The Application of a Computerized Cognitive Screening Tool in Naval Aviators.

INTRODUCTION: The CogScreen-Aeromedical Edition (CogScreen-AE) is a computerized neurocognitive assessment screening tool developed for the Federal Aviation Administration as a rapid, reliable means of measuring neurocognitive deficiency in civilian airline pilots. This has potential use and assessment of military aviators flying high performance aircraft under extreme conditions; however, no data exist on how the dynamic flight environment affects CogScreen-AE scores. The objectives of this study were to determine what changes in performance on CogScreen-AE scores are seen post-flight in Naval Aviators flying high performance aircraft and to determine the potential for use of CogScreen-AE as a screening tool to evaluate degree of impairment, recovery from neurological illness, and return to duty status of a military aviator. MATERIALS AND METHODS: Repeated measures, within-subjects experimental design with three CogScreen-AE administrations-introduction session, preflight session, and postflight session. An experimental study group was exposed to dynamic flight between preflight and postflight sessions, while a control group flew a desktop computer flight simulator between sessions. Data were analyzed by mixed model ANOVA using Statistical Package for the Social Sciences to compare CogScreen-AE pre- and postflight performance on 5 composite scores of variables that account for 45% of the variance in predicting flight performance. RESULTS: Preflight versus postflight scores demonstrated no significant differences in performance attributable to flight in high performance aircraft. CONCLUSIONS: The CogScreen-AE performance is shown to be consistent preflight to post-flight. These data show that CogScreen-AE may be a reliable clinical instrument for assessing aviators' cognitive function with regard to return to flight duty decision-making. We anticipate future work in determining how CogScreen-AE can be utilized in the operational environment and documenting recovery from neurologic illness.

Effects of ascorbic acid on carcinogenicity and acute toxicity of nickel subsulfide, and on tumor transplants growth in gulonolactone oxidase knock-out mice and wild-type C57BL mice.

The aim of this study was to test a hypothesis that ascorbate depletion could enhance carcinogenicity and acute toxicity of nickel. Homozygous L-gulono--lactone oxidase gene knock-out mice (Gulo-/- mice) unable to produce ascorbate and wild-type C57BL mice (WT mice) were injected intramuscularly with carcinogenic nickel subsulfide (Ni3S2), and observed for the development of injection site tumors for 57 weeks. Small pieces of one of the induced tumors were transplanted subcutaneously into separate groups of Gulo-/- and WT mice and the growth of these tumors was measured for up to 3 months. The two strains of mice differed significantly with regard to (1) Ni3S2 carcinogenesis: Gulo-/- mice were 40% more susceptible than WT mice; and (2) transplanted tumors development: Gulo-/- mice were more receptive to tumor growth than WT mice, but only in terms of a much shorter tumor latency; later in the exponential phase of growth, the growth rates were the same. And, with adequate ascorbate supplementation, the two strains were equally susceptible to acute toxicity of Ni3S2. Statistically significant effects of dietary ascorbate dosing levels were the following: (1) reduction in ascorbate supplementation increased acute toxicity of Ni3S2 in Gulo-/- mice; (2) ascorbate supplementation extended the latency of transplanted tumors in WT mice. In conclusion, the lack of endogenous ascorbate synthesis makes Gulo-/- mice more susceptible to Ni3S2 carcinogenesis. Dietary ascorbate tends to attenuate acute toxicity of Ni3S2 and to extend the latency of transplanted tumors. The latter effects may be of practical importance to humans and thus deserve further studies.