Inflammation in the developing preterm lung leads to disrupted airway morphogenesis and chronic lung disease in human neonates. However, the molecular mechanisms linking inflammation and the pathways controlling airway morphogenesis remain unclear. In this article, we show that IL-1β released by activated fetal lung macrophages is the key inflammatory mediator that disrupts airway morphogenesis.
View Article and Find Full Text PDFDivision of large, immature alveolar structures into smaller, more numerous alveoli increases the surface area available for gas exchange. Alveolar division requires precise epithelial-mesenchymal interactions. However, few experimental models exist for studying how these cell-cell interactions produce changes in 3-dimensional structure.
View Article and Find Full Text PDFInhibitors of apoptosis proteins (IAP) are key regulators of apoptosis and are inhibited by the second mitocondrial activator of caspases (SMAC). Previously, a small subset of TNF-α-expressing non-small cell lung cancers (NSCLC) was found to be sensitive to SMAC mimetics alone. In this study, we determined if a SMAC mimetic (JP1201) could sensitize nonresponsive NSCLC cell lines to standard chemotherapy.
View Article and Find Full Text PDFA method was developed for using an inexpensive and widely available protein, hen egg white lysozyme, as a patterning agent for commercial high surface area silicas. The basic patterning methodology involved spontaneous adsorption of the protein from aqueous solution, alkylation of the uncovered surface with an alkylsiloxane, and protein desorption in a slightly alkaline solution of morpholine. Adsorption kinetic studies using Bradford assays assisted in determining protein deposition conditions.
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