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7. The co-evolution of technology and institution in the Korean information and communications industry

Author

Choung, Jae-Yong, Hwang, Hye-Ran, and Yang, Heeseung

Subjects
Information technology -- Analysis, Information technology, Business, international, High technology industry, Science and technology
Abstract

Byline: Jae-Yong Choung, Hye-Ran Hwang, Heeseung Yang The Korean IT industry has shown distinct patterns in learning mechanisms and organisational configuration throughout its entry into advanced information technology. Innovation systems in the area of information technology have also evolved along with technological capability, thereby changing the focus of technological strategies and the role of public institutions. It is found that distinctive patterns of learning and diffusion mechanisms in the case of DRAMs, TDX, and CDMA systems represent successful catch-up situations in Korea as presented in this paper. This paper characterises the stylised facts of the Korean innovation system in the IT sector and traces how technology and institutions coevolved throughout the development process. The transition from technology-using to technology-generating is not an automatic process. Cumulative learning in both technology and organisation is a critical factor to upgrade technological capabilities. The main policy implication of the paper is that it is important to design the corresponding organisational and institutional arrangement in accordance with the changing need of technological upgrading.

Published
2006

10. Inhibition of Pseudomonas aeruginosa LPS-Induced airway inflammation by RIPK3 in human airway.

Author

Yun M, Park SH, Kang DH, Kim JW, Kim JD, Ryu S, Lee J, Jeong HM, Hwang HR, and Song KS

Subjects
Humans, Histones, Receptor-Interacting Protein Serine-Threonine Kinases genetics, Receptor-Interacting Protein Serine-Threonine Kinases metabolism, Necrosis, Inflammation metabolism, Cytokines metabolism, Lipopolysaccharides, Pseudomonas aeruginosa
Abstract

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.)

Published
2022
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