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Benjamin E. L. Lauffer Robert Mintzer Rina Fong Susmith Mukund Christine Tam Inna Zilberleyb Birgit Flicke Allegra Ritscher Grazyna Fedorowicz Roxanne Vallero Daniel F. Ortwine Janet Gunzner Zora Modrusan Lars Neumann Christopher M. Koth Patrick J. Lupardus Joshua S. Kaminker Christopher E. Heise Pascal Steiner 《The Journal of biological chemistry》2013,288(37):26926-26943
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Renee W. Y. Chan Michael C. W. Chan Sudhakar Agnihothram Louisa L. Y. Chan Denise I. T. Kuok Joanne H. M. Fong Y. Guan Leo L. M. Poon Ralph S. Baric John M. Nicholls J. S. Malik Peiris 《Journal of virology》2013,87(12):6604-6614
Since April 2012, there have been 17 laboratory-confirmed human cases of respiratory disease associated with newly recognized human betacoronavirus lineage C virus EMC (HCoV-EMC), and 7 of them were fatal. The transmissibility and pathogenesis of HCoV-EMC remain poorly understood, and elucidating its cellular tropism in human respiratory tissues will provide mechanistic insights into the key cellular targets for virus propagation and spread. We utilized ex vivo cultures of human bronchial and lung tissue specimens to investigate the tissue tropism and virus replication kinetics following experimental infection with HCoV-EMC compared with those following infection with human coronavirus 229E (HCoV-229E) and severe acute respiratory syndrome coronavirus (SARS-CoV). The innate immune responses elicited by HCoV-EMC were also investigated. HCoV-EMC productively replicated in human bronchial and lung ex vivo organ cultures. While SARS-CoV productively replicated in lung tissue, replication in human bronchial tissue was limited. Immunohistochemistry revealed that HCoV-EMC infected nonciliated bronchial epithelium, bronchiolar epithelial cells, alveolar epithelial cells, and endothelial cells. Transmission electron microscopy showed virions within the cytoplasm of bronchial epithelial cells and budding virions from alveolar epithelial cells (type II). In contrast, there was minimal HCoV-229E infection in these tissues. HCoV-EMC failed to elicit strong type I or III interferon (IFN) or proinflammatory innate immune responses in ex vivo respiratory tissue cultures. Treatment of human lung tissue ex vivo organ cultures with type I IFNs (alpha and beta IFNs) at 1 h postinfection reduced the replication of HCoV-EMC, suggesting a potential therapeutic use of IFNs for treatment of human infection. 相似文献
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Jack Fong 《Ethnic and racial studies》2013,36(2):327-357
My paper examines the Karen ethnic nationality and their fifty-eight-year self-determination struggle against ethnic cleansing resulting from the ethnocratic and military governments of Burma. I frame Karen self-determination as a development issue by employing Rodolfo Stavenhagen's ethnodevelopment model. Ethnodevelopment argues that, if asymmetrical development occurs within a multi-ethnic state, state-oriented ethnic minority development strategies are needed to neutralize the asymmetry. However, Stavenhagen's ethnodevelopment does not question the premise of an authoritarian state or the systemic crisis experienced by ethnic minorities under authoritarian rule. Thus, I revise ethnodevelopment from its top-to-bottom trajectory where ethnic minority development is dependent upon the centralized state, to a bottom-to-top trajectory I designate as liberation ethnodevelopment. I argue that Karen liberation ethnodevelopment is also a development process, but one that develops and shields the Karen from ethnic cleansing. 相似文献
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