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Abstract: Objective: To examine whether trends in death rate from diabetes according to multiple-cause-of-death (MCOD) data differed from those according to underlying-cause-of-death (UCOD) data in Taiwan and the United States. Study Design and Setting: We used multiple cause mortality files for the years 1987, 1992, 1997, 2002, and 2007 to calculate the age-adjusted death rates from diabetes according to MCOD and UCOD and the ratio between diabetes mortality according to UCOD and that according to MCOD (U/M ratio) in Taiwan and the United States. Results: In Taiwan, diabetes mortality according to MCOD increased persistently from 1987 to 2007, but no prominent changes were found according to UCOD in men. For women, the death rates according to MCOD did not change significantly between 1987 and 2007 but decreased drastically from 1992 to 2007 according to UCOD. In the United States, the patterns of change in diabetes mortality according to MCOD were similar to those according to UCOD in both sexes. The U/M ratio of diabetes mortality declined persistently between 1987 and 2007 in Taiwan, but no prominent change was found in the United States. Conclusion: Trends in death rate from diabetes according to MCOD differed from that according to UCOD in Taiwan but not in the United States. To properly interpret cause-specific mortality trends, it is important to provide both MCOD and UCOD data. [Copyright &y& Elsevier]

Asthma, a complex pulmonary allergic disease, major therapy is applied of drugs to control the disease, but quickly recur after the drugs are stopped. In patients with severe asthma may show steroid resistance and would benefit from the development of novel therapeutic drugs. Ovatodiolide, a unique macrocyclic diterpenoid isolated from Anisomeles indica , showed therapeutic potential for the treatment of allergic asthma. As a model of allergic inflammation, we used ovalbumin (OVA)-immunized mice, which displayed T helper cell type 2 (T H 2) cytokine expression in bronchoalveolar lavage fluid (BALF), as well as airway inflammation and hyperresponsiveness (AHR). The results showed that ovatodiolide suppressed T H 2 activation, including cell proliferation and production of the T H 2 related cytokines, interleukin (IL)-4, IL-5, IL-13, IL-33, eosinophil chemotactic protein (eotaxin), and also reduced airway hyperresponsiveness. In this study, ovatodiolide inhibited allergic asthma through downregulation of T H 2 responses in a murine model of asthma. [ABSTRACT FROM AUTHOR]