Cadmium (Cd) is an environmental toxic heavy metal that predominantly causes renal failure. Although changes in gene expression are important factors affecting Cd toxicity, the genes that determine Cd toxicity have not been identified. In this study, we tested 36 genes that are highly expressed in the kidney for their effects on Cd toxicity. After human proximal tubular cells (HK-2 cells) were transfected with small interfering RNAs (siRNAs) targeting these genes, Cd toxicity was examined. The expression of the five genes selected from the primary screen was knocked down and the effect on Cd toxicity evaluated. The knockdown of CRYAA and DPYS significantly enhanced Cd toxicity, but not the toxicity of mercury compounds. The CRYAA protein plays a chaperone role and DPYS protein regulates nucleic acid metabolism. The regulation of CRYAA and DPYS expression may affect the Cd renal toxicity.

The contamination levels of benzotriazole ultraviolet absorbers (BUVAs) were determined in breast milk samples from 36 Japanese mothers. BUVAs were detected in all samples in the ranges of 11.0-803 ng/g lipid weight. Especially, 2-(2H-benzotriazol-2-yl)-4,6-bis(1,1-dimethylethyl) phenol (UV-320) accounted for 36% of the total. The BUVAs levels were comparable to some previous reports. The total BUVAs levels in this study were higher than those of Vietnam and Korea. A comparison of primiparas and multiparas showed that the mean total BUVAs level in multiparas was 2.1 times higher than that in primiparas. In particular, UV-320 levels were significantly higher in multiparas than in primiparas (p<0.05). Subsequently, the estimated daily intake of infants was calculated to be 76.5-4,410 ng/kg/day. Further studies are needed to help develop regulations for these chemicals in our living environment and prevent harmful exposure.

As the number of consumers suffering from rough hands and dermatitis caused by the frequent daily use of synthetic surfactants increases, biocompatible materials are required. Biosurfactants (BSs), compounds excreted or produced by microbial cells, attract attention as cosmetic substrates suitable for human skin and the environment. This study evaluated the utility of the glycolipid-type sophorolipid (SL) produced by the non-pathogenic yeast Starmerella bombicola, as a BS. The cytotoxicity of open-chain acid type SL (SL acid) among SLs, is approximately 100–250 times less than that of commercially available surfactants in all cells. Therefore, SL acid is a promising surfactant with a high safety profile. In contrast, the critical micelle concentration (CMC) of SL acid, surfactin, and rhamnolipid were 1,000 mg/L, 16 mg/L, and 38 mg/L, respectively, indicating that SL acid has lower functionality than the other BSs. Finally, the safety range was analyzed for each BS to indicate practicality. The safety range, the concentration range where each BS can exhibit its function without cytotoxicity, was defined based on the lethal concentration 50 (LC₅₀)/CMC value. As a result, the safety range of SL acid is 3.9–4.4 times wilder than that of surfactin and rhamnolipids. Consequently, SL acid could be a promising BS with a wider safety range than other BSs, such as surfuctin and rhamnolipids.

Plasminogen activator inhibitor 1 (PAI-1) stabilizes the thrombus by suppressing the activation of plasminogen to plasmin at the site where the thrombus is formed, thereby inhibiting fibrinolytic reaction. Because inhibition of PAI-1 production or activity facilitates fibrin degradation and eliminates unnecessary thrombus, it is believed that suppression of PAI-1 production or activity prevent thrombosis. Some natural substances that inhibit PAI-1 production and activity were found from medicinal plants, health foods, and purified natural substances and they have potential for realistic use in clinical field or as functional foods. Here, we reviewed these natural products that inhibit PAI-1 production and activity. In addition, we described the potential applications of these substances in clinical field or as functional foods.

Alzheimer’s disease (AD) is one of the most common types of progressive dementia. Recently, endoplasmic reticulum (ER) stress was suggested as a potential event involved in AD development. Thus, targeting ER stress may be an effective AD treatment. The involvement of ER stress in the brains of amyloid precursor protein knock-in AD model mice (App^{NL-G-F/NL-G-F}) with Swedish/Iberian/Arctic mutations found in human familial AD remains unclear. This study aimed to clarify whether the expression of ER stress marker C/EBP homologous protein (CHOP) was enhanced in the brains of App^{NL-G-F/NL-G-F} AD model mice. Our immunofluorescence staining results showed that similar to the expression pattern of amyloid-β (Aβ), CHOP demonstrated an age-dependent increase in the numbers and sizes of spotted signals in the cerebral cortex and hippocampus of these 4- to 10-month-old AD model mice but not in their age-matched controls. These findings suggested that CHOP expression was upregulated in close association with Aβ expression, and that CHOP was involved in neuropathy caused by Aβ accumulation. Future investigations of the localization and variations in expression levels of other ER stress-related proteins in this mouse model using immunofluorescence staining will lead to a more detailed estimation of the relationship between ER stress and AD pathogenesis.

