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Climate change is considered to be one of the greatest threats to biodiversity in this century, especially for range-restricted island species. This study explored the potential effects of climate change on Arborophila crudigularis, a weak-flying endemic bird species in Taiwan. The potential effects of climate change on climatically suitable habitat for A. crudigularis were analyzed in biomod2 and ArcGIS software. Future climate change could increase the availability of climatically suitable habitat for A. crudigularis while decreasing the mean suitability for both the entire suitable area and the area with known presence records. By 2050 and 2080, climatically suitable habitat is expected to increase by an average of 4.57% and 5.18%, respectively; the mean suitability of the entire climatically suitable habitat is expected to decrease by 4.80% and 6.61%; and the mean suitability of known presence records is expected to decrease by 2.70% and 4.62%, respectively. Future climate change will not be disastrous for A. crudigularis in Taiwan. Future efforts to conserve this species should focus on northwestern Taiwan. [ABSTRACT FROM AUTHOR]

Cooking oil fumes (COF) exposure was demonstrated to be associated with lung cancer development in Taiwanese nonsmoking women. Previous studies identified Cox-2 overexpression and oxidative DNA damage in lung adenocarcinoma cells after exposure to COF. Involvement of COF in lung tumorigenesis may be associated with cell survival, as well as proliferation of lung adenocarcinoma. To test this hypothesis, A549, a lung adenocarcinoma cell line, was used, and MTT assay data showed that the cell viability of A549 was significantly increased in a concentration-dependent manner by COF treatment for 48h. Flow cytometery results indicated that the proportion of A549 cell at S-phase was markedly increased after exposure of COF. To elucidate whether the antiapoptotic c-IAP2 (IAP2) was involved in COF-improved cell survival, IAP2 protein levels was determined by Western blot, and the results showed it was significantly induced by COF in a concentration-dependent manner. Moreover, the suppression of BAY, a nuclear factor (NF)-κB binding inhibitor, or the COF-induced IAP2 protein levels indicated that NF-κB activation by COF may partly be involved in IAP2 induction. These results showed that the positive impact of COF on cell survival and proliferation of A549 lung tumor cells may be through an induction of IAP2 overexpression. [ABSTRACT FROM AUTHOR]