15-epi-lipoxin A4-mediated induction of nitric oxide explains how aspirin inhibits acute inflammation.

The established model for the mechanism of action of aspirin is the inhibition of prostaglandin synthesis. However, this has never fully explained aspirin's repertoire of antiinflammatory properties. We found in acute pleuritis that aspirin, but not salicylate, indomethacin, or piroxicam, increased plasma nitric oxide (NO), which correlated with a reduction in inflammation.

Optimal strategy for management of pituitary disease in the growth hormone-deficient teenager.

The optimal treatment of chronic conditions spanning pediatric and adult clinical practice requires the establishment of clear and robust systems for managing the important period of transition of care. This principle is particularly relevant to the treatment of ongoing pituitary dysfunction after the achievement of final height and, in addition to the vital component of maintaining the confidence of the patient, encompasses a number of considerations that are particularly relevant to long-term health as an adult. These considerations include the achievement of peak bone mass, optimization of gonadal steroid and glucocorticoid replacement, and determination of the need for continuing growth hormone replacement.

Signal transduction pathways involved in cytokine stimulation of endothelin-1 release from human vascular smooth muscle cells.

Endothelin-1 (ET-1) mRNA expression and peptide production in human vascular smooth muscle cells (HVSMCs) are markedly increased by exposure to cytokines. As the transcription factor nuclear factor-kappaB (NF-kappaB) often mediates the effects of cytokines in target cells the aim of this study was to determine whether the production of ET-1 following exposure of HVSMCs to cytokines depends upon activation of NF-kappaB. BAY 11-7082, an inhibitor of cytokine-induced inhibitor protein (IkappaB) phosphorylation, inhibited cytokine-stimulated upregulation of preproendothelin-1 mRNA expression and ET-1 peptide production.

Cyclic AMP regulates cytokine stimulation of endothelin-1 release in human vascular smooth muscle cells.

Exposure of human vascular smooth muscle cells (HVSMCs) to cytokines markedly elevates endothelin-1 (ET-1) mRNA expression and peptide production. Cyclic AMP is a key regulator of many physiological processes. The aim of this study was to determine whether an elevation of intracellular cAMP may affect cytokine-induced production of ET-1 in HVSMCs.