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In this paper, we analyze the extent to which low-income countries integrate into the global knowledge production network. We develop an (undirected) research collaboration model based on which we identify the drivers of global research collaboration using publication data of the field Business and Economics from the Web of Science and macroeconomic data from the United Nations Educational, Scientific and Cultural Organization Institute for Statistics. Network and dynamic panel regression techniques are employed. Our results show that (i) reciprocal preferential attachment and the homophily between countries reinforce scientific collaboration, (ii) there is no evidence that low-income countries are becoming better integrated into the global knowledge production over the years, despite their active participation in international reserach collaboration, while (iii) high-income countries show a basic willingness to cooperate with them, which, in turn, promotes the integration of low-income countries, although this willingness seems to decline; and (iv) as to low-income countries, they have little choice but to invest more in education and R&D in order to advance in the global knowledge production network. [ABSTRACT FROM AUTHOR]

Airway remodeling is a key characteristic of allergic asthma. Epithelial-mesenchymal transition (EMT) induced by various factors, particularly transforming growth factor (TGF)-β1, orchestrates airway remodeling. Protein phosphatase 2A (PP2A), an important serine-threonine phosphatase, is involved in TGF-β1 production and EMT. Long noncoding RNAs (lncRNAs) have emerged as novel players in regulating EMT. Here, we aimed to explore the effects and mechanisms of action of lincR-PPP2R5C, a lncRNA that affects PP2A activity, on airway remodeling in a mouse model of chronic allergic asthma. LincR-PPP2R5C knockout (KO) alleviated inflammatory responses in house dust mite (HDM)-induced chronic allergic asthma. Moreover, airway remodeling and EMT were reduced in lung tissues of lincR-PPP2R5C KO mice. HDM extract induced EMT in airway epithelial cells, which was decreased following lincR-PPP2R5C KO. Mechanistically, lincR-PPP2R5C deficiency enhanced PP2A activity, which inhibited TGF-β1 production in epithelial cells. In conclusion, lincR-PPP2R5C deficiency prevented HDM-induced airway remodeling in mice by reversing EMT, which was mediated by the PP2A/TGF-β1 signaling pathway. Thus, lncRNAs, i.e. , lincR-PPP2R5C, may be potential targets to prevent airway remodeling in allergic asthma., Competing Interests: There are no financial or other issues that might lead to a conflict of interest., (Copyright © 2024 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease.)