflammatory skin disease characterized by the hyperproliferative epidermal keratinocytes and significant immune cells infiltration, leading to cytokines production such as IL-1β, TNF-α, IL-23, and IL-17. Recent study highlights the critical role of IL-1β in the induction and activation of pathogenic Th17 and IL-17-producing γδ T cells, contributing to psoriasis. However, the mechanism underlying IL-1β dysregulation in psoriasis pathogenesis is unclear. Autophagy regulates IL-1β production and has a pleiotropic effect on inflammatory disorders. Previous studies showed controversial role of autophagy in psoriasis pathogenesis, either pro-inflammatory in autophagy-deficient keratinocyte or anti-inflammatory in pharmacologically autophagy-promoting macrophages. Thus, the direct role of autophagy and its therapeutic potential in psoriasis remains unclear. Methods: We used myeloid cell-specific autophagy-related gene 7 (Atg7)-deficient mice and determined the effect of autophagy deficiency in myeloid cells on neutrophilia and disease pathogenesis in an imiquimod-induced psoriasis mouse model. We then assessed the pathogenic mechanism focusing on immune cells producing IL-1β and IL-17 along with gene expression profiles associated with psoriasis in mouse model and public database on patients. Moreover, therapeutic potential of IL-1β blocking in such context was assessed. Results: We found that autophagy deficiency in myeloid cells exacerbated neutrophilic inflammation and disease pathogenesis in mice with psoriasis. This autophagy-dependent effect was associated with a significant increase in IL-1β production from myeloid cells, particularly macrophages, Cxcl2 expression, and IL-17 A producing T cells including γδ T cells. Supporting this, treatment with systemic IL-1 receptor blocking antibody or topical saccharin, a disaccharide suppressing pro-IL-1β expression, led to the alleviation of neutrophilia and psoriatic skin inflammation linked to autophagy deficiency. The pathophysiological relevance of this finding was supported by dysregulation of autophagy-related genes and their correlation with Th17 cytokines in psoriatic skin lesion from patients with psoriasis. Conclusions: Our results suggest that autophagy dysfunction in myeloid cells, especially macrophages, along with IL-1β dysregulation has a causal role in neutrophilic inflammation and psoriasis pathogenesis. [ABSTRACT FROM AUTHOR]

A remote color converter with a phosphor in silicone (PiS) structure was fabricated using CsPbBr3 perovskite nanocrystal embedded glass (PNEG) as a green phosphor. When the PNEG was pasted on a glass substrate and mounted on a blue LED, it showed enhanced thermal and photo stability compared with the bulk PNEG. The remote color converter was used to prepare a white LED, which had a wide color gamut of up to 130% of the National Television Standards Committee (NTSC) defined area with the addition of K2SiF6:Mn4+ (KSF:Mn4+) as a red phosphor. The feasibility of a flexible remote white color converter using ultra-thin glass (UTG) as a substrate was examined and discussed. [ABSTRACT FROM AUTHOR]

Drawing on various studies, we provide a holistic view incorporating different nested cultural contexts, organizational shame, and health outcomes. We introduce the concept of organizational shame and explain its two key domains: conformity and status/competition. Then, we comprehensively review prior studies on cultural approaches to shame and propose our cultural variance model of organizational shame. Our model illustrates an equilibrium, exhibiting dominant and stable patterns of shame domains formed by reinforcing relationships among three key nested contextual layers: individuals (workers), organizations (firms), and the labor market. We apply our model to discuss general and occupational implications and outline future research directions. Thus, we hope to conceptualize organizational shame within the dynamic contexts of organizations and cultures. [ABSTRACT FROM AUTHOR]

Drawing on various studies, we provide a holistic view incorporating different nested cultural contexts, organizational shame, and health outcomes. We introduce the concept of organizational shame and explain its two key domains: conformity and status/competition. Then, we comprehensively review prior studies on cultural approaches to shame and propose our cultural variance model of organizational shame. Our model illustrates an equilibrium, exhibiting dominant and stable patterns of shame domains formed by reinforcing relationships among three key nested contextual layers: individuals (workers), organizations (firms), and the labor market. We apply our model to discuss general and occupational implications and outline future research directions. Thus, we hope to conceptualize organizational shame within the dynamic contexts of organizations and cultures. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial dysfunction in the thyroid due to defective mitophagy has been observed in lymphocytic thyroiditis (LT). However, the effect of impaired mitophagy on the pathogenesis of LT is not well understood. The aim of this study is to investigate the role of mitophagy dysregulation in the thyroid gland. Methods: We analyzed RNA sequencing data of human thyroid glands with/without LT from Genotype-Tissue Expression (GTEx; n = 653) and performed RNA sequencing in thyroid glands of phosphatase and tensin homolog-induced putative protein kinase 1 ( Pink1 ) knock-out and wild-type mice. We evaluated the phenotypic and histopathologic characteristics of the human ( n = 16) and mouse thyroids. Additionally, we assessed cell proliferation, reactive oxygen species (ROS) production, and cytokine secretion of human thyroid epithelial cells (HTori-3) treated with PINK1 siRNA or a mitophagy inhibitor. Results: We found that expression of PINK1 , a key regulator of mitophagy, was compromised in human thyroids with LT. Thyroid glands of Pink1 -deficient mice exhibited increased inflammatory responses and nodular hyperplasia. Furthermore, mitophagy defects led to the production of pro-inflammatory cytokines and ROS in thyroid cells, resulting in immune cell recruitment. Notably, these mitophagy defects upregulated both the RNA expression and protein secretion of amphiregulin (AREG), an epidermal growth factor receptor (EGFR) ligand, in thyroid cells, while decreasing the protein expression of cAMP response element-binding protein (CREB), a transcription factor that suppresses AREG transcription. Finally, we demonstrated that aberrant cell proliferation in thyroid cells, driven by mitophagy defects, was mitigated after treatment with cetuximab, an EGFR inhibitor. Conclusions: In this study, we observed that mitophagy defects in the thyroid not only intensify inflammation through the accumulation of ROS, cytokine production, and immune cell recruitment but also contribute to hyperplasia via the EGFR pathway, facilitated by increased secretion of AREG from thyroid cells.