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To investigate whether changes in outdoor air pollutants, meteorology data, certain personal or environmental factors explain the changing prevalence of current wheeze, ever wheeze and physician-diagnosed asthma among Taiwanese middle-schools children.Data from two cross-sectional national surveys between 1995 and 2001 were used. Study population was limited from 22 middle schools located within one-kilometer catchment areas of 22 air-monitoring stations in Taiwan. The main outcome measures were physician-diagnosed asthma, lifetime wheezy symptoms, and wheeze in current 12 months, as reported by parents. The effects of several personal and environmental factors on the change of three diseases were assessed by multiple logistic regression. Changes in air pollutants and meteorology data in communities were also compared with estimated prevalence changes of three diseases.44,118 data from 1995 survey and 11,738 data from 2001 survey were left for final analysis. The prevalence of ever wheeze and physician-diagnosed asthma increased from 1995 to 2001 in both sexes. Prevalence of current wheeze decreased significantly in boys but not in girls. Three diseases were more commonly reported among children of lower age, higher parental education level, higher parental reported ambient air pollution level, and those who were exposed to ETS or incense, performed less exercise, and suffered from atopic eczema. When adjusted for these factors, the relative odds of three diseases (2001 to 1995) did not show significant changes. Communities with lower decreasing rate in sulfur dioxides level had higher increasing percentage in prevalence of three diseases.Changes in listed personal and environmental factors did not seem to explain any of the observed changes in prevalence. However, correlates of these factors which have changed over time may still underlie recent changes in diseases. Sulfur dioxides may play an essential role as an indicator in trends of three diseases. [ABSTRACT FROM AUTHOR]

We recently reported that domain 5 (D5) of high-molecular-weight kininogen inhibited critical steps required for angiogenesis. Thus, it was named kininostatin. To understand its mechanism of action, we further investigated the effects of D5 on basic fibroblast growth factor (bFGF)-induced endothelial cell proliferation and cell viability. We report here that D5-inhibited cell proliferation of human endothelial cells stimulated by bFGF was associated with a significant reduction of cyclin D1 expression, which is a critical component required for the transition from G(1) to S phase of the cell cycle. However, inhibition of cell proliferation by D5 was not due to an inhibition of extracellular signal-regulated protein kinase activity. Endothelial cells underwent apoptosis when cultured in a serum-free medium, which was prevented by bFGF. D5 reversed the protective effect of bFGF by 80%. Cells treated with D5 in the presence of bFGF showed typical morphological features of apoptosis, which was further confirmed by 2 additional assays: Hoechst 33258 cell staining and DNA fragmentation analysis. We conclude that the inhibition of endothelial cell proliferation and induction of apoptosis together represent a major contribution to the antiangiogenic activity of D5.