959 resultados para University of Pennsylvania
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Comprehensive annual financial report of the University of Northern Iowa, Cedar Falls, Iowa for the years ended June 30, 2008 and 2007
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Audit report on Iowa State University of Science and Technology as of and for the year ended June 30, 2008
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Audit report for the State University of Iowa for the year ended June 30, 2008
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Report on the review of selected general and application controls over the State University of Iowa PeopleSoft Human Resources Information System (HRIS) for the period June 3, 2008 through July 25, 2008
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Report on a special investigation of the University of Northern Iowa, Camp Adventure Youth Services program for the period April 1, 2007 through March 31, 2008
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Report on the State University of Iowa, Iowa City, Iowa for the year ended June 30, 2008
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Report on Iowa State University of Science and Technology, Ames, Iowa, for the year ended June 30, 2008
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Report on the University of Northern Iowa for the year ended June 30, 2008
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Schedule of Debt Service and Coverage for Iowa State University of Science and Technology for the Academic Building Revenue Bond Funds for the year ended June 30, 2009
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Audit report on the Student Health Facility Revenue Bond Funds of Iowa State University of Science and Technology for the year ended June 30, 2009
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OBJECTIVE: Fibrotic changes are initiated early in acute respiratory distress syndrome. This may involve overproliferation of alveolar type II cells. In an animal model of acute respiratory distress syndrome, we have shown that the administration of an adenoviral vector overexpressing the 70-kd heat shock protein (AdHSP) limited pathophysiological changes. We hypothesized that this improvement may be modulated, in part, by an early AdHSP-induced attenuation of alveolar type II cell proliferation. DESIGN: Laboratory investigation. SETTING: Hadassah-Hebrew University and University of Pennsylvania animal laboratories. SUBJECTS: Sprague-Dawley Rats (250 g). INTERVENTIONS: Lung injury was induced in male Sprague-Dawley rats via cecal ligation and double puncture. At the time of cecal ligation and double puncture, we injected phosphate-buffered saline, AdHSP, or AdGFP (an adenoviral vector expressing the marker green fluorescent protein) into the trachea. Rats then received subcutaneous bromodeoxyuridine. In separate experiments, A549 cells were incubated with medium, AdHSP, or AdGFP. Some cells were also stimulated with tumor necrosis factor-alpha. After 48 hrs, cytosolic and nuclear proteins from rat lungs or cell cultures were isolated. These were subjected to immunoblotting, immunoprecipitation, electrophoretic mobility shift assay, fluorescent immunohistochemistry, and Northern blot analysis. MEASUREMENTS AND MAIN RESULTS: Alveolar type I cells were lost within 48 hrs of inducing acute respiratory distress syndrome. This was accompanied by alveolar type II cell proliferation. Treatment with AdHSP preserved alveolar type I cells and limited alveolar type II cell proliferation. Heat shock protein 70 prevented overexuberant cell division, in part, by inhibiting hyperphosphorylation of the regulatory retinoblastoma protein. This prevented retinoblastoma protein ubiquitination and degradation and, thus, stabilized the interaction of retinoblastoma protein with E2F1, a key cell division transcription factor. CONCLUSIONS: : Heat shock protein 70-induced attenuation of cell proliferation may be a useful strategy for limiting lung injury when treating acute respiratory distress syndrome if consistent in later time points.
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Audit report of the University of Northern Iowa, Cedar Falls, Iowa, for the years ended June 30, 2009 and 2008