Conclusion: Our study suggests that CD105 and CD166 would be valuable surface markers associated with chondrogenic potential; thus, CD105- and CD166-enriched cells derived from human synovium would be practical and valuable sources for cartilage selleck chemicals llc regeneration. (C) 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“SETTING: A tertiary care research centre in Sao Paolo, Brazil.
OBJECTIVE: To
quantify interleukin (IL) 8, tumour necrosis factor alpha (TNF-alpha), vascular endothelial growth factor (VEGF) and transforming growth factor beta(1), (TGF-beta(1))in pleural fluid from tuberculous patients, correlating its values with the histopathological patterns in pleural biopsies.
DESIGN: Cytokines were quantified in patients with transudatcs secondary to congestive heart failure (n = 8) and exudates secondary to tuberculosis (TB; n = 39). In parietal pleural biopsies from TB patients,
the histological patterns of the inflammatory response were click here quantified by morphometric analysis (stereological point-counting method).
RESULTS: IL-8, TNF-alpha, VEGF and TGF-beta(1) levels were higher in TB than in transudates. A positive correlation existed between components of the fibrinoid exudative phase with pleural fluid IL-8 (R = 0.52, P = 0.004) and VEGF (R = 0.42, P = 0.0021) levels. A negative correlation existed between pleural fluid IL-8 (R = -0.37, P = 0.048) and VEGF (R = -0.44, P = 0.0015) levels with tissue components of fibroproliferation.
CONCLUSION: The high pleural levels of TNF-a, IL-8, VEGF and TGF-beta(1) suggest the involvement of these cytokines BIX 01294 molecular weight in the TB immunological response. The positive correlation between pleural fluid IL-8 and VEGF with the components of the acute exudative phase and the negative correlation between these cytokines with the fibroproliferative components suggest a temporary inflammatory response in the pleural
space.”
“Objective: A novel impaction fracture insult technique, developed for modeling post-traumatic osteoarthritis in porcine hocks in vivo, was tested to determine the extent to which it could replicate the cell-level cartilage pathology in human clinical intra-articular fractures.
Design: Eight fresh porcine hocks (whole-joint specimens with fully viable chondrocytes) were subjected to fracture insult. From the fractured distal tibial surfaces, osteoarticular fragments were immediately sampled and cultured in vitro for 48 h. These samples were analyzed for the distribution and progression of chondrocyte death, using the Live/Dead assay. Five control joints, in which “”fractures”" were simulated by means of surgical osteotomy, were also similarly analyzed.