Navigating and riding the double bind of economic and political hedging: Japan and the US-China strategic competition

Japan finds itself in a double bind. On the one hand, the United States (US) has been a committed military ally, guaranteeing the national security of Japan since 1952. Any discussion of abandonment by the US sends shockwaves throughout the conservative security establishment of Japan. On the other hand, the rise of the People’s Republic of China (PRC) has transformed it into the most important trade partner of Japan, by far. Japan is interested in a continued expansion of the PRC economy. This paper analyzes the foreign economic policy of Japan and the security policy of the conservative, LDP-led governments under the leadership of Prime Minister Shinzō Abe (2012–2020) and his successors in this complex interplay of international relations and national politics

Japanese Political Economy Revisited: Diverse Corporate Change, Institutional Transformation, and Abenomics

This article has been published as the introduction of the special issue in Japan Forum (“Japanese Political Economy Revisited: Abenomics and Institutional Change”) and as an introduction to the book (Japanese Political Economy Revisited: Abenomics and Institutional Change, Routledge)This introductory article to the special issue on “Japanese Political Economy Revisited: Diverse Corporate Change, Institutional Transformation, and Abenomics” starts with a short summaryof the changing perceptions of Japan’s political economy from its meteoric rise as worldwide leading model in the 1970s and 1980s to its demotiontoa problem and reform case since the later 1990s. Based on this overview, it identifies some striking issue and open questions in this conventional view of Japan’s political economy as problem and the high expectations on Abenomics as Japan’s current economic reform programme. Then we discuss the articles of the special issue and their new contributionsto a better understanding of the developments at the corporate level as well as institutional change and economic reforms at the macro level in the last two decades. Finally, this introductory article ends with a short outlineof a new research programme and four central research questions about the Japanese political economy

China’s and Japan’s winding path to the refugee convention: state identity transformations and the evolving international refugee regime

In the early 1980s, the People’s Republic of China (PRC) and Japan joined the international refugee regime. This timing similarity is puzzling due to the stark differences between the PRC as a communist and authoritarian state versus Japan as a prime example of capitalist development and democratization. Moreover, although both signed the 1951 Refugee Convention and the 1967 Refugee Protocol without major reservations, neither of them has fully implemented these treaties. Discussions regarding the PRC’s and Japan’s engagement with the international refugee regime tend to start with the beginning of the Indochina refugee crisis in 1975. However, this article shows that the early decades of their interaction with the international refugee regime are of crucial importance for a full understanding of the timing and form of accession to the international refugee regime. Although the Southeast Asian refugee crisis played an important role as a trigger, it was the changing character of the international refugee regime and the transformations of state identity in both countries that set the ground for the signing of the refugee-related conventions

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Meta-analysis of shared genetic architecture across ten pediatric autoimmune diseases

Genome-wide association studies (GWASs) have identified hundreds of susceptibility genes, including shared associations across clinically distinct autoimmune diseases. We performed an inverse χ(2) meta-analysis across ten pediatric-age-of-onset autoimmune diseases (pAIDs) in a case-control study including more than 6,035 cases and 10,718 shared population-based controls. We identified 27 genome-wide significant loci associated with one or more pAIDs, mapping to in silico-replicated autoimmune-associated genes (including IL2RA) and new candidate loci with established immunoregulatory functions such as ADGRL2, TENM3, ANKRD30A, ADCY7 and CD40LG. The pAID-associated single-nucleotide polymorphisms (SNPs) were functionally enriched for deoxyribonuclease (DNase)-hypersensitivity sites, expression quantitative trait loci (eQTLs), microRNA (miRNA)-binding sites and coding variants. We also identified biologically correlated, pAID-associated candidate gene sets on the basis of immune cell expression profiling and found evidence of genetic sharing. Network and protein-interaction analyses demonstrated converging roles for the signaling pathways of type 1, 2 and 17 helper T cells (TH1, TH2 and TH17), JAK-STAT, interferon and interleukin in multiple autoimmune diseases