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"Island X delves into the compelling political lives of Taiwanese migrants who came to the United States as students from the 1960s through the 1980s. Often depicted as compliant model minorities, many were in fact deeply political, shaped by Taiwan's colonial history and influenced by the global social movements of their times. As activists, they fought to make Taiwanese people visible as subjects of injustice and deserving of self-determination. Under the distorting shadows of Cold War geopolitics, the Kuomintang regime and collaborators across U.S. campuses attempted to control Taiwanese in the diaspora through extralegal surveillance and violence, including harassment, blacklisting, imprisonment, and even murder. Drawing on interviews with student activists and extensive archival research, Wendy Cheng documents how Taiwanese Americans developed tight-knit social networks as infrastructures for identity formation, consciousness development, and anticolonial activism. They fought for Taiwanese independence, opposed state persecution and oppression, and participated in global political movements"--

Examining the San Gabriel Valley, Wendy Cheng unpacks questions of how identity-especially racial identity-is shaped by place. Informed by nearly seventy interviews, Cheng argues that people's daily experiences deeply influence their racial consciousness, providing a model for considering the spatial dimensions of racial formation and the significant demographic shifts taking place across the national landscape

While Los Angeles's San Gabriel Valley is best known for being the "first suburban Chinatown," it is actually a lively, multiethnic, and multiracial community with a complex past, and an emerging arts scene that celebrates that complexity. Today, the "SGV" constitutes the largest, majority-Asian American and Latino community in the United States. Its social and cultural mix make it a vibrant example of suburban cosmopolitanism, in which diverse residents live in relative harmony, with mutual respect for difference. Local groups such as the South El Monte Arts Posse have begun to make work that reflects this ethos, and could reshape normative ideas of what it means to be American.

Black and Brown in Los Angeles is a timely and wide-ranging, interdisciplinary foray into the complicated world of multiethnic Los Angeles. The first book to focus exclusively on the range of relationships and interactions between Latinas/os and African Americans in one of the most diverse cities in the United States, the book delivers supporting evidence that Los Angeles is a key place to study racial politics while also providing the basis for broader discussions of multiethnic America. Students, faculty, and interested readers will gain an understanding of the different forms of cultural borrowing and exchange that have shaped a terrain through which African Americans and Latinas/os cross paths, intersect, move in parallel tracks, and engage with a whole range of aspects of urban living. Tensions and shared intimacies are recurrent themes that emerge as the contributors seek to integrate artistic and cultural constructs with politics and economics in their goal of extending simple paradigms of conflict, cooperation, or coalition. The book features essays by historians, economists, and cultural and ethnic studies scholars, alongside contributions by photographers and journalists working in Los Angeles

International Liver Disease Genetics Consortium. ; Cirrhosis likely shares common pathophysiological pathways despite arising from a variety of liver diseases. A recent GWAS identified rs641738, a polymorphism in the MBOAT7 locus, as being associated with the development of alcoholic cirrhosis. Here we explore the role of this variant on liver inflammation and fibrosis in two cohorts of patients with chronic hepatitis C. In 2,051 patients, rs641738 associated with severe hepatic inflammation and increased risk of fibrosis, as well as fast fibrosis progression. At functional level, rs641738 associated with MBOAT7 transcript and protein levels in liver and blood, and with serum inflammatory, oxidative stress and macrophage activation markers. MBOAT7 was expressed in immune cell subsets, implying a role in hepatic inflammation. We conclude that the MBOAT7 rs641738 polymorphism is a novel risk variant for liver inflammation in hepatitis C, and thereby for liver fibrosis. ; M.E., M.W.D. and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and Project grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432). H.G. received support from The NOVO Nordisk Foundation the Danish Strategic Research Council (10-092797). U.S. and J.N. are supported by DFG SFB-TR57 and the Hector-Foundation (M63). K.T. is supported by Scholarship from the Egyptian government.

International Liver Disease Genetics Consortium (ILDGC). ; Hepatocarcinogenesis is tightly linked to liver fibrosis. Recently, two GWAS variants, MICA rs2596542 and DEPDC5 rs1012068 were identified as being associated with the development of HCV-induced hepatocellular carcinoma (HCC) in Japanese patients. The role of these variants on hepatic inflammation and fibrosis that are closely associated with HCC development is not known, nor are the biological mechanisms underlying their impact on the liver. Here, we demonstrate in 1689 patients with chronic hepatitis C (CHC) (1,501 with CHC and 188 with HCV-related HCC), that the MICA (T) allele, despite not being associated with HCC susceptibility, is associated with increased fibrosis stage (OR: 1.47, 95% CI: 1.05–2.06, p = 0.02) and fibrosis progression rate (hazards ratio: 1.41, 95% CI: 1.04–1.90, p = 0.02). The DEPDC5 variant was not associated with any of these phenotypes. MICA expression was down-regulated in advanced fibrosis stages. Further, (T) allele carriage was associated with lower MICA expression in liver and serum. Transforming growth factor-β1 (TGF-β1) expression suppresses MICA expression in hepatic stellate cells. Our findings suggest a novel mechanism linking susceptibility to advanced fibrosis and subsequently indirectly to HCC, to the level of MICA expression through TGF-β1-dependent mechanisms. ; M.E., C.L., M.D. and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (APP1053206, APP1149976) and Project grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432). U.S. and J.N. are supported by DFG SFB-TR57 and the Hector-Foundation (M63). R.E. and K.T. are supported by a scholarship from the Egyptian government. A.B. is supported by an Australian Government Research Training Program (RTP) scholarship. ; Peer reviewed