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Ded many of the proteins that had been found to be decreased under baseline conditions in uninfected SP-A-/- mice as compared to WT mice. Our working hypotheses to explain these differences are: a) that expression of these proteins is stimulated by the induction of infection, probably as a consequence of increased levels of regulatory molecules such as cytokines; b) in order to compensate for the
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Unteers' lung found significant decreases in levels of SP-A [28]. Unfortunately, there was little overlap in the sets of identified proteins between our studies and therefore little basis for comparison. When the DEF and RED proteins are individually examined as subgroups of the identified proteins, the changes are similar to those noted for all proteins. In both of these groups of proteins, more
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To the mineralization process [56]. Further, Wendy Shaw's group used NMR spectroscopy to examine the WT mouse and mutant amelogenins to confirm the pre-mature self-assembly of the mutant proteins [57]. Other studies show how the amelogenin structure is modified during its interaction with HA, phospholipids, other enamel proteins [58] and even collagen (remember that amelogenin does not interact wi
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Ed. RAW, DRAW and CDRAW cells were grown in Dulbecco's modified Eagle medium (DMEM) with 2.5 fetal bovine serum (FBS).L929 cells, originally derived from normal subcutaneous areolar and adipose tissue of a 100-day-old male C3H/An mouse and purchased from ATCC, were used for plaque assay. Cells were grown as monolayers in minimal essential medium supplemented with Earle's salts, nonessential amino
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D, phase and slice-select direction) and a total scan time of 8 minutes. The magnitude contrast-to-noise ratio (CNR) between artery and vessel wall was 12:1. The phase CNR between the arterial wall and the lumen was 7:1. A total of 19 calcifications in the femoral vessel wall were identified with SWI in 8 subjects. The mean area of calcification measured on CT, magnitude and phase images was 0.37
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