Thin alloy films of Pd and Ni (8%<Ni<20% in at. %) formed by dual-electron-beam evaporation techniques have been found to give durable and quickly reversible detectors of high H2 concentrations (pH2 0.1%–100%, 0.7–700 Torr) near 1 atm and 300 K, including accurate determinations of pH2 around the lower explosive limit of 4% in air. The addition of Ni suppresses the α to β phase transition found in pure Pd under these conditions. The measurement of resistivity changes in the thin films along with flatband shifts of metal-oxide-semiconductor capacitors on the same Si wafer gives accurate values of pH2 over more than six decades.

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The addition of Ag to Pd in the gate metal of a metal-insulator-semiconductor gas sensing diode can improve the performance and change the selectivity of the sensors for a variety of reactions. Data on the response of diodes with 12 different ratios of Ag to Pd in alloys and layers of Pd and Ag to hydrogen and other gases are reported. Diodes with as much as 32% Ag respond very well to H2 gas and the films are much more durable to high hydrogen exposure than pure Pd films. Improvements in the rate of response and aging behavior are found for certain Ag combinations; others give poorer performance. The presence of Ag on the surface changes the catalytic activity in some cases and examples of H2 mixed with O2 and/or NO2, propylene oxide, ethylene, and formic acid are given. Such selectivity forms the basis for miniature chemical sensor arrays which could analyze complex gas mixtures.

Despite greater than 23 years of study, an incomplete understanding of the etiology, epidemiology and pathogenesis of Reye's syndrome persists. Better understanding of the disease has been hampered by the lack of a good animal model on which hypotheses of its pathogenesis could be tested. Human studies indicate that a primary mitochondrial injury may lead to complex metabolic disturbances that produce the observed pathophysiology. Specific directions regarding avenues for future research should pursue two lines: a good animal model still needs to be developed in which the biochemical and morphologic alterations identified in Reye's syndrome are duplicated. This model should include an antecedent viral illness but may not require aspirin exposure as an essential ingredient. With the identification of a satisfactory model, specific questions about the roles of environmental toxins or medications may be answered. Study of noncomatose cases of Reye's syndrome should continue. The specific emphasis should be to delineate what factors (NH3, free fatty acids and dicarboxylic acids) may be implicated in the pathogenesis of the CNS disease with the hopes of devising strategies for more effective treatment of encephalopathy and its attendant morbidity and mortality.