Average Four-Year Cost Per Graduate for Maine Public High Schools: Class of 2004

The results of this analysis appear in the tables titled “Average Four-Year Cost Per Graduate For Maine High Schools By School Size (Class of 2004)”. (The first table and graph represent school size breakdowns every 200 students with the exception of an additional breakout of schools with less than 100 students. The second table and chart represent school size breakdowns for every 100 students.) As the cohort shows, Maine high schools followed the economies of scale model with the lowest average cost per graduate being found in high schools with enrollments of 800-1000 students. Small high schools (especially those with enrollments of less than 200 students) had the highest average cost per graduate and those high schools with enrollments higher than 1000 students also showed increases in the average cost per graduate. Three island schools that had unusually high average cost per graduate compared to mainland schools were considered outliers and removed from the data set. However, even with these outliers removed the economies of scale model was clear. As may be seen from this data set, that while the economy of scale model declines appropriately for the state-wide data, there are exceptions in each enrollment category. That is, some high schools are more costly than others within each school size category. Consequently, further analysis is needed to determine why some high schools are more costly than others for graduating students

Prohibitin Inhibits Tumor Necrosis Factor alpha–induced Nuclear Factor-kappa B Nuclear Translocation via the Novel Mechanism of Decreasing Importin α3 Expression

Expression of prohibitin 1 (PHB), a multifunctional protein in the cell, is decreased during inflammatory bowel disease (IBD). Little is known regarding the regulation and role of PHB during intestinal inflammation. We examined the effect of tumor necrosis factor alpha (TNF-α), a cytokine that plays a central role in the pathogenesis of IBD, on PHB expression and the effect of sustained PHB expression on TNF-α activation of nuclear factor-kappa B (NF-κB) and epithelial barrier dysfunction, two hallmarks of intestinal inflammation. We show that TNF-α decreased PHB protein and mRNA abundance in intestinal epithelial cells in vitro and in colon mucosa in vivo. Sustained expression of prohibitin in intestinal epithelial cells in vitro and in vivo (prohibitin transgenic mice, PHB TG) resulted in a marked decrease in TNF-α–induced nuclear translocation of the NF-κB protein p65, NF-κB/DNA binding, and NF-κB–mediated transcriptional activation despite robust IκB-α phosphorylation and degradation and increased cytosolic p65. Cells overexpressing PHB were protected from TNF-α–induced increased epithelial permeability. Expression of importin α3, a protein involved in p50/p65 nuclear import, was decreased in cells overexpressing PHB and in colon mucosa of PHB TG mice. Restoration of importin α3 levels sustained NF-κB activation by TNF-α during PHB transfection. These results suggest that PHB inhibits NF-κB nuclear translocation via a novel mechanism involving alteration of importin α3 levels. TNF-α decreases PHB expression in intestinal epithelial cells and restoration of PHB expression in these cells can protect against the deleterious effects of TNF-α and NF-κB on barrier function

Assessment of network module identification across complex diseases

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