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The phase-transformation temperatures of a nickel-titanium-based shape-memory alloy (SMA) were initially evaluated under stress-free conditions by the differential scanning calorimetric (DSC) technique. Results show that the phase-transformation temperature is significantly higher for the transition from detwinned martensite to austenite than for that from twinned martensite (or R phase) to austenite. To further examine transformation temperatures as a function of initial state, a tensile-test apparatus with in-situ electrical resistance (ER) measurements was used to evaluate the transformation properties of SMAs at a variety of stress levels and initial compositions. The results show that stress has a significant influence on the transformation of detwinned martensite, but a small influence on the R-phase and twinned martensite transformations. The ER changes linearly with strain during the transformations from both kinds of martensite to austenite. The linearity between the ER and strain during the transformation from detwinned martensite to austenite is not affected by the stress, facilitating application to control algorithms. A revised phase diagram is drawn to express these results.

Nitric oxide (NO) has been shown to be an important mediator in several forms of neurotoxicity. We previously reported that NO alters intracellular Ca2+ concentration ([Ca2+]i) homeostasis in cultured hippocampal neurons during 20‐min exposures. In this study, we examine the relationship between late alterations of [Ca2+]i homeostasis and the delayed toxicity produced by NO. The NO‐releasing agent S‐nitrosocysteine (SNOC; 300 µM) reduced survival by about one half 1 day after 20‐min exposures, as did other NO‐releasing agents. SNOC also was found to produce prolonged elevations of [Ca2+]i, persisting at 2 and 6 h. Hemoglobin, a scavenger of NO, blocked both the late [Ca2+]i elevation and the delayed toxicity of SNOC. Removal of extracellular Ca2+ during the 20‐min SNOC treatment failed to prevent the late [Ca2+]i elevations and did not prevent the delayed toxicity, but removal of extracellular Ca2+ for the 6 h after exposure as well blocked most of the toxicity. Western blots showed that SNOC exposure resulted in an increased proteolytic breakdown of the structural protein spectrin, generating a fragment with immunoreactivity suggesting activity of the Ca2+‐activated protease calpain. The spectrin breakdown and the toxicity of SNOC were inhibited by treatment with calpain antagonists. We conclude that exposures to toxic levels of NO cause prolonged disruption of [Ca2+]i homeostatic mechanisms, and that the resulting persistent [Ca2+]i elevations contribute to the delayed neurotoxicity of NO.