Sumio Murase

Development of long-range and high-speed wireless LAN for the transmission of telemedicine from disaster areas

A computer network is indispensable for realizing the use of telemedicine. Recently, experiments to provide telemedicine to residents in remote places over a broadband Internet access have been reported. However, if a disaster were to occur with devastation over a wide mountainous area, and telephones and Internet access were to become unavailable, the provision of telemedicine for injured residents in this area becomes difficult. To solve this problem, we have developed 2.4 GHz wireless LAN units with the longest coverage in Japan to date, of 30 km plus at 54 Mbps which complies with the IEEE802.11 g standard and the Japanese radio regulations to re-establish communications temporally between disaster devastated areas and hospitals, and so on. We tested them in the disaster prevention drill with the regional fire bureau and concluded that wireless LAN units we developed can transfer high-quality video images and sound good enough for use in telemedicine.

Contribution of the stress-induced degeneration of the locus coeruleus noradrenergic neurons to the pathophysiology of depression: a study on an animal model.

A novel theory on the pathophysiology of depression would be expected to resolve a contradiction between therapeutic time lag and monoamine hypothesis. On the basis of the fact that a subgroup of depression appears during or after stress, we exposed rats to a long-term (2 weeks) forced walking stress and produced depression-model rats in one group and spontaneous recovery rats in another. The density of axon terminals of the locus coeruleus (LC) neurons in the frontal cortex stained by dopamine β-hydroxylase antiserum was lower in the depression-model rats than in the spontaneous recovery rats and in the control rats without stress. The density was higher in the model rats daily treated with imipramine than in those treated with saline. Morphological projection (MP) index (a percentage of horseradish peroxidase-positive LC cells in total number of LC cells) and electrophysiological projection index (a percentage of LC neurons activated antidromically by electrical stimulation of the cerebral cortex) were lower in the depression-model rats than in the recovery and control rats. MP index was higher in the imipramine-treated rats than that in the saline-treated rats. Electron microscopic examination of the LC disclosed such degenerative changes as low-dense areas without structure, aggregation of intracellular organs, destroyed membranes around the rough endoplasmic reticulum (rER), a decreased number of deformed subsurface cisterns, glia invaginated into the LC neurons and prominent appearance of microglia containing increased number of lipofustin or lysosome in the model rats, but not in the spontaneous recovery rats. These findings suggest that the terminals and cell bodies of the LC noradrenergic neurons degenerate in the stress-induced depression-model rats and regenerate in the imipramine-treated model rats. This degenerative change may possibly contribute to the decrease in synthesis and metabolism of noradrenaline (NA), the slowing of axonal flow, the accumulation of NA in the neurons, the decrease in discharge rate of LC neurons without stress and the increase in release of NA in response to an additional stress. It may also explain the therapeutic time lag that is required to repair the noradrenergic neurons.

Histogenesis of congenital and acquired melanocytic nevi based on histological study of lesion size and thickness

The histogenesis of melanocytic nevi is poorly understood. It is important to determine the differences and similarities in histogenesis between congenital and acquired nevi. To clarify the histogenic differences between acquired melanocytic nevi (AMN) and congenital melanocytic nevi (CMN), diameter and depth of nevus cells (tumor thickness) were examined in histological specimens from 80 cases of CMN and 71 cases of AMN, and these nevi were classified according to Mark’s pathological CMN criteria. In all cases, giant CMN nevus cells were found in the lower marginal portion of excised specimens. The mean diameter and lesional thickness were significantly higher in CMN than in AMN. AMN diameter showed a significant correlation (r = 0.567, P < 0.05) with lesional thickness, while no such relation was observed in CMN. In addition, a significant correlation between lesion diameter and thickness was observed in small (<10 mm) non‐Mark’s type CMN (r = 0.626, P < 0.05). CMN may be classified into three subtypes: (i) caused by increased proliferation of melanoblasts during the course of migration from the neural crest to the epidermis; (ii) proliferation of nevus cells after arrival at the epidermis, and nevus cell distribution affected by adnexa and dermal differentiation; and (iii) arising after completion of skin development before birth.