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The cyclization of allylic thioamides is postulated to operate via a modified mechanism in which oxidation of the thioamide, rather than the alkene, is responsible for the observed reactivity.
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The relationship is postulated to follow the Mooney Rivlin function.
These rapid actions of corticosteroids are thought to operate either at the pituitary (11, 12) or suprapituitary levels (13, 14) and have been postulated to play important roles both in terminating the response to acute stressors (15– 17) and in generating the ultradian pattern of basal HPA activity (18, 19).
Organizational factors have been postulated to be a major reason.
The growth is postulated to occur in two stages.
Then, two possible explanations were postulated to explain the results.
Epigenetic mechanisms are postulated to mediate migraine susceptibility.
These changes were postulated to result in degraded electrocoating protectiveness.
Three hypotheses may be postulated to explain these data.
It was postulated to initiate and regulate membrane fusion.
Several possible mechanisms could be postulated to explain these findings.
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