Regionalization and Regionalism: The Process of Mutual Interaction

This paper analyzes the evolution of regionalism in East Asia and derives implications for the role and influence of the United States and Japan in the region. In the introductory section, this paper identifies three major driving forces and three factors that acted as a brake throughout the evolutionary process of regionalism. Section 1 analyses the regionalization in East Asia to understand the characteristics of the second driving force, intra-regional economic interdependence, which has had a consistent and ever-increasing impact on the shape and nature of the regionalism. Section 2 reveals changing impacts of different factors through an overview of interactions of the driving forces and obstacles through the four distinct periods identified in the introductory section. The concluding section deals with the interaction between the regionalism and the influence of the United States, Japan and China on it.

Whither East Asian Economic Integration?

This paper looks back on the evolution of institutional frameworks for economic integration in East Asia, which accelerated after the Asian financial crisis, analyzes its dynamics and future prospects, and identifies Japan's roles in the process that are consistent with the institutional transformation of its economy and society as well as the fundamental interests the United States have in Asian integration and constructive roles it can play in the process. In Section I, it analyzes the forces influencing the development and performance of various regional frameworks. In Section II, the paper assesses the prospects for Asian economic integration in light of these forces as well as perceived obstacles. Section III examines the link between Japan's policy efforts to overcome economic and political challenges, and the development of various institutional frameworks for East Asian economic integration. In Section IV, this paper presents positive implications for the U. S. policy for Asia.

Importance of the interferon-α system in murine large intestine indicated by microarray analysis of commensal bacteria-induced immunological changes

Abstract Background Although microbiota play a critical role in the normal development and function of host immune systems, the underlying mechanisms, especially those involved in the large intestine (LI), remain unknown. In the present study, we performed transcriptome analysis of the LI of germ-free (GF) and specific pathogen-free (SPF) mice of the IQI strain, an inbred strain established from ICR mice. Results GeneChip analysis, quantitative real-time RT-PCR, and reconfirmation using bacteria-inoculated GF mice revealed differences in the expression levels of several immune-related genes, such as cryptdin-related sequences (CRS), certain subsets of type 1 interferon (IFN)-related genes, class Ib MHC molecules, and certain complements. LI expressed no authentic cryptdins but predominantly expressed CRS2, 4, and 7. The mRNA levels of IFN-related genes, including Irf7, Isgf3g, Ifit1 and Stat1, were lower in SPF- and flora-reconstituted mice. When an oral IFN-α inducer tilorone analog, R11567DA, was administered to SPF mice, IFN-α was induced rapidly in the LI at 4 h, whereas no IFN-α protein was detected in the small intestine (SI) or blood. In situ hybridization and immunohistochemistry suggested that the IFN-α production originated from Paneth cells in the SI, and portions of lamina proprial CD11b- or mPDCA1-positive cells in the LI. Conclusion The present study suggests that microbial colonization, while inducing the expression of anti-microbial peptides, results in the down-regulation of certain genes responsible for immune responses, especially for type I IFN synthesis. This may reflect the adaptation process of the immune system in the LI to prevent excessive inflammation with respect to continuous microbial exposure. Further, the repertoire of anti-microbial peptides and the extraordinary role of interferon producing cells in the LI have been found to be distinct from those in the SI.</p