The Classification of Cyclooxygenase Inhibitors

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The Classification of Cyclooxygenase Inhibitors

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Cyclooxygenase in biology and disease

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Salivary cortisol and cold pain sensitivity in female twins

BackgroundThere is a dearth of knowledge about the link between cortisol and pain sensitivity.PurposeWe examined the association of salivary cortisol with indices of cold pain sensitivity in 198 female twins and explored the role of familial confounding.MethodsThree-day saliva samples were collected for cortisol levels and a cold pressor test was used to collect pain ratings and time to threshold and tolerance. Linear regression modeling with generalized estimating equations examined the overall and within-pair associations.ResultsLower diurnal variation of cortisol was associated with higher pain ratings at threshold (p?=?0.02) and tolerance (p?<?0.01). The relationship of diurnal variation with pain ratings at threshold and tolerance was minimally influenced by familial factors (i.e., genetics and common environment).ConclusionsUnderstanding the genetic and non-genetic mechanisms underlying the link between HPA axis dysregulation and pain sensitivity may help to prevent chronic pain development and maintenance

The production of interleukin-1β from human fetal membranes is not obligatory for increased prostaglandin output

Bacterial endotoxin increased the expression of mRNA (maximal after 4 hr) for interleukin-1β (IL-1β) and the release of mature protein from intact human fetal membranes. In contrast, the change in expression of mRNA for type 2 cyclo-oxygenase (COX-2) was biphasic, with peaks after 0·5–1 hr and after 8 hr of culture. An antibody to IL-1β was without effect after 4 hr of culture, inhibited endotoxin-stimulated prostaglandin E2 (PGE2) production after 8 hr of culture, and caused a parallel decrease in the expression of mRNA for COX-2. We conclude that endotoxin induced the expression of COX-2 through IL-1β-independent and IL-1β-dependent mechanisms, and these differences are time dependent. Corticotrophin-releasing hormone (CRH) or platelet-activating factor (PAF) also increased the expression of mRNA for IL-1β and the release of IL-1β from some, but not all, fetal membranes. The antibody to IL-1β did not affect CRH-stimulated or PAF-stimulated PGE2 production or COX-2 expression. We conclude that CRH and PAF can induce the expression of IL-1β, but this is not obligatory for increased PGE2 release, and the effect of these stimuli on COX-2 expression is a direct, IL-1β-independent effect