Shinrin-yoku or forest bathing refers to a therapeutic, immersive nature experience that aids to improve well-being. The goal of the current research was to compare the effects of a physical urban nature versus virtual nature experience on stress, affect, vitality, and restoration. Previous research suggested that an immersive nature experience—such as shinrin-yoku—can be beneficial for health, but direct comparisons between physical and virtual reality (VR) experiences are scarce. In the current study, fifty participants navigated self-paced through a forest scene that was either an urban physical forest or an immersive VR forest with similar characteristics as the physical one. Before and after the intervention, we measured positive and negative affect, subjective vitality, and perceived daily stress. After the intervention, we measured perceived restorative outcomes. Results revealed that both VR and physical nature experience resulted in expected effects on well-being indicators: Affect was more positive and less negative, subjective vitality increased slightly, and stress decreased slightly after both interventions. There were no significant differences between the two settings on any of the variables, but slightly stronger effect sizes over time within the physical condition. Overall, these findings suggest that immersive VR nature experiences can have restoration effects similar to physical nature experiences, suggesting intervention strategies when physical nature options are scarce.
Nature experiences usually lead to restorative effects, such as positive affective states and reduced stress. Even watching nature compared to urban images, which are known to differ in several image properties that are processed at early stages, can lead to such effects. One potential pathway explaining how the visual input alone evokes restoration is that image properties processed at early stages in the visual system evoke positive associations. To study these automatic bottom-up processes and the role of lower-level visual processing involved in the restoring effects of nature, we conducted two studies. First, we analyzed nature and urban stimuli for a comprehensive set of image properties. Second, we investigated implicit associations in a dichotomous set of nature and urban images in three domains, namely, valence, mood, and stress restoration. To examine the role of lower-level processing in these associations, we also used stimuli that lacked the spatial information but retained certain image properties of the original photographs (i.e., phase-scrambled images). While original nature images were associated with “good,” “positive mood,” and “restoration,” urban images were associated with “bad” and “stress.” The results also showed that image properties differ between our nature and urban images and that they contribute to the implicit associations with valence, although spatial information and therefore recognition of the environment remained necessary for positive associations. Moreover, lower-level processed image properties seem to play no or only minor roles for associations with mood and stress restoration.
Adaptive immune responses are induced in liver after major stresses such as hemorrhagic shock (HS) and trauma. There is emerging evidence that the inflammasome, the multiprotein platform that induces caspase-1 activation and promotes interleukin (IL)-1β and IL-18 processing, is activated in response to cellular oxidative stress, such as after hypoxia, ischemia and HS. Additionally, damage-associated molecular patterns, such as those released after injury, have been shown to activate the inflammasome and caspase-1 through the NOD-like receptor (NLR) NLRP3. However, the role of the inflammasome in organ injury after HS and trauma is unknown. We therefore investigated inflammatory responses and end-organ injury in wild-type (WT) and caspase-1 -/-mice in our model of HS with bilateral femur fracture (HS/BFF). We found that caspase-1 -/-mice had higher levels of systemic inflammatory cytokines than WT mice. This result corresponded to higher levels of liver damage, cell death and neutrophil influx in caspase-1 -/-liver compared with WT, although there was no difference in lung damage between experimental groups. To determine if hepatoprotection also depended on NLRP3, we subjected NLRP3 -/-mice to HS/BFF, but found inflammatory responses and liver damage in these mice was similar to WT. Hepatoprotection was also not due to caspase-1-dependent cytokines, IL-1β and IL-18. Altogether, these data suggest that caspase-1 is hepatoprotective, in part through regulation of cell death pathways in the liver after major trauma, and that caspase-1 activation after HS/BFF does not depend on NLRP3. These findings may have implications for the treatment of trauma patients and may lead to progress in prevention or treatment of multiple organ failure (MOF).
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