Narrow Results

Investigation of the radiation-induced bystander effect plays an important role in the understanding of the mechanisms of radiation response after low-dose irradiation. Sphingomyelinase (SMase) was activated by radiation and required the metal element for its activation. For further elucidation of the bystander effect, we investigated the relationship between its induction by acid SMase and a factor secreted from the irradiated tumor cells. In the cell culture medium transfer experiment after irradiation at a dose of 0.1 Gy, cell death was induced in non-irradiated cells. However, when cells received prior treatment with SMase inhibitor, cell death was not induced. When fluctuations in the activation of SMase and metal elements were detected, both intracellularly and extracellularly after irradiation, an increase in SMase activity and Zn concentration occurred within the cells at 5 min and outside of the cells at 15 min after irradiation. This increase in zinc concentration at 15 min after irradiation was suppressed by treatment with SMase inhibitor. These results suggest that activation of SMase, which is related to the bystander effect, is dependent on zinc.

Although Astragalus polysaccharide (APS) has been shown to have various pharmacological effects, there have been no studies concerning the inhibitory effects of APS on the radiation-induced bystander effects (RIBE). The aim of this study was to investigate whether APS could suppress RIBE damage by inhibiting cell growth, micronucleus (MN) formation and 53BP1 foci number increased in bone marrow mesenchymal stem cells (BMSCs), named bystander cells, as well as to explore its mechanism. In this study, APS decreased proliferation and colony rate of bystander cells by inducing cell cycle arrest at G1 phase via extrinsic and intrinsic DNA damage. Regarding mechanism, APS inhibited mitogen-activated protein kinase (MAPK) signal pathway by down-regulating the expression of the key proteins, phosphorylated JNK (p-JNK), phosphorylated ERK (p-ERK) but not phosphorylated P38 (p-P38), and down-regulating their downstream function protein and molecule, cyclooxygenase-2 (COX-2) and reactive oxygen species (ROS). Moreover, in bystander cells, APS inhibits expression of transforming growth factor $\beta$ receptor II (TGF-$\beta$R II), a cell membrane receptor, resulting in lower ROS production and secretion via TGF-$\beta$R-JNK/ERK-COX-2/ROS not P38 signaling. They gave a hint that the decreased RIBE damage induced by APS treatment involved TGF-$\beta$R-JNK/ERK-COX-2/ROS down-regulation.

Everyone has a role to play in the fight against the spread of fake news. While there are many actions that members of the community can do to intervene in the spread of fake news (e.g., flagging on social media platforms, warning others), most of them choose not to do so. This is a concern as the number of fake news, which is propagating online, shows no signs of abating. Hence, this exploratory study aims to identify factors that influence people’s decision to not intervene in the spread of fake news. Utilizing insights from extant research on fake news and bystander intervention model, a 22-item survey was created by the research team to understand participants’ perceptions toward stopping the spread of fake news, and measure their willingness to curb the spread of fake news. Implications for countering fake news will also be identified.