Olfactory Facilitation of Takeover Performance in Highly Automated Driving.

OBJECTIVE: This study aims to quantify the impact of olfactory stimulation and takeover modality on the performance of takeovers in conditionally automated driving. BACKGROUND: Takeover requests are important for the safety of automated vehicles. The reaction time and subsequent performance of drivers in the takeover process are crucial for safety. In this study, peppermint was adopted as an auxiliary modality to the tactile and auditory design of takeover requests. METHODS: Sixty participants took part in the experiment, which required participants to avoid a stalled vehicle after they were awoken from a state of light sleep by a takeover request. Takeover modality (tactile, auditory, and combined) was the within-subjects factor. In the between-subjects design, half of the participants received a peppermint odor stimulation when the takeover request occurred, and the other half received a placebo (air). RESULTS: The presence of peppermint odor did not influence the reaction time, but participants did show signs of being more alert afterwards. For the moment of takeover, use of the auditory modality had a significant positive effect on reaction time compared to the tactile conditions. CONCLUSION: Peppermint odor had a positive impact on drivers' takeover quality when engaged in nondriving-related activities such as light sleep, and the takeover request modalities were shown to be crucial for a safe and successful takeover. APPLICATION: The results will be useful as a reference for developers of automated driving systems to design human-machine interfaces, shorten the driver's reaction time, and improve takeover quality.

Mesenchymal Wnt/ß-catenin signaling induces Wnt and BMP antagonists in dental epithelium.

Previous studies indicated that the elevated mesenchymal Wnt/ß-catenin signaling deprived dental mesenchyme of odontogenic fate. By utilizing ex vivo or pharmacological approaches, Wnt/ß-catenin signaling in the developing dental mesenchyme was suggested to suppress the odontogenic fate by disrupting the balance between Axin2 and Runx2. In our study, the Osr2-creKI; Ctnnb1ex3f mouse was used to explore how mesenchymal Wnt/ß-catenin signaling suppressed the odontogenic fate in vivo. We found that all of the incisor and half of the molar germs of Osr2-creKI; Ctnnb1ex3fmice started to regress at E14.5 and almost disappeared at birth. The expression of Fgf3 and Msx1 was dramatically down-regulated in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor and molar mesenchyme, while Runx2transcription was only diminished in incisor mesenchyme. Intriguingly, in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor epithelium, the expression of Noggin was activated, while Shh was abrogated. Similarly, the Wnt and BMP antagonists, Ectodin and Noggin were also ectopically activated in the E14.5 Osr2-creKI; Ctnnb1ex3f molar epithelium. Recombination of E13.5 Osr2-creKI; Ctnnb1ex3f molar mesenchyme with E10.5 and E13.5 WT dental epithelia failed to develop tooth. Taken together, the mesenchymal Wnt/ß-catenin signaling resulted in the loss of odontogenic fate in vivo not only by directly suppressing odontogenic genes expression but also by inducing Wnt and BMP antagonists in dental epithelium.

Persistent Wnt/ß-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme.

Tooth development is accomplished by a series of epithelial-mesenchyme interactions. Epithelial Wnt/ß-catenin signaling is sufficient to initiate tooth development by activating Shh, Bmps, Fgfs and Wnts in dental epithelium, which in turn, triggered the expression of odontogenic genes in the underlying mesenchyme. Although constitutive activation of Wnt/ß-catenin signaling in oral ectoderm resulted in the continuous tooth formation throughout the life span, if the epithelial Wnt/ß-catenin signaling could induce the mesenchyme other than oral mesenchyme still required to be elucidated. In this study, we found that in the K14-cre; Ctnnb1ex3f mice, the markers of dental epithelium, such as Pitx2, Shh, Bmp2, Fgf4, and Fgf8, were not only activated in the oral ectoderm, but also in the cheek epithelium. Surprisingly, the underlying cheek mesenchymal cells were elongated and expressed Dspp. Further investigations detected that the expression of Msx1 and Runx2 extended from oral to cheek mesenchyme. These findings suggested that epithelial Wnt/ß-catenin signaling was capable of inducing Dspp expression in non-dental mesenchyme. Moreover, Dspp expression in the K14-cre; Ctnnb1ex3f oral mesenchyme was activated earlier than that in the wild type littermates. In contrast, although the elongated oral epithelial cells were detected in the K14-cre; Ctnnb1ex3f mice, the Amelogenin expression was suppressed. The differential effects of the persistent epithelial Wnt/ß-catenin signaling on ameloblast and odontoblast differentiation might result from the altered BMP signaling. In summary, our findings suggested that the epithelial Wnt/ß-catenin signaling could induce craniofacial mesenchyme into odontogenic program and promote odontoblast differentiation.