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D O Brown

Publications and source records attributed to D O Brown.

6 recordsLinked to original sources

Characteristics of microwave evoked body movements in mice.

Microwave evoked body movements were studied in mice. A resonant cavity was used to provide head and neck exposure of the mouse to pulsed and gated continuous wave (CW) 1.25 GHz microwaves. No difference in response to pulsed and gated CW stimuli of equal average power was found. The incidence of the microwave evoked body movements increased proportionally with specific absorption (dose) when the whole-body average specific absorption rate was at a constant level (7300 W/kg). Under a constant average specific absorption rate, the response incidence reached a plateau at 0.9 kJ/kg. For doses higher than 0.9 kJ/kg, response incidence was proportional to the specific absorption rate and reached a plateau at 900 W/kg. Body movements could be evoked by a single microwave pulse. The lowest whole-body specific absorption (SA) tested was 0.18 kJ/kg, and the corresponding brain SA was 0.29 kJ/kg. Bulk heating potentials of these SAs were less than 0.1 degree C. For doses higher than 0.9 kJ/kg, the response incidence was also proportional to subcutaneous temperature increment and subcutaneous heating rate. The extrapolated absolute thresholds (0% incidence) were 1.21 degrees C temperature increment and 0.24 degree C/s heating rate. Due to high subcutaneous heating rates, these microwaves must be perceived by the mouse as an intense thermal sensation but not a pain sensation because the temperature increment was well below the threshold for thermal pain. Results of the present study should be considered in promulgation of personnel protection guideline against high peak power but low average power microwaves.

Analysis of Variance↗

Abnormal cardiovascular responses induced by localized high power microwave exposure.

A hypothesis of microwave-induced circulatory under perfusion was tested in ketamine anesthetized rats whose heart rate, mean arterial pressure, pulse pressure, respiration rate, and body temperatures were monitored continuously. Fifty-eight ventral head and neck exposures in a waveguide consisted of sham-exposure and exposure to continuous wave (CW) and pulsed 1.25 GHz microwaves for 5 min. The 0.5 Hz (10 microseconds, 2 W average) and 16 Hz (1 microsecond, 6.4 W average) pulse-modulated microwaves were delivered at 400 kW peak power. The CW microwaves were 2 and 6.4 W. The average specific absorption rate was 4.75 W/kg per watt transmitted in the brain and 17.15 W/kg per watt transmitted in the neck. Respiration rate and mean arterial pressure were not altered. Changes in heart rate and pulse pressure were observed in rats exposed to higher power (16 Hz pulses and 6.4 W CW) but not to the lower average power microwaves (0.5 Hz pulses and 2 W CW). Depression of pulse pressure, an indication of a decrease in stroke volume, and increased (tachycardia) or decreased (bradycardia) heart rate were noted in presence of whole-body hyperthermia. The cardiac output of those animals exposed to higher average power microwaves was considered to be below normal as hypothesized. Decreased cardiac output and normal mean arterial pressure resulted in an increase in the total peripheral resistance which was contrary to the anticipated thermal response of animals.

Animals↗

In vitro studies of microwave-induced cataract. II. Comparison of damage observed for continuous wave and pulsed microwaves.

Depth of damage caused by pulsed (PU) and continuous wave (CW) microwaves was estimated by scanning electron microscopy in rat lenses fixed immediately, after irradiation in vitro in circulating thermostatically controlled buffered saline. Pulses of 10 microseconds width and 24 kW peak power were delivered to the lens at different repetition rates in order to permit the same total energy to be delivered during 6, 20 or 60 min of irradiation at specific absorption rate (SAR) values of 0, 5.75, 11.5, 23, 69, 231 and 750 mW g-1; total energy [power (pow) x time] deposited in the lens was 0, 0.23, 0.46, 1.38, 4.6, and 15 W min g-1. Damage (granular degeneration of cells at the lens equator) was measured at the apex of penetration of the degeneration. The depth of degeneration (dep) of Pu or CW was compared either: (1) by a one-way analysis of variance (ANOVA) for the CW data alone and the 11 combinations of (pow x time); or (2) by using two alternative models to fit the data, to permit experimental distinguishment between: (a) reciprocal effects of pow x time; and (b) separate effects. Using the ANOVA analysis, the Pu mode of irradiation resulted in more damage at the same average power for every combination tested except one (23 mW g-1, 6 min). Although the separate-effects models explained more of the variation in depth of damage, the reciprocal effects model may provide an adequate fit for practical purposes and has the advantage of greater simplicity. For both models, the pulsed irradiation mode produced 4.7 times the depth of damage caused by CW irradiation. These results are discussed in relation to previous Pu-CW comparisons. It is proposed that this additional damage at the same average power is caused by thermoelastic expansion (TEE).

Animals↗