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This study took Chiayi City—a tropical, medium-sized city—as an example to investigate the urban heat island (UHI) effect using mobile transects and built environment characteristics in 2018. The findings were compared to those from a study in 1999 to explore the spatiotemporal changes in the built environment characteristics and UHI phenomenon. The result for the UHI intensity (UHII) during the day was approximately 4.1 °C and at midnight was approximately 2.5 °C. Compared with the survey in 1999, the UHII during the day increased by approximately 1.3 °C, and the UHII at midnight decreased by approximately 1.2 °C. The trend of the spatial distribution of the increasing artificial area ratio (AAR) proved the importance of urban land use expansion on UHI. The results of the air temperature survey were incorporated with the nesting space in GIS to explore the role of built environment characteristics in UHI effects. The higher the population density (PD) and artificial area ratio (AAR) were, the closer the proximity was to the downtown area. The green area ratio (GAR) was less than 0.2 in the downtown area and increased closer to the rural areas. The built environment factors were analyzed in detail and correlated with the UHI effect. The air temperature in the daytime increased with the population density (PD) and artificial area ratio (AAR), but decreased with the green area ratio (GAR) (r = ±0.3–0.4). The result showed good agreement with previous studies.

Background: Hepatotoxicity is the most severe adverse effect of anti-tuberculosis therapy. Isoniazid’s metabolite hydrazine is a mitochondrial complex II inhibitor. We hypothesized that mitochondrial DNA variants are risk factors for drug-induced liver injury (DILI) due to isoniazid, rifampicin or pyrazinamide. Methods: We obtained peripheral blood from tuberculosis (TB) patients before anti-TB therapy. A total of 38 patients developed DILI due to anti-TB drugs. We selected 38 patients with TB but without DILI as controls. Next-generation sequencing detected point mutations in the mitochondrial DNA genome. DILI was defined as ALT ≥5 times the upper limit of normal (ULN), or ALT ≥3 times the ULN with total bilirubin ≥2 times the ULN. Results: In 38 patients with DILI, the causative drug was isoniazid in eight, rifampicin in 14 and pyrazinamide in 16. Patients with isoniazid-induced liver injury had more variants in complex I’s NADH subunit 5 and 1 genes, more nonsynonymous mutations in NADH subunit 5, and a higher ratio of nonsynonymous to total substitutions. Patients with rifampicin- or pyrazinamide-induced liver injury had no association with mitochondrial DNA variants. Conclusions: Variants in complex I’s subunit 1 and 5 genes might affect respiratory chain function and predispose isoniazid-induced liver injury when exposed to hydrazine, a metabolite of isoniazid and a complex II inhibitor.

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