Contrastingly, in brain tissue XXY* males expressed all four genes higher than male and female controls.\n\nConclusion:\n\nAltered expression of genes escaping X inactivation probably contributes directly to the XXY* phenotype.”
“Background: Structural and inflammatory changes in asthma involve both the large and small airways, with involvement of the distal lung being related to disease severity. We have previously shown that changes in the extracellular matrix (ECM) composition of the distal

lung are associated with loss of alveolar attachments in patients with fatal asthma. However, major ECM elements, such as collagen I and fibronectin and their regulators, have not been addressed at the distal level.\n\nObjective: We sought to evaluate ECM remodeling in the distal lungs of asthmatic patients.\n\nMethods: Using immunohistochemistry and image analysis, we determined the content of collagen I and III, fibronectin, and matrix LB-100 metalloproteinases; (MMPs) 1, 2, and 9 and tissue inhibitors of metalloproteinase (MMPs) 1 and 2 in the large and small airways and lung parenchyma of 24

patients with fatal asthma and compared the results with those of 11 nonasthmatic control subjects. Protein content was defined as the area of positive staining divided by basement membrane or septum length.\n\nResults: We observed increased collagen I and decreased collagen III content in the small airways of asthmatic PARP activation patients compared with that seen in control subjects. Greater fibronectin and MMP-1, MMP-2, and MMP-9 content was observed at the outer area of the small airways in asthmatic patients. NIMP content was also increased in the peribronchiolar parenchyma in asthmatic patients. In contrast, TIMP expression was only increased in the large airways of asthmatic patients compared with that seen in control subjects.\n\nConclusions: The outer area of the small airways is a major site of ECM remodeling in fatal asthma, potentially contributing to functional changes and the loss of airway-parenchyma

interdependence observed in patients with fatal asthma. (J Allergy Clin Immunol 2009;123:1090-7.)”
“von Willebrand factor (VWF) levels are elevated and a disintegrin-like and metalloprotease with thrombospondin type MK-2206 in vivo I repeats-13 (ADAMTS13) activity is decreased in both acute and chronic inflammation. We hypothesized that by cleaving hyperactive ultralarge VWF (ULVWF) multimers, ADAMTS13 down-regulates both thrombosis and inflammation. Using intravital microscopy, we show that ADAMTS13 deficiency results in increased leukocyte rolling on unstimulated veins and increased leukocyte adhesion in inflamed veins. Both processes were dependent on the presence of VWF. Depletion of platelets in Adamts13(-/-) mice reduced leukocyte rolling, suggesting that platelet interaction with ULVWF contributes to this process.