The Differential Effects of Multisensory Attentional Cues on Task Performance in VR Depending on the Level of Cognitive Load and Cognitive Capacity.

As the utilization of VR is expanding across diverse fields, research on devising attentional cues that could optimize users' task performance in VR has become crucial. Since the cognitive load imposed by the context and the individual's cognitive capacity are representative factors that are known to determine task performance, we aimed to examine how the effects of multisensory attentional cues on task performance are modulated by the two factors. For this purpose, we designed a new experimental paradigm in which participants engaged in dual (N-back, visual search) tasks under different levels of cognitive load while an attentional cue (visual, tactile, or visuotactile) was presented to facilitate search performance. The results showed that multi-sensory attentional cues are generally more effective than uni-sensory cues in enhancing task performance, but the benefit of multi-sensory cues changes according to the level of cognitive load and the individual's cognitive capacity; the amount of benefit increases as the cognitive load is higher and the cognitive capacity is lower. The findings of this study provide practical implications for designing attentional cues to enhance VR task performance, considering both the complexity of the VR context and users' internal characteristics.

Lactobacillus plantarum Metabolites Elicit Anticancer Effects by Inhibiting Autophagy-Related Responses.

Lactobacillus plantarum (L. plantarum) is a probiotic that has emerged as novel therapeutic agents for managing various diseases, such as cancer, atopic dermatitis, inflammatory bowel disease, and infections. In this study, we investigated the potential mechanisms underlying the anticancer effect of the metabolites of L. plantarum. We cultured L. plantarum cells to obtain their metabolites, created several dilutions, and used these solutions to treat human colonic Caco-2 cells. Our results showed a 10% dilution of L. plantarum metabolites decreased cell viability and reduced the expression of autophagy-related proteins. Moreover, we found co-treatment with L. plantarum metabolites and chloroquine, a known autophagy inhibitor, had a synergistic effect on cytotoxicity and downregulation of autophagy-related protein expression. In conclusion, we showed the metabolites from the probiotic, L. plantarum, work synergistically with chloroquine in killing Caco-2 cells and downregulating the expression of autophagy-related proteins, suggesting the involvement of autophagy, rather than apoptosis, in their cytotoxic effect. Hence, this study provides new insights into new therapeutic methods via inhibiting autophagy.

Modulation of Intestinal Epithelial Permeability via Protease-Activated Receptor-2-Induced Autophagy.

Protease-activated receptor 2 (PAR2) alleviates intestinal inflammation by upregulating autophagy. PAR2 also modulates tight junctions through ß-arrestin signaling. Therefore, we investigated the effect of PAR2-induced autophagy on intestinal epithelial tight junctions and permeability. RT-PCR, Western blot analysis, and immunoprecipitation were performed to investigate the underlying molecular mechanisms by which PAR2 regulates autophagy and intestinal epithelial tight junctions. Inhibition of PAR2 by GB83, a PAR2 antagonist, decreased the expression of autophagy-related and tight-junction-related factors in Caco-2 cells. Moreover, inhibition of PAR2 decreased intestinal transepithelial electrical resistance. When PAR2 was activated, intestinal permeability was maintained, but when autophagy was suppressed by chloroquine, intestinal permeability was significantly increased. In addition, the prolongation of ERK1/2 phosphorylation by PAR2-ERK1/2-ß-arrestin assembly was reduced under autophagy inhibition conditions. Therefore, PAR2 induces autophagy to regulate intestinal epithelial permeability, suggesting that it is related to the ß-arrestin-ERK1/2 pathway. In conclusion, regulating intestinal epithelial permeability through PAR2-induced autophagy can help maintain mucosal barrier integrity. Therefore, these findings suggest that the regulation of PAR2 can be a suitable strategy to treat intestinal diseases caused by permeability dysfunction.