Abstract. In South Korea, scrub typhus is one of the most common rickettsial diseases. The number of scrub typhus patients has increased in South Korea, a total of 69,210 cases were reported from 2001 to 2013. The seasonality and relation of scrub typhus cases to latitude were analyzed in this article using data obtained from the National Notifiable Diseases Surveillance System website of the Korea Centers for Disease Control and Prevention. The incidence of scrub typhus tended to increase in the later months of the year, especially in October-December. In general, lower latitudes were associated with a later peak incidence. Our results suggest for the first time that the monthly observed incidence tended to increase in the later months of the year as the latitude decreased, and on a yearly basis in Korea.
Inhaled particulate matter (PM) might influence many adverse health effects in human body, including increased exacerbations of pulmonary and cardiovascular diseases. In this study, we examined the associations between PM and pulmonary adverse effects. Two types of particles, Asian dust (AD) and titanium dioxide (TiO(2)), were administered intratracheally to C57BL/6 mice. The mice were exposed to saline and saline suspensions of 20 mg/kg of AD, TiO(2) particles twice a week for 12 weeks. Following exposure with these particles, the lungs were analyzed histopathologically by hematoxylin and eosin (H&E) and Masson's trichrome (MT) staining. Oxidative injuries were determined by immunohistochemistry (IHC) for 8-oxoguanine in the lungs and Comet assays in peripheral blood mononuclear cells (PBMCs) of C57BL/6 mice. Mice exposed to AD and TiO(2) showed significant inflammatory changes and oxidative damages in the lungs as compared with the control group. DNA damage in PBMCs was also increased significantly in AD and TiO(2)-exposed mice. However, lung fibrosis was minimal and there was no significant difference between PM exposed and control mice. Exposure to AD and TiO(2) particles-induced similar inflammatory damages in the lungs and elicited oxidative DNA damage in the PBMCs.
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