This study investigated the characteristics of personal PM2.5 exposure among 109 participants residing in Seoul over a two-month period, from February 2024 to April 2024. The participants were categorized into four sub-populations, and personal exposure to PM2.5 was assessed using portable monitors, GPS, and time-activity diaries. To understand the time-activity patterns, the daily occupancy rate for different microenvironments was calculated. Additionally, daily PM2.5 exposure contribution and integrated exposure were quantified. A time series analysis was conducted to identify differences in time-activity patterns and PM2.5 exposure among the sub-populations. ANOVA analysis indicated statistically significant differences in PM2.5 concentrations across populations and microenvironments (p<0.05). However, post-hoc analysis revealed specific microenvironments within certain sub-populations where PM2.5 concentration differences were not significant (p>0.05). All sub-populations spent more than 90% of their time indoors, and the results for exposure contribution and integrated exposure indicated that the home, which had the highest occupancy rate, was the most significant contributor to PM2.5 exposure. This study is expected to serve as foundational data for future indoor air quality management and the development of personalized strategies for reducing PM2.5 exposure.

Recently, the importance of inflammation in carcinogenesis has been recognized and studied extensively. As a result, a clear correlation between inflammation and carcinogenesis has been well established in some types of cancers. Despite a high prevalence of chronic periodontitis, one of the most common inflammatory diseases in the general population, there are only a few reports on the role of chronic periodontitis in oral cancer progression. In this study, we aimed to investigate genetic changes in oral cancer cells induced by repetitive Porphryomonas gingivalis infections to mimic chronic periodontitis in a clinical setting. Cells of oral squamous cell carcinoma (OSCC), the most common type of oral cancer, and P. gingivalis 381 were used for the present study. ID1 and ID3 were mRNAs of higher expression in the P. gingivalis-infected group compared to the uninfected control. These mRNAs have been regarded as important modulators participating in cancer progression. Future studies will provide an insight into the roles of the molecules we identified in oral cancer progression. Outcomes from these studies will also shed light on the significance of chronic periodontitis induced by bacterial pathogen, such as P. gingivalis, in progression of oral cancer and relevant molecular mechanisms underlying altered cancer cell behaviors.

Embryonic stem cell-preconditioned microenvironment is important for cancer cells properitities by change cell morphology and proliferation. This microenvironment induces cancer cell reprogramming and results in a change in cancer cell properties such as differentiation and migration. The cancer microenvironment affects cancer cell proliferation and growth. However, the mechanism has not been clarified yet. Using the ES-preconditioned 3-D microenvironment model, we provide evidence showing that the ES microenvironment inhibits proliferation and reduces oncogenic gene expression. But ES microenvironment has no effect on telomerase activity, cell viability, cellular senescence, and methylation on Oct4 promoter region. Furthermore, methylation of Nanog was increase on ES-preconditioned microenvironment and supports results that no difference on RNA expression levels. Taken together, these results demonstrated that in the ES-preconditioned 3-D microenvironment is a crucial role for cancer cell proliferation not senescence.