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MICHAEL LOBSIGER;MARC ZAHNER 경제연구소 2012 Journal of Economic Development Vol.37 No.2
This paper aims at estimating the effect of different types of institutions on economic development. To tackle the endogeneity problem that is prevalent, an identification strategy exploiting the heteroskedasticity in the data is used. This also allows to analyze the reverse effect, running from economic development to institutions. In a sample of about 100 countries, an impact of property rights institutions but not contracting institutions on economic development is detected. Furthermore, the results suggest that a higher level of economic development improves contracting institutions, but not property rights institutions.
MICHAEL LOBSIGER,MARC ZAHNER 중앙대학교 경제연구소 2012 Journal of Economic Development Vol.37 No.2
This paper aims at estimating the effect of different types of institutions on economic development. To tackle the endogeneity problem that is prevalent, an identification strategy exploiting the heteroskedasticity in the data is used. This also allows to analyze the reverse effect, running from economic development to institutions. In a sample of about 100 countries, an impact of property rights institutions but not contracting institutions on economic development is detected. Furthermore, the results suggest that a higher level of economic development improves contracting institutions, but not property rights institutions
LIGHT-HVEM Signaling in Innate Lymphoid Cell Subsets Protects Against Enteric Bacterial Infection
Seo, Goo-Young,Shui, Jr-Wen,Takahashi, Daisuke,Song, Christina,Wang, Qingyang,Kim, Kenneth,Mikulski, Zbigniew,Chandra, Shilpi,Giles, Daniel A.,Zahner, Sonja,Kim, Pyeung-Hyeun,Cheroutre, Hilde,Colonna, Elsevier 2018 Cell host & microbe Vol.24 No.2
<P><B>Summary</B></P> <P>Innate lymphoid cells (ILCs) are important regulators of early infection at mucosal barriers. ILCs are divided into three groups based on expression profiles, and are activated by cytokines and neuropeptides. Yet, it remains unknown if ILCs integrate other signals in providing protection. We show that signaling through herpes virus entry mediator (HVEM), a member of the tumor necrosis factor (TNF) receptor superfamily, in ILC3 is important for host defense against oral infection with the bacterial pathogen <I>Yersinia enterocolitica.</I> HVEM stimulates protective interferon-γ (IFN-γ) secretion from ILCs, and mice with HVEM-deficient ILC3 exhibit reduced IFN-γ production, higher bacterial burdens and increased mortality. In addition, IFN-γ production is critical as adoptive transfer of wild-type but not IFN-γ-deficient ILC3 can restore protection to mice lacking ILCs. We identify the TNF superfamily member, LIGHT, as the ligand inducing HVEM signals in ILCs. Thus HVEM signaling mediated by LIGHT plays a critical role in regulating ILC3-derived IFN-γ production for protection following infection.</P> <P><B>Video Abstract</B></P> <P>Display Omitted</P> <P><B>Highlights</B></P> <P> <UL> <LI> ILC3 are required for early host defense during <I>Y. enterocolitica</I> infection </LI> <LI> IFN-γ from CCR6<SUP>−</SUP> ILC3 is essential for protection of mice from <I>Yersinia</I> </LI> <LI> HVEM expression by ILC3 is important for IFN-γ production following infection </LI> <LI> LIGHT is the ligand for HVEM signaling in regulating ILC3-derived IFN-γ production </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>