We investigated the characteristic changes in the physiology of cybersickness when subjects were exposed to virtual reality. Sixty-one participants experienced a virtual navigation for a total of 9.5 min, and were required to detect specific virtual objects. Three questionnaires for sickness susceptibility and immersive tendency were obtained before the navigation. Sixteen electrophysiological signals were recorded before, during, and after the navigation. The severity of cybersickness experienced by participants was reported from a simulator sickness questionnaire after the navigation. The total severity of cybersickness had a significant positive correlation with gastric tachyarrhythmia, eyeblink rate, heart period, and EEG delta wave and a negative correlation with EEG beta wave. These results suggest that cybersickness accompanies the pattern changes in the activities of the central and the autonomic nervous systems.

RNA-guided endonucleases (RGENs), derived from the prokaryotic Type II CRISPR-Cas system, enable targeted genome modification in cells and organisms. Here we describe the establishment of gene-knockout mice and zebrafish by the injection of RGENs as Cas9 protein:guide RNA complexes or Cas9 mRNA plus guide RNA into one-cell-stage embryos of both species. RGENs efficiently generated germline transmittable mutations in up to 93% of newborn mice with minimal toxicity. RGEN-induced mutations in the mouse Prkdc gene that encodes an enzyme critical for DNA double-strand break repair resulted in immunodeficiency both in F0 and F1 mice. We propose that RGEN-mediated mutagenesis in animals will greatly expedite the creation of genetically engineered model organisms, accelerating functional genomic research.

In virtual reality (VR), users can experience symptoms of motion sickness, which is referred to as VR sickness or cybersickness. The symptoms include but are not limited to eye fatigue, disorientation, and nausea, which can impair the VR experience of users. Though many studies have attempted to reduce the discomfort, they produced conflicting results with varying degrees of VR sickness. In particular, a visually improved VR does not necessarily result in decreased VR sickness. To understand these unexpected results, we surveyed the causes of VR sickness and measurement of symptoms. We reorganized the causes of the VR sickness into three major factors (hardware, content, and human factors) and investigated the sub-component of each factor. We then surveyed frequently used measures of VR sickness, both subjective and objective approaches. We also investigated emerging approaches for reducing VR sickness and proposed a multimodal fidelity hypothesis to give an insight into future studies.

In order to investigate whether and how medial prefrontal cortex (mPFC) of the rat is involved in processing of information related to fear conditioning, we recorded from single units in the prelimbic and infralimbic cortex of fear-conditioned rats in response to an explicit conditional stimulus (CS; an auditory tone) or contextual cues (conditioning box). The majority of units changed their activities significantly in response to the CS in a delay or trace conditioning paradigm. Both transient and tonic activity changes, including delay cell activity, were observed as in other behavioral tasks. When exposed to the context without CS delivery, most units changed their activities as well. These results show that both tone and contextual information are processed in the rat mPFC in expectation of the delivery of an aversive stimulus (electric foot shock). Interestingly, fast spiking cells (putative inhibitory interneurons) and regular spiking cells (putative projection neurons) showed different patterns of responses. Fast spiking cells tended to show transient responses and increased their firing rates following CS presentation, whereas a complementary pattern was observed in the regular spiking cells. Our results enhance our understanding of the neural mechanisms underlying prediction of an aversive stimulus in the mPFC.

By defining the chromosomal breakpoint of a balanced t(10;12) translocation from a subject with Kallmann syndrome and scanning genes in its vicinity in unrelated hypogonadal subjects, we have identified WDR11 as a gene involved in human puberty. We found six patients with a total of five different heterozygous WDR11 missense mutations, including three alterations (A435T, R448Q, and H690Q) in WD domains important for β propeller formation and protein-protein interaction. In addition, we discovered that WDR11 interacts with EMX1, a homeodomain transcription factor involved in the development of olfactory neurons, and that missense alterations reduce or abolish this interaction. Our findings suggest that impaired pubertal development in these patients results from a deficiency of productive WDR11 protein interaction.