Two different binocular cues are known for detecting motion in depth. One is disparity change in time and the other is inter-ocular velocity difference. In contrast to the well known fact of the use of the disparity cues, no evidence of contribution of inter-ocular velocity differences for detecting motion in depth has been reported. We demonstrate that motion in depth can be seen based solely on inter-ocular velocity differences using binocularly uncorrelated random-dot kinematograms. This indicates that the visual system uses monocular velocity signals for processing motion in depth in addition to disparity change in time.
We investigated the effect of attention on the flash-lag effect (FLE) in order to determine whether the FLE can be used to estimate the effect of visual attention. The FLE is the effect that a flash aligned with a moving object is perceived to lag the moving object, and several studies have shown that attention reduces its magnitude. We measured the FLE as a function of the number or speed of moving objects. The results showed that the effect of cueing, which we attributed the effect of attention, on the FLE increased monotonically with the number or the speed of the objects. This suggests that the amount of attention can be estimated by measuring the FLE, assuming that more amount of attention is required for a larger number or faster speed of objects to attend. On the basis of this presumption, we attempted to measure the spatial spread of visual attention by FLE measurements. The estimated spatial spreads were similar to those estimated by other experimental methods.
There are two types of binocular cues available for perception of motion in depth. One is the binocular disparity change in time and the other is the velocity difference between the left and the right retinal images (inter-ocular velocity differences). We measured the luminance contrast threshold for seeing motion in depth while isolating either of the cues at various temporal modulations of velocity in the stimulus. To isolate disparity cues, dynamic random-dot stereograms were used (the disparity condition) while binocularly uncorrelated random-dot kinematograms were used to isolate velocity cues (the velocity condition). Results showed that sensitivity peaked at a temporal frequency (approximately 1 cps) in the velocity condition while the peak in the disparity condition was at the lowest frequency (0.35 cps) or at least at a frequency lower than that in the velocity condition. This suggests that the visual system has different temporal frequency properties for the velocity and disparity cues for motion in depth.
Intensive nutritional support followed by balloon dilatation is the first choice of treatment for esophageal strictures complicating recessive epidermolysis bullosa. By following this regime, invasive surgery can be avoided.
Endothelin (ET)-1 is a 21-amino acid peptide which has vasoconstrictor and growth regulatory activity. Recently, cultured keratinocytes have been reported to express ET-1 and its receptor when irradiated by ultraviolet (UV) B. In order to further understand the role of ET-1 in vivo during UVB-induced inflammation, we examined the localization, intensity and time course of the expression levels of ET-1 and its binding sites in UVB-exposed BALB/c mouse skin. Frozen and paraffin sections prepared from mouse skin 48 h after treatment with UVB irradiation (0.36 or 0.72 J/cm2) or after injection with tumor necrosis factor (TNF)-alpha (1.0 microgram) or interleukin (IL)-1 alpha (0.05 microgram) were incubated with monoclonal anti-ET-1 IgG and then visualized by peroxidase staining. In normal skin, faint ET-1 immunoreactivity was observed in the epidermis, pilosebaceous structures and blood vessels. Upon exposure to UVB irradiation or administration of TNF-alpha injection or IL-1 alpha injection, such immunoreactivity was found to be significantly enhanced. Subsequently, the frozen sections were incubated with 125I ET-1 for 30 min, and visualized by autoradiographic technique. In normal skin, ET-1 weakly bound to the skin, while UVB irradiation and TNF-alpha injection significantly enhanced ET-1 binding in the epidermis, pilosebaceous structures and blood vessels. Time course experiments (1, 2, 4 and 7 days) indicated that ET-1 immunoreactivity and ET-1 binding peaked 1 or 2 days after UVB irradiation or TNF-alpha injection. These results suggest that the up-regulated expression of ET-1 and its binding sites in the epidermis and pilosebaceous structures may act as an autocrine/paracrine factor during UVB-induced inflammation.
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