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Although the physiological function of receptor‐interacting protein kinase (RIPK) 3 has emerged as a critical mediator of programmed necrosis/necroptosis, the intracellular role it plays as an attenuator in human lungs and human bronchial epithelia remains unclear. Here, we show that the expression of RIPK3 dramatically decreased in the inflamed tissues of human lungs, and moved from the nucleus to the cytoplasm. The overexpression of RIPK3 dramatically increased F‐actin formation and decreased the expression of genes for pro‐inflammatory cytokines (IL‐6 and IL‐1β), but not siRNA‐RIPK3. Interestingly, whereas RIPK3 was bound to histone 1b without LPS stimulation, the interaction between them was disrupted after 15 min of LPS treatment. Histone methylation could not maintain the binding of RIPK3 and activated movement towards the cytoplasm. In the cytoplasm, overexpressed RIPK3 continuously attenuated pro‐inflammatory cytokine gene expression by inhibiting NF‐κB activation, preventing the progression of inflammation during Pseudomonas aeruginosa infection. Our data indicated that RIPK3 is critical for the regulation of the LPS‐induced inflammatory microenvironment. Therefore, we suggest that RIPK3 is a potential therapeutic candidate for bacterial infection‐induced pulmonary inflammation. [ABSTRACT FROM AUTHOR]

This paper explores the patterns of knowledge production of science and engineering from catching-up via overtaking to the achievement of leadership in global industries. In particular, it examines the depth and direction of knowledge production with proxy variables of patents and bibliometric data of a latecomer firm. Moreover, it explores the changing patterns of knowledge sourcing in the firm during the transition from catch-up to forging ahead and with specific references to the experience of Samsung Electronics Company. This study shows that the patterns of scientific and engineering activities increased as the firm proceeds to the forging ahead period, the patterns of knowledge sourcing evolved in the direction of increasing importance of the domestic knowledge base, and the collaborative partners for generating knowledge changed as the firm's capabilities were enhanced to approach cutting-edge technologies. This paper illuminates the importance of intraorganizational capabilities and domestic knowledge bases to advance a latecomer firm's knowledge generating capabilities into a stage of forging ahead. [ABSTRACT FROM AUTHOR]

This paper explores the industrial specialisation of latecomer countries, particularly Korea and Taiwan, which are often referred to as successful catch-up cases. The traditional wisdom is that the ‘developmental state’, resource leverage, and technological sophistication in an export-oriented strategy have been the factors for success. However, firm strategies and a supportive government are not sufficient to explain the different features of catch-up patterns. In this paper we propose that differences in industrial specialisation of catch-up countries are attributable to the interaction between technological characteristics and institutional settings, including corporate organisation, industrial structure, and the role of the public sector. [ABSTRACT FROM PUBLISHER]

Although the physiological function of receptor-interacting protein kinase (RIPK) 3 has emerged as a critical mediator of programmed necrosis/necroptosis, the intracellular role it plays as an attenuator in human lungs and human bronchial epithelia remains unclear. Here, we show that the expression of RIPK3 dramatically decreased in the inflamed tissues of human lungs, and moved from the nucleus to the cytoplasm. The overexpression of RIPK3 dramatically increased F-actin formation and decreased the expression of genes for pro-inflammatory cytokines (IL-6 and IL-1β), but not siRNA-RIPK3. Interestingly, whereas RIPK3 was bound to histone 1b without LPS stimulation, the interaction between them was disrupted after 15 min of LPS treatment. Histone methylation could not maintain the binding of RIPK3 and activated movement towards the cytoplasm. In the cytoplasm, overexpressed RIPK3 continuously attenuated pro-inflammatory cytokine gene expression by inhibiting NF-κB activation, preventing the progression of inflammation during Pseudomonas aeruginosa infection. Our data indicated that RIPK3 is critical for the regulation of the LPS-induced inflammatory microenvironment. Therefore, we suggest that RIPK3 is a potential therapeutic candidate for bacterial infection-induced pulmonary inflammation., (© 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Background and Purpose: The objective of this study was to determine the benefits of cognitive training in patients with amnestic mild cognitive impairment (aMCI) and those with early Alzheimer's disease (AD)., Methods: Eleven patients with aMCI and nine with early AD (stage 4 on the Global Deterioration Scale) participated in this study. Six participants with aMCI and six with AD were allocated to the cognitive training group, while five participants with aMCI and three with AD were allocated to a wait-list control group. Multicomponent cognitive training was administered in 18 weekly, individual sessions. Outcome measures were undertaken at baseline, and at 2 weeks and 3 months of follow-up., Results: In the trained MCI group, there were significant improvements in the delayed-recall scores on the Seoul Verbal Learning Test at both the 2-week and 3-month follow-ups compared with baseline (baseline, 1.6±1.5; 2 weeks, 4.4±1.5, p=0.04; 3 months, 4.6±2.3, p=0.04). The phonemic fluency scores (1.0±0.8 vs. 5.0±1.8, p=0.07) and Korean Mini-Mental State Examination scores (18.8±0.5 vs. 23.8±2.2, p=0.07) also showed a tendency toward improvement at the 2-week follow-up compared to baseline in the trained AD group., Conclusions: This study provides evidence of the effectiveness of cognitive training in aMCI and early AD. The efficacy of cognitive training programs remains to be verified in studies with larger samples and a randomized design.