Publications by authors named "C Kawai"

Noise from unmanned aerial vehicles, commonly referred to as "drones," will likely shape our acoustic environment in the near future. Yet, reactions of the population to this new noise source are still little explored. The objective of this study was to investigate short-term noise annoyance reactions to drones in a controlled laboratory experiment.

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Estimating the direction of functional connectivity (FC) can help further elucidate complex brain function. However, the estimation of directed FC at the voxel level in fMRI data, and evaluating its performance, has yet to be done. We therefore developed a novel directed seed-based connectivity analysis (SCA) method based on normalized pairwise Granger causality that provides greater detail and accuracy over ROI-based methods.

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Traumatic brain injury (TBI) has been found to be associated with certain peripheral organ injuries; however, a few studies have explored the chronological influences of TBI on multiple organs and the systemic effects of therapeutic interventions. Particularly, high-mobility group box 1 (HMGB1) is a potential therapeutic target for TBI; however, its effects on peripheral organs remain unclear. Therefore, this study aimed to determine whether severe TBI can lead to multiple organ injury and how HMGB1 inhibition affects peripheral organs.

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This paper introduces a methodology tailored to capture, post-process, and replicate audio-visual data of outdoor environments (urban or natural) for VR experiments carried out within a controlled laboratory environment. The methodology consists of 360 video and higher order ambisonic (HOA) field recordings and subsequent calibrated spatial sound reproduction with a spherical loudspeaker array and video played back via a head-mounted display using a game engine and a graphical user interface for a perceptual experimental questionnaire. Attention was given to the equalisation and calibration of the ambisonic microphone and to the design of different ambisonic decoders.

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Compared with naïve B cells, the B cell receptor (BCR) signal in germinal center (GC) B cells is attenuated; however, the significance of this signaling attenuation has not been well defined. Here, to investigate the role of attenuation of BCR signaling, we employed a Csk mutant mouse model in which Csk deficiency in GC B cells resulted in augmentation of net BCR signaling with no apparent effect on antigen presentation. We found that Csk is required for GC maintenance and efficient antibody affinity maturation.

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