Under aerobic conditions, glucose is primarily catabolized by vascular smooth muscle to lactate, in spite of an adequate oxidative capacity. Although this is often considered to be indicative of some nonspecific metabolic insufficiency, there is evidence that aerobic glycolysis is specifically coupled to sodium and potassium transport processes, whereas oxidative metabolism is couple to contracticle energy requirements.

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Inflammation contributes to the development of fibrotic and malignant diseases. We assessed the ability of inflammatory cytokines to modulate endothelial cell survival and functions related to tissue repair/remodeling. Treatment with interleukin (IL)-1β or tumor necrosis factor (TNF)-α (2 ng/mL) led to human pulmonary artery endothelial cells becoming spindle-shaped fibroblast-like cells. However, immunoblot and DNA microarray showed no change in most endothelial and mesenchymal markers. In the presence of IL-1β or TNF-α, cells were resistant to apoptosis induced by deprivation of serum and growth factor, and were more migratory. In addition, cells treated with IL-1β or TNF-α contracted collagen gels more robustly. In contrast, transforming growth factor-β1 did not induce these responses. RNA interference targeting nuclear factor (NF)-κB p65 blocked the effects of IL-1β or TNF-α on cell morphologic change, survival, migration, and collagen gel contraction. These results suggest that endothelial cells may contribute to tissue repair/remodeling via the NF-κB signaling in a milieu of airway inflammation.

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Large-array surface electromyography produced data from patients with back pain that differed from data on subjects without back pain. This method may be useful in evaluating patients with low back pain.