Report on a special investigation of the Coggon Municipal Light Plant for the period July 1, 2004 through August 27, 2012

Report on a special investigation of the Coggon Municipal Light Plant for the period July 1, 2004 through August 27, 2012

Report on a special investigation of the City of Stockport for the period July 1, 2007 through October 31, 2011

Report on a special investigation of the City of Stockport for the period July 1, 2007 through October 31, 2011

Report on a special investigation of the City of Muscatine for the period July 1, 2008 through March 8, 2012

Report on a special investigation of the City of Muscatine for the period July 1, 2008 through March 8, 2012

Special investigation of the Iowa Department of Transportation for the period January 29, 1994 through July 7, 2011

Special investigation of the Iowa Department of Transportation for the period January 29, 1994 through July 7, 2011

Special investigation of the University of Northern Iowa Events Complex Concessions for the period October 1, 2006 through March 31, 2012

Special investigation of the University of Northern Iowa Events Complex Concessions for the period October 1, 2006 through March 31, 2012

Report on a special investigation of the City of Indianola for the period June 1, 2006 through August 31, 2012

Report on a special investigation of the City of Indianola for the period June 1, 2006 through August 31, 2012

Report on a special investigation of the Lyon County Engineer’s Office for the period August 1, 2006 through May 31, 2012

Report on a special investigation of the Lyon County Engineer’s Office for the period August 1, 2006 through May 31, 2012

Report on a special investigation of the Creston Water Works for the period July 1, 2005 through November 16, 2012

Report on a special investigation of the Creston Water Works for the period July 1, 2005 through November 16, 2012

Report on special investigation of the Department of Inspections and Appeals, Office of the State Public Defender, for the period August 31, 2007 through March 31, 2011

Report on a special investigation of the State Public Defender’s Office for the period August 31, 2007 through March 31, 2011

Report on special investigation of the City of Farmington for the period July 1, 2009 through November 30, 2012

Special investigation of the City of Farmington for the period July 1, 2009 through November 30, 2012

Report on a special investigation of the City of Grand River for the period July 1, 2004 through March 7, 2012

Report on a special investigation of the City of Grand River for the period July 1, 2004 through March 7, 2012

Investigation of Deterioration of Joints in Concrete Pavements , TPF-5(224), 2012

Premature deterioration of concrete at the joints in concrete pavements and parking lots has been reported across the northern states. The distress is first observed as shadowing when microcracking near the joints traps water, later exhibiting as significant loss of material. Not all roadways are distressed, but the problem is common enough to warrant attention. The aim of the work being conducted under this and parallel contracts was to improve understanding of the mechanisms behind premature joint deterioration and, based on this understanding, develop training materials and guidance documents to help practitioners reduce the risk of further distress and provide guidelines for repair techniques. While work is still needed to understand all of the details of the mechanisms behind premature deterioration and prevention of further distress, the work in this report has contributed to advancing the state of knowledge.

Inhibition of death receptor signals by cellular FLIP.

The widely expressed protein Fas is a member of the tumour necrosis factor receptor family which can trigger apoptosis. However, Fas surface expression does not necessarily render cells susceptible to Fas ligand-induced death signals, indicating that inhibitors of the apoptosis-signalling pathway must exist. Here we report the characterization of an inhibitor of apoptosis, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues. The short form, FLIPs, contains two death effector domains and is structurally related to the viral FLIP inhibitors of apoptosis, whereas the long form, FLIP(L), contains in addition a caspase-like domain in which the active-centre cysteine residue is substituted by a tyrosine residue. FLIPs and FLIP(L) interact with the adaptor protein FADD and the protease FLICE, and potently inhibit apoptosis induced by all known human death receptors. FLIP(L) is expressed during the early stage of T-cell activation, but disappears when T cells become susceptible to Fas ligand-mediated apoptosis. High levels of FLIP(L) protein are also detectable in melanoma cell lines and malignant melanoma tumours. Thus FLIP may be implicated in tissue homeostasis as an important regulator of apoptosis.