Visualization and automatic detection of defect distribution in GaN atomic structure from sampling Moiré phase.

Quantitative detection of defects in atomic structures is of great significance to evaluating product quality and exploring quality improvement process. In this study, a Fourier transform filtered sampling Moiré technique was proposed to visualize and detect defects in atomic arrays in a large field of view. Defect distributions, defect numbers and defect densities could be visually and quantitatively determined from a single atomic structure image at low cost. The effectiveness of the proposed technique was verified from numerical simulations. As an application, the dislocation distributions in a GaN/AlGaN atomic structure in two directions were magnified and displayed in Moiré phase maps, and defect locations and densities were detected automatically. The proposed technique is able to provide valuable references to material scientists and engineers by checking the effect of various treatments for defect reduction.

[Objective assessment of senile changes in visual function by visually evoked cortical potentials].

The P100 peak latency of pattern visually evoked cortical potentials (P-VECP) was found to increase and amplitude decrease in the elderly depending on stimulus conditions. Using either of these as a criterion, changes of visual function with aging were quantitatively assessed both in humans and animals. Contrast threshold was found to increase at higher spatial frequency ranges and the luminance threshold increased more than 0.8 log unit. Also, the contrast threshold increased due to a smaller pupillary area and there was progressive decrease of the temporal frequency curves with age for lower frequency ranges of less than 10 rev/sec. In addition, a sensitivity decrease for the upper visual field was detected plus blue-yellow defects and a decrease in the amplitude of accommodation. In order to exclude the effect of senile changes of the crystalline lens, the luminance threshold, the accommodation power and color sense were investigated in pseudo-phakic eyes with a posterior chamber lens. No significant differences were found between phakic and pseudo-phakic eyes. Accordingly, it was suggested that reduced transparency and yellowish changes of the crystalline lens do not essentially contribute to the loss of function in the elderly found in the present study, but the neuronal pathway was responsible. As a clinical model of senescence, cases of juvenile parkinsonism were investigated, during L-dopa treatment and after ceasing it. The deficiency of the neural-transmitter of the higher visual pathway was indicated in the elderly, also. Animal experiments on neuronal dysfunction in rats and mice suggested no aging effects in ERGs, whereas VECP peak latency for higher temporal frequencies increased with age. The assumption that the elderly changes occur at the neuronal level was supported by a loss of optic nerve fibers in mice with age. The numbers of optic nerve fibers measured were 48,115, 50,875 in the 3-month-old and 6-month-old groups, respectively, and decreased to 43,175 in the 30-month-old group. Though our results indicated the senescence of visual function at the neuronal level, it was not as much as shown by other sensory organs. It was therefore presumed that there might be a certain feed-back system from the brain to the retina.

Uveoscleral outflow following cyclodialysis in the monkey eye using a fluorescent tracer.

Cyclodialysis was performed in one eye of each of eight cynomolgus monkeys. Two days later, the intraocular pressure was 1.6 +/- 0.7 mmHg in eyes with cyclodialysis and 12.0 +/- 0.7 mmHg in fellow control eyes. 10(-4) M fluorescein-isothiocyanate dextran (70,000 molecular weight) was perfused into the anterior chamber of each eye for 30 min. The eyes were enucleated and dissected into sclera, choroid, retina, iris, and ocular fluid. Samples were homogenized and centrifuged, and the fluorescence of the supernatant was measured. Expressed as equivalent volumes of aqueous, the rate of anterior chamber movement of tracer via uveoscleral pathways was 1.40 +/- 0.17 microliter/min in cyclodialysis eyes and 0.34 +/- 0.10 microliter/min in control eyes. Cyclodialysis results in a fourfold increase in uveoscleral outflow, contributing to the observed hypotony.