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We present a way of predicting spatial nonuniformity in deep reactive ion etching ͑DRIE͒. In addition to well-known feature size or aspect-ratio-dependent etch ͑ARDE͒ nonuniformity, etch rate can vary between regions of the wafer, such that supposedly identical microelectromechanical systems ͑MEMS͒ fabricated on that wafer may vary in performance or fail in use. Wafer-and die-scale uniformity may be improved by changing conditions in the etching chamber, but this usually compromises etching speed and may accentuate ARDE. An alternative approach is to lay out the patterns being etched so that they compete for reactants in a controlled way. We demonstrate a way of precharacterizing any DRIE tool plus associated "recipes" of operating parameters. Several test wafers are etched and measured, and simple data-fitting algorithms are run. The model constructed captures etch nonuniformity occurring over the diameter of a wafer plus variations caused by the localization of patterns within the wafer. Our technique models etch rate variation across experimental wafers with fitting errors of between 0.8 and 4.5% root-mean-square per wafer. Our model can then predict etch rate on a 1 mm lateral grid for any etched pattern. We envisage this method being integrated into computer-aided MEMS design systems.

Background:The mechanism of action of sweet substance-induced analgesia is thought to involve activation of the endogenous opioid system. The nitric oxide (NO) pathway has a pivotal role in pain modulation of analgesic compounds such as opioids.Objectives:We investigated the role of NO and the opioid receptor-mediated system in the analgesic effect of sucrose ingestion in mice.Materials and Methods:We evaluated the effect of intraperitoneal administration of 10 mg/kg of NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME) and 20 mg/kg of opioid receptor antagonist, naltrexone on the tail flick response in sucrose ingesting mice.Results:Sucrose ingestion for 12 days induced a statistically significant increase in the latency of tail flick response which was unmodified by L-NAME, but partially inhibited by naltrexone administration.Conclusions:Sucrose-induced nociception may be explained by facilitating the release of endogenous opioid peptides. Contrary to some previously studied pain models, the NO/cyclic guanosine monophosphate (cGMP) pathway had no role in thermal hyperalgesia in our study. We recommend further studies on the involvement of NO in other animals and pain models.

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