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“Study Design. The influence of mechanical load on pleiotrophin (PTM) and aggrecan expression by intervertebral disc (IVD) cells, and the effects of disc cell conditioned medium on endothelial cell migration was investigated.
Objective. To examine possible interactions of mechanical loads and known pro- and antiangiogenic factors, which may regulate disc angiogenesis during degeneration.
Summary of Background Data. Pleiotrophin expression can be influenced by mechanical stimulation check details and has been
associated with disc vascularization. Disc aggrecan inhibits endothelial cell migration, suggesting an antiangiogenic role. A possible interplay between these factors is unknown.
Methods. The influence of the respective predominant load (cyclic strain for anulus fibrosus and hydrostatic pressure for nucleus pulposus cells) on PTN and aggrecan expression by IVD cells was determined by real-time RT-PCR and Western blotting (PTN only). The effects of IVD cell conditioned medium on endothelial cell migration were analyzed in a bioassay using human microvascular endothelial (HMEC-1) cells.
Results. Application of both mechanical loads resulted in significant alterations of gene expression of PTN (+67%, P = 0.004 in anulus cells; +29%, P = 0.03 in nucleus cells) and aggrecan (+42%, P = 0.03 in anulus
cells, -25%, P = 0.03 in nucleus cells). These effects depended on the cell type, the applied load, and timescale. JAK inhibitor Conditioned media of nucleus pulposus cells enhanced HMEC-1 migration, but this effect was diminished after 2.5 MPa hydrostatic pressure, when aggrecan expression was diminished, but not 0.25 MPa, when expression levels were unchanged.
Conclusion. Mechanical loading influences PTN expression by human IVD cells. Conditioned media from nucleus pulposus cell cultures stimulated HMEC-1 endothelial cell migration. This study demonstrates that Selleck LCL161 the influence of mechanical loads on vascularization of the human IVD is likely to be complex and does not correlate simply with altered expression of known pro- and antiangiogenic factors.”
“BACKGROUND: Increased vascularity of the airway mucosa
in asthma potentially increases heat loss in the airways.
OBJECTIVE: To determine if the inflamed airways of subjects with uncontrolled asthma show increased exhaled breath temperature (EBT).
PATIENTS AND METHODS: In 100 patients with persistent asthma and 50 healthy volunteers, we measured lung function by post-bronchodilator forced spirometry, the asthma control test (ACT) and EBT.
RESULTS: Patients with asthma, of whom 49 (49%) were female, with a mean (+/- standard error of the mean) age of 44 (+/- 17) years and a predicted forced expiratory volume in one second of 71% (+/- 16), had a significantly increased EBT, particularly those with uncontrolled asthma (n = 50, ACT <= 19, EBT 34.9 +/- 0.8 degrees C), compared to patients with controlled asthma (n = 50, ACT >= 20, EBT 33.7 +/- 0.