210Po is a naturally occurring radionuclide of 238U decay series with a half-life of 138.4 days. 210Po is decay products of 222Rn, which escapes into the atmosphere and present in all environments with aerosol particles. Also, 210Po has high radiotoxicity and emits a high alpha energy of 5.305 MeV, and it decays to finally become a stable isotope, 206Pb. Therefore, 210Po entering the body by continuously ingestion or inhalation is likely to cause severe damage to the bone marrow, kidney and spleen and other sites in the body. Accordingly, the World Health Organization (WHO) recommends that screening level of gross alpha for drinking water not exceed 0.5 Bq·L−1. Alpha spectrometry has been mainly used for analysis of 210Po, and for the accurate measurement of alpha particle with short range, it is essential to prepare suitable source for alpha detection. The 210Po alpha source is made by a spontaneous deposition method in which polonium is adsorbed thin and flat onto a metal disc, such as silver, nickel and copper. There are various pretreatment methods to separate and concentrate polonium from water samples prior to spontaneous deposition, including Fe(OH)3 or MnO2 co-precipitation and evaporation. However, in the case of co-precipitation, sample contamination or loss of polonium may occur through the experimental processes, and evaporation lead to not only time-consuming process but also may cause loss of polonium due to the low boiling point of polonium. Therefore, in order to compensate for these problems, an efficient polonium analysis method that directly collects polonium from the original sample without a pretreatment is required. In this study, 210Po in bottled drinking water sold in Korea was analyzed using alpha spectrometry. A high purity silver disc (99.99%) was inserted into a newly designed polonium deposition kit to quickly and conveniently collect polonium from a water sample. The polonium alpha detecting source was made effectively only by the spontaneous deposition method without a complicated pretreatment. The source was measured using a PIPS detector, and the radioactivity concentration of 210Po was calculated using 209Po as a yield tracer.

Periodontal disease, a form of chronic inflammatory bacterial infectious disease, is known to be a risk factor for cardiovascular disease (CVD). Porphyromonas gingivalis has been implicated in periodontal disease and widely studied for its role in the pathogenesis of CVD. A previous study demonstrating that periodontopathic P. gingivalis is involved in CVD showed that invasion of endothelial cells by the bacterium is accompanied by an increase in cytokine production, which may result in vascular atherosclerotic changes. The present study was performed in order to further elucidate the role of P. gingivalis in the process of atherosclerosis and CVD. For this purpose, invasion of human aortic smooth muscle cells (HASMC) by P. gingivalis 381 and its isogenic mutants of KDP150 (fimA⁻), CW120 (ppk⁻) and KS7 (relA⁻) was assessed using a metronidazole protection assay. Wild type P. gingivalis invaded HASMCs with an efficiency of 0.12%. In contrast, KDP150 failed to demonstrate any invasive ability. CW120 and KS7 showed relatively higher invasion efficiencies, but results for these variants were still negligible when compared to the wild type invasiveness. These results suggest that fimbriae are required for invasion and that energy metabolism in association with regulatory genes involved in stress and stringent response may also be important for this process. ELISA assays revealed that the invasive P. gingivalis 381 increased production of the proinflammatory cytokine interleukin (IL)-1β and the chemotactic cytokines (chemokine) IL (interleukin)-8 and monocyte chemotactic (MCP) protein-1 during the 30-90 min incubation periods (P<0.05). Expression of RANTES (regulation upon activation, normal T cell expressed and secreted) and Toll-like receptor (TLR)-4, a pattern recognition receptor (PRR), was increased in HASMCs infected with P. gingivalis 381 by RT-PCR analysis. P. gingivalis infection did not alter interferon--inducible protein-10 expression in HASMCs. HASMC nonspecific necrosis and apoptotic cell death were measured by lactate dehydrogenase (LDH) and caspase activity assays, respectively. LDH release from HASMCs and HAMC caspase activity were significantly higher after a 90 min incubation with P. gingivalis 381. Taken together, P. gingivalis invasion of HASMCs induces inflammatory cytokine production, apoptotic cell death, and expression of TLR-4, a PRR which may react with the bacterial molecules and induce the expression of the chemokines IL-8, MCP-1 and RANTES. Overall, these results suggest that invasive P. gingivalis may participate in the pathogenesis of atherosclerosis, leading to CVD.