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Describes a simple nomenclature for defects on metal-oxide-semiconductor (MOS) devices. Outline of the revised nomenclature; Discussion of three classes of physical models of border traps; Details of the long-term buildup and annealing of radiation-induced trapped charge in non-radiation-hardened MOS transistors.

We examine the total-dose radiation response of capacitors and transistors with stacked Al&sub2;O&sub3; On oxynitride gate dielectrics with Al and poly-Si gates after irradiation with 10 keV X-rays. The midgap voltage shift increase monotonically with dose and depends strongly on both Al&sub2;O&sub3; and SiOxNy thickness! The thinnest dielectrics, of most interest to industry, are extrenely hard to ionizing irradiation, exhibiting only ∼50 mV of shift at a total dose of 10 Mrad(SiO&sub2;) for the worst case bias condition. Oxygen anneals are found to improve the total dose radiation response by ∼SO% and induce a small amount of capacitance-voltage hysteresis. Al&sub2; O&sub3; /SiOxNy dielectrics which receive a ∼1000°C dopaut activation anneal trap ∼12% more of the initial charge than films annealed at 550°C. Charge pumping measurements show that the interface trap density decreases with dose up to 500 krad(SiO&sub2;). This surprising result is discussed with respect to hydrogen effects in alternative dielectric materials, and may be the result of radiation-induced hydrogen passivation of some of the near-interfacial defects in these gate dielectrics. [ABSTRACT FROM AUTHOR]

Presents a study that examined the mechanism of the reliability degradation of dielectric films due to high-energy ion irradiation using a percolation approach. Analysis of parameters that affect postirradiation reliability degradation; Investigation of the enhancement of the reliability of degradation due to increasing ion fluence incident; Results and implications.

A procedure for quantifying whole-body tremors in mice was developed. Displacement of a free-floating platform by animal movement created a change in resistance across a strain gauge. The resulting resistive changes were assessed as voltage fluctuations by a wheatstone bridge and converted into an intensity-frequency profile by a series of calculations involving Fourier transformations. Movement profiles of normal mice were characterized by high-intensity, low-frequency peaks. Administration of oxotremorine, 2.5 mg/kg, ip, produced numerous high-frequency, high-intensity peaks within 5 min of administration. The peak frequency at 5 min after oxotremorine was approximately 15 Hz, and within 30 min the intensity-frequency profile had returned to control levels. In dose-response studies, a slight decrease in exploratory activity and initiation of low-level tremors was observed after 0.5 mg/kg. The most severe tremors were detected after a dose of 1.0 mg/kg. The peak frequency remained at approximately 15 Hz at 1.0 to 5.0 mg/kg, but varied greatly in intensity. This study describes an inexpensive, quantitative, sensitive, and rapid technique for quantifying tremors in mice.

The effect of cyanide on whole-brain calcium levels was determined in mice administered KCN and correlated with the neurotoxic signs manifested during acute cyanide poisoning. KCN (10mg/kg, sc) significantly increased whole-brain total calcium levels from 48.1 +/- 1.8 to 66.5 +/- 3.9 micrograms/g dry wt within 15 min after administration. The levels remained elevated for 3 hr and returned to control readings after 12 hr. Dose-response studies revealed KCN, at doses of 10-15 mg/kg, produced significant elevations of whole-brain calcium 30 min after administration. No measurable effect was obtained from lower doses which suggested a threshold effect. Pretreatment 15 min before KCN with diltiazem, a calcium channel blocker, prevented the cyanide-induced rise in whole-brain total calcium. Cyanide-induced tremors, which are centrally mediated symptoms of intoxication, were quantified and correlated with the observed changes in whole-brain calcium. Tremors were detected at 10 and 12 mg/kg KCN and peak intensity was observed at 15 min postcyanide. Pretreatment with diltiazem markedly attenuated the cyanide-induced tremors. It appears that a correlation exists between cyanide-induced change in whole-brain calcium and tremors. This study suggests that intraneuronal calcium may play an important role in mediating cyanide neurotoxicity and calcium channel blocking agents may be useful in limiting the severity of the centrally mediated symptoms of acute cyanide intoxication.