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A new cost-effective process to fabricate aluminide coatings was developed. Coating layers consisting of nickel aluminides could be formed by electrodeposition of Al layers from a dimethylsulfone-AlCl₃ electrolyte on Ni substrates and subsequent annealing in air or vacuum at temperatures of 700–1150°C. Analysis of the intermetallic layers by XRD, SEM and EDX indicated the formation of Al₃Ni and Al₃Ni₂ at 700°C, AlNi at 900°C and 1000°C, and AlNi and AlNi₃ at 1150°C. The Annealing atmosphere did not affect the resulting intermetallic products.

The ability of dimethyl sulfoxide to inhibit insulin-stimulated glucose oxidation is not the result of the increased lipolysis observed in the absence of insulin with DMSO. Free fatty acids have been shown to inhibit insulin action on fat cells but DMSO still inhibited insulin-stimulated glucose oxidation under conditions (0.56 M DMSO plus insulin) in which there was no lipolytic action of DMSO. The lipolytic effect of DMSO and its ability to potentiate lipolysis due to agents such as noreipinephrine or glucagon may result from DMSO's potentiation of cyclic AMP accumulation due to these agents. Cyclic AMP accumulation due to DMSO alone was slight, but there was a potentiation of the rise in cyclic AMP due to norepinephrine or norepinephrine plus theophylline. The mechanism by which DMSO increased cyclic AMP accumulation due to catecholamines could result from stimulation of adenylate cyclase activity. However, DMSO did not stimulate adenylate cyclase activity caused by catecholamines in the presence of a phosphodiesterase inhibitor. A much more likely effect predominates in intact cells, the activation of lipolysis by DMSO may be secondary to an elevation of cyclic AMP accumulation resulting from inhibition of cyclic AMP phosphodiesterase., This article is from 'Conference on Biological Actions and Medical Applications of Dimethyl Sulfoxide (DMSO), 15-17 September 1982,' AD-A133 175. p135-140.