The Ministry of Health, Labour and Welfare of Japan has set the guideline values for indoor air concentrations of 13 volatile organic compounds (VOCs) and semi-volatile organic compounds from 1997 to 2002. However, in 2019, the guideline values for three of these substances, including xylene, were revised and regulated more strictly. Additionally, the manual for analysis of VOCs in indoor air, established in 2001 by the Committee on Sick House Syndrome: Indoor Air Pollution, has not been updated for over 20 years. In this study, we confirmed that the current analytical method for VOCs in indoor air using solvent extraction which was established in 2001, is applicable to VOCs that have been revised or added since then. We proposed it as a standard test method and performed an inter-laboratory validation study in five laboratories to prove this. This validation study included nine substances: six VOCs with current guideline values and three VOCs as candidates for newly setting guideline values. Additional amount in this study was set as 1 µg, less than one-tenth of the guideline value for xylene. The results showed that the average recovery, repeatability, and reproducibility for the nine substances in the five laboratories were 75.4%–115%, 0.78%–9.6%, and 3.6%–21%, respectively. These values satisfied the determined criteria ranges, suggesting that our proposed analytical method can be used as a standard test method.

To clarify the relationship between smartphone addiction and headaches, we conducted a questionnaire survey of women who were aware of having headaches. A questionnaire survey was conducted on the Internet of 600 women between the ages of 20 and 40 who had suffered from headaches in the past three months. The subjects were divided into a smartphone addiction group (n = 120) and a smartphone non-addiction group (n = 480). The addiction group had more complaints of photophobia and phonophobia, which are accompanying symptoms of headaches, and the impact of headache attacks on daily life was greater than the non-addiction group. There was no significant difference in sleep time between the groups, but the addiction group used their smartphones longer on average and felt more sleepy during the day. More respondents in the addiction group complained of decreased visual acuity, dry eyes, and blurred vision than the non-addiction group, suggesting that blue light from computers and smartphones affected their eyes. Moreover, the frequency of headaches, stiff shoulders, fatigue, sleeping disorders, hormonal imbalance, and dark circles and wrinkles around the eyes were higher in the addiction group compared to the non-addiction group. Although smartphone addiction has not been established as a disease, our findings suggest that it reduces sleep quality and worsens headaches.

In humans, influenza A virus (IAV) causes mild to severe respiratory disease, posing a major threat to public health worldwide. Increasing evidence suggests that myeloid-derived suppressor cells (MDSCs) are involved in viral infection outcomes in genetically modified mice; however, the mechanisms by which MDSCs contribute to lung pathology under normal genetic conditions remain controversial. In the present study, we intranasally infected mice with mouse-adapted IAV (A/Puerto Rico/8/1934 [PR8]) and adoptively transferred MDSCs differentiated in vitro intravenously to assess their functional relevance in vivo. After PR8 infection, the adoptive transfer of MDSCs significantly improved the survival of mice. Furthermore, MDSC transfer increased CD4⁺ T cell and eosinophil infiltration into the lungs and decreased interleukin-6 and tumor necrosis factor-α levels in the bronchoalveolar lavage fluid. However, the viral load did not significantly decrease; this suggests that MDSCs affect virus clearance. Inducible nitric oxide synthase (iNOS) is a key factor responsible for the immunosuppressive activity of MDSCs. However, the transfer of Nos2-deficient MDSCs can decrease PR8 infection-induced mortality; nevertheless, the absence of iNOS in MDSCs did not affect the infiltration of inflammatory cells into the lung, suggesting that MDSCs function independently of their iNOS expression and downstream pathways. Taken together, our findings suggest that transferred MDSCs decrease IAV disease-induced mortality in vivo in an iNOS-independent manner. The adoptive cellular transfer of MDSCs may be an attractive therapeutic strategy for IAV infections.