The Taiwan Strait Crisis of 1954-55 and U.S.-R.O.C Relations

On September 3, 1954, Chinese artillery began shelling Quemoy (Jinmen), one of the Kuomintang-held offshore islands, setting off the first Taiwan Strait Crisis. This paper focuses on the crisis and analyzes the following three questions: (1) What was the policy the U.S. took towards the Republic of China (R.O.C), especially towards the offshore islands, to try to end the Taiwan Strait Crisis? (2) What were the intentions of the U.S. government in trying to end the Taiwan Strait Crisis? And (3) how should U.S. policy towards the R.O.C. which led to solving the Taiwan Strait Crisis be positioned in the history of Sino-American relations? Through analysis of these questions, this study concludes that the position the U.S. took to bring an end to crisis, one which prevented China from “liberating Taiwan†and the Kuomintang from “attacking the mainland,†brought about the existence of a de facto “two-China†situation.Taiwan Strait Crisis, Quemoy, Jinmen, U.S.-R.O.C. Relations, Two-China, Taiwan, China, United States, International Relations, Foreign Policy

The Evolution of the "One China" Concept in the Process of Taiwan\u27s Democratization

This paper investigates how Taiwan\u27s "one China" concept evolved during the democratization process that occurred under the leadership of former President Lee Teng-hui. The author argues that there was a crucial evolution of the "one China" concept and that the transformation of the concept resulted from changes in Taiwan\u27s internal political circumstances. The evolution of the concept creates a real possibility that the "status quo" sought by the ROC in the Taiwan Strait both during and after the Cold War might be destroyed. In addition, any further evolution of the "one China" concept will surely make the "status quo" of Taiwan untenable, in that it would induce Taiwan to seek de jure instead of de facto independence, possibly initiating a conflict between the PRC and the ROC. To prevent such a conflict in the Taiwan Strait, the international community must persuade the ROC not to go beyond the "status quo" and to stay within the framework of de facto independence. At the same time, both the PRC and the ROC should be urged to maintain an open conduit of communication for productive talks on the reunification of China

The Taiwan Strait Crisis of 1954-55 and U.S.-R.O.C Relations

On September 3, 1954, Chinese artillery began shelling Quemoy (Jinmen), one of theKuomintang-held offshore islands, setting off the first Taiwan Strait Crisis. This paper focuses on the crisis and analyzes the following three questions: (1) What was the policy the U.S. took towards the Republic of China (R.O.C), especially towards the offshore islands, to try to end the Taiwan Strait Crisis? (2) What were the intentions of the U.S. government in trying to end the Taiwan Strait Crisis? And (3) how should U.S. policy towards the R.O.C. which led to solving the Taiwan Strait Crisis be positioned in the history of Sino-American relations? Through analysis of these questions, this study concludes that the position the U.S. took to bring an end to crisis,one which prevented China from “liberating Taiwan” and the Kuomintang from“attacking the mainland,” brought about the existence of a de facto “two-China”situation

NOX1/NADPH Oxidase Expressed in Colonic Macrophages Contributes to the Pathogenesis of Colonic Inflammation in Trinitrobenzene Sulfonic Acid-Induced Murine Colitis s

ABSTRACT NOX1/NADPH oxidase, a nonphagocytic isoform of reactive oxygen species-producing enzymes, is highly expressed in the colon, but the physiologic and pathophysiologic roles of this isoform are not fully understood. The present study investigated the role of NOX1 in the development of colonic inflammation in a trinitrobenzene sulfonic acid (TNBS)-induced murine colitis model. Intrarectal injection of TNBS caused severe colitis accompanied by body weight loss, diarrhea, and increased myeloperoxidase (MPO) activity in wild-type (WT) mice. In contrast, the severity of colitis was significantly attenuated in NOX1-deficient (NOX1KO) mice (the inhibitions of macroscopic damage score, body weight loss, diarrhea score, and MPO activity were 73.1%, 36.8%, 83.3%, and 98.4%, respectively). TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-a and interleukin (IL)-1b), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Expression of NOX1 mRNA was detected not only in the lamina propria but also in peritoneal macrophages isolated from WT mice. Increased expression of TNF-a, IL-1b, and iNOS in peritoneal macrophages exposed to lipopolysaccharide was significantly attenuated in macrophages isolated from NOX1KO mice (68.1%, 67.0%, and 79.3% inhibition, respectively). These findings suggest that NOX1/NADPH oxidase plays an important role in the pathogenesis of TNBS-induced colonic inflammation via upregulation of inflammatory cytokines, chemokines, and iNOS. NOX1 in colonic macrophages may become a potential target in pharmacologic intervention for inflammatory bowel disease

DNA hypomethylation characterizes genes encoding tissue-dominant functional proteins in liver and skeletal muscle

Abstract Each tissue has a dominant set of functional proteins required to mediate tissue-specific functions. Epigenetic modifications, transcription, and translational efficiency control tissue-dominant protein production. However, the coordination of these regulatory mechanisms to achieve such tissue-specific protein production remains unclear. Here, we analyzed the DNA methylome, transcriptome, and proteome in mouse liver and skeletal muscle. We found that DNA hypomethylation at promoter regions is globally associated with liver-dominant or skeletal muscle-dominant functional protein production within each tissue, as well as with genes encoding proteins involved in ubiquitous functions in both tissues. Thus, genes encoding liver-dominant proteins, such as those involved in glycolysis or gluconeogenesis, the urea cycle, complement and coagulation systems, enzymes of tryptophan metabolism, and cytochrome P450-related metabolism, were hypomethylated in the liver, whereas those encoding-skeletal muscle-dominant proteins, such as those involved in sarcomere organization, were hypomethylated in the skeletal muscle. Thus, DNA hypomethylation characterizes genes encoding tissue-dominant functional proteins