ISAI: Investigating Solar Axion by Iron-57

The existence of the axion is a unique solution for the strong CP problem, and the axion is one of the most promising candidates of the dark matter. Investigating Solar Axion by Iron-57 (ISAI) is being prepared as a complemented table-top experiment to confirm the solar axion scenario. Probing an X-ray emission from the nuclear transitions associated with the axion-nucleon coupling is a leading approach. ISAI searches for the monochromatic 14.4 keV X-ray from the first excited state of 57Fe using a state-of-the-art pixelized silicon detector, dubbed XRPIX, under an extremely low-background environment. We highlight scientific objectives, experimental design and the latest status of ISAI

Terpinen-4-ol inhibits colorectal cancer growth via reactive oxygen species

Terpinen-4-ol (TP4O) is the main component of the essential oil extracted from Melaleuca alternifolia, known as the tea tree, of the botanical family Myrtaceae. The anticancer effects of TP4O have been reported in several cancer cell lines. Previous reports have demonstrated that TP4O exerts anticancer effects by inducing apoptotic cell death in several cell lines; however, the underlying molecular mechanisms of these effects remain unclear. In the present study, the anticancer effects of TP4O against the colorectal cancer (CRC) cell lines HCT116 and RKO were evaluated using WST‑8 and bromodeoxyuridine assays. The mechanism of cell death was investigated by the measurement of caspase‑3/7, Annexin V and lactate dehydrogenase release. Reactive oxygen species (ROS) levels induced by TP4O were evaluated by electron spin resonance and quantitative measurement of dihydroethidium. Localization of the ROS derived from mitochondria was observed by confocal inverted microscopy. Protein levels of ROS scavengers were assessed by western blotting analysis. To confirm the role of ROS, cell viability was measured in the presence of antioxidant reagents. In an in vivo xenograft model of ICR‑SCID mice implanted with HCT116 cells, 200 mg/kg TP4O was injected locally, and tumor growth was compared with that of the control. TP4O induced apoptotic cell death in HCT116 and RKO cells in a dose‑dependent manner, and TP4O also increased the levels of ROS generated by mitochondria. TP4O‑induced cell death was rescued by administration of antioxidant regents. In vivo, TP4O inhibited the proliferation of HCT116 xenografts compared with that of the control group. The results of the present study suggest that TP4O induces apoptosis in CRC cells through ROS generation. Furthermore, TP4O is potentially useful for the development of novel therapies against CRC