11 research outputs found
A retrospective and agenda for future research on Chinese outward foreign direct investment
Our original paper “The determinants of Chinese Outward Foreign Direct Investment” was the first
theoretically based empirical analysis of the phenomenon. It utilised internalisation theory to show that
Chinese state-owned firms reacted to home country market imperfections to surmount barriers to
foreign entry arising from naivety and the lack of obvious ownership advantages, leveraging
institutional factors including favourable policy stimuli. This special theory explained outward foreign
direct investment (OFDI) but provided surprises. These included the apparent appetite for risk evinced
by these early investors, causing us to conjecture that domestic market imperfections, particularly in
the domestic capital market, might be responsible. The article stimulated a massive subsequent, largely
successful, research effort on emerging country multinationals. In this Retrospective article we review
some of the main strands of research that ensued, for the insight they offer for the theme of our
commentary. Our theme is that theoretical development can only come through embracing yet more
challenging, different, and new contexts, and we make suggestions for future research directions
H5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades
Highly pathogenic avian influenza H5N1 viruses cause severe disease in humans, and dysregulation of cytokine responses is believed to contribute to the pathogenesis of human H5N1 disease. However, mechanisms leading to the increased induction of proinflammatory cytokines by H5N1 viruses are poorly understood. We show that the innate sensing receptor RIG-I is involved in interferon regulatory factor 3 (IRF3), NF-κB nuclear translocation, p38 activation, and the subsequent interferon (IFN) β, IFN-λ1, and tumor necrosis factor α induction during H5N1 infection. Soluble mediators from H5N1-infected human macrophages upregulate RIG-I, MDA5, and TLR3 to much higher levels than those from seasonal H1N1 in uninfected human macrophages and alveolar epithelial cells via paracrine IFNAR1/JAK but not IFN-λ receptor signaling. Compared with H1N1 virus-induced mediators, H5N1 mediators markedly enhance the cytokine response to PolyIC and to both seasonal and H5N1 virus infection in a RIG-I-dependent manner. Thus, sensitizing neighboring cells by upregulation of RIG-I contributes to the amplified cytokine cascades during H5N1 infection. © 2011 The Author.link_to_OA_fulltex
Simeprevir potently suppresses SARS-CoV-2 replication and synergizes with remdesivir
202307 bcchVersion of RecordRGCOthersH2020 SC1-PHE-Coronavirus-2020; National Institute of Allergy and Infectious Diseases; Croucher Foundation; Hong Kong Baptist University; Fondation pour la Recherche Médicale; National Research Foundation of Korea; Chinese University of Hong Kong; Faculty of Medicine, Prince of Songkla University; Ministry of Science and ICT, South KoreaPublishe