Enhancing safety in conditionally automated driving: Can more takeover request visual information make a difference in hazard scenarios with varied hazard visibility?

Autonomous driving technology has the potential to significantly reduce the number of traffic accidents. However, before achieving full automation, drivers still need to take control of the vehicle in complex and diverse scenarios that the autonomous driving system cannot handle. Therefore, appropriate takeover request (TOR) designs are necessary to enhance takeover performance and driving safety. This study focuses on takeover tasks in hazard scenarios with varied hazard visibility, which can be categorized as overt hazards and covert hazards. Through ergonomic experiments, the impact of TOR interface visual information, including takeover warning, hazard direction, and time to collision, on takeover performance is investigated, and specific analyses are conducted using eye-tracking data. The following conclusions are drawn from the experiments: (1) The visibility of hazards significantly affects takeover performance. (2) Providing more TOR visual information in hazards with different visibility has varying effects on drivers' visual attention allocation but can improve takeover performance. (3) More TOR visual information helps reduce takeover workload and increase human-machine trust. Based on these findings, this paper proposes the following TOR visual interface design strategies: (1) In overt hazard scenarios, only takeover warning is necessary, as additional visual information may distract drivers' attention. (2) In covert hazard scenarios, the TOR visual interface should better assist drivers in understanding the current hazard situation by providing information on hazard direction and time to collision to enhance takeover performance.

S100A8/A9 Molecular Complexes Promote Cancer Migration and Invasion via the p38 MAPK Pathway in Nasopharyngeal Carcinoma.

Nasopharyngeal carcinoma (NPC) is one type of malignancy associated with migration and invasion through a currently unclear mechanism. We previously discovered S100A8/A9 levels were roughly elevated in the plasma of NPC patients as the promising biomarkers. However, their expressions and underlying functions in NPC tissues are still unknown. In the present study, we analyzed 49 NPC tissues and 20 chronic pharyngitis (CP) tissues. Immunohistochemical staining was performed in different tissues and analyzed by the Mann-Whitney U test statistically. Transwell migration and invasion experiments were further performed to determine S100A8/A9 effects on NPC. Our results showed that S100A8/A9 in NPC tissues were significantly higher than those in CP tissues, closely associated with NPC clinical stages. Intriguingly, exogenous S100A8/A9 protein stimulation could dramatically enhance NPC migration and invasion abilities. In addition, p38 MAPK pathway blockade could diminish the migration and invasion of NPC cells stimulated by S100A8/A9 proteins. The downstream tumor invasion and migration associated proteins (e.g., MMP7) were also elevated in NPC tissues, consistent with S100A8/A9 overexpression. Taken together, our present findings suggest that the secreted soluble inflammatory factors S100A8/A9 might promote cancer migration and invasion via the p38 MAPK signaling pathway along with invasion/migration associated proteins overexpression in the tumor microenvironment of NPC. This may shed light on the mechanism understanding of NPC prognosis and provide more novel clues for NPC diagnosis and therapy.

Effects of silencing S100A8 and S100A9 with small interfering RNA on the migration of CNE1 nasopharyngeal carcinoma cells.

The calcium-binding S100 proteins are involved in functions such as cell growth, differentiation, migration, adhesion and signal transduction. S100A8 and S100A9 are highly expressed in a variety of tumor cells, and are implicated in tumor development and progression. However, the role of S100A8 and S100A9 in nasopharyngeal carcinoma (NPC) cell migration is unclear. The present study investigated the effect of S100A8 and S100A9 on migration using a NPC cell line, CNE1. The CNE1 cells were transfected with S100A8 or S100A9 small interfering RNA (siRNA). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect S100A8 and S100A9 gene expression. Following the downregulation of S100A8 or S100A9, the effects on cell migration were determined using wound-healing assays. The expression of matrix metalloproteinase-7 (MMP7), a member of the MMP family that is associated with tumor cell invasion and migration, was also detected by RT-qPCR. S100A8 and S100A9 siRNAs effectively suppressed S100A8 and S100A9 gene expression, and substantially inhibited the migration of the CNE1 cells. In addition, MMP7 expression was reduced to varying extents in S100A8 and S100A9 siRNA-treated cells compared with controls. Thus, S100A8 and S100A9 promoted the migration of CNE1 NPC cells.