Iowa Department of Transportation Major Items - Preliminary Quantity Report, May 17, 2011; With Addendums

Weekly letting report.

Estimated Target for Construction Lettings, May 17, 2011

Recognize that plans and proposals are not currently available for the following projects. The letting dates indicated are estimated target dates only and they are subject to change

Myeloid differentiation factor-88/interleukin-1 signaling controls cardiac fibrosis and heart failure progression in inflammatory dilated cardiomyopathy.

RATIONALE: The myeloid differentiation factor (MyD)88/interleukin (IL)-1 axis activates self-antigen-presenting cells and promotes autoreactive CD4(+) T-cell expansion in experimental autoimmune myocarditis, a mouse model of inflammatory heart disease. OBJECTIVE: The aim of this study was to determine the role of MyD88 and IL-1 in the progression of acute myocarditis to an end-stage heart failure. METHODS AND RESULTS: Using alpha-myosin heavy chain peptide (MyHC-alpha)-loaded, activated dendritic cells, we induced myocarditis in wild-type and MyD88(-/-) mice with similar distributions of heart-infiltrating cell subsets and comparable CD4(+) T-cell responses. Injection of complete Freund's adjuvant (CFA) or MyHC-alpha/CFA into diseased mice promoted cardiac fibrosis, induced ventricular dilation, and impaired heart function in wild-type but not in MyD88(-/-) mice. Experiments with chimeric mice confirmed the bone marrow origin of the fibroblasts replacing inflammatory infiltrates and showed that MyD88 and IL-1 receptor type I signaling on bone marrow-derived cells was critical for development of cardiac fibrosis during progression to heart failure. CONCLUSIONS: Our findings indicate a critical role of MyD88/IL-1 signaling in the bone marrow compartment in postinflammatory cardiac fibrosis and heart failure and point to novel therapeutic strategies against inflammatory cardiomyopathy.

Characterization of a specific 20- to 25-kD interleukin-1 inhibitor from cultured human lung macrophages.

Alveolar macrophages have the ability to downregulate immune processes in vitro. We have recently suggested the presence of interleukin-1 (IL-1) inhibitors in the supernatants of human bronchoalveolar lavage cells from patients with idiopathic pulmonary fibrosis or sarcoidosis. In the present study, we further analyze the cellular origin and the biologic properties of a 20- to 25-kD IL-1 inhibitor spontaneously produced by cultured human alveolar macrophages (AM). The inhibitor blocks IL-1-induced prostaglandin E2 production by human fibroblasts and the IL-1-related increase of phytohemagglutinin-induced murine thymocyte proliferation. After rigorous IL-1 alpha and IL-1 beta depletion, supernatants of lung macrophages specifically block the binding of IL-1 to its receptor on the murine thymoma cell line EL4-6.1 in a dose-dependent manner. These results indicate that AM from both normal donors and patients produce a specific IL-1 inhibitor that may be of importance in protecting the alveolar environment from the deleterious effects of excessive IL-1 production.

List of Bid Proposal Holders, May 17, 2011

List of Bid Proposal Holders

Lottery Action Newsletter, November 17-30, 2008, Vol. 15, no. 22

Newsletter for Iowa Lottery Retailers.

Lottery Action Newsletter, August 17-30, 2009, Vol. 16, no. 16

Lottery Newsletter for Lottery Retailers

Lottery Action Newsletter, August 31-September 13, 2009, Vol. 16, no. 17

Lottery Newsletter for Lottery Retailers

Lottery Action Newsletter, January 4-January 24, 2010, Vol. 17, no. 1

Lottery Newsletter for Lottery Retailers

Lottery Action Newsletter, February 8-21, 2010, Vol. 17, no. 3

Lottery Newsletter for Lottery Retailers

Lottery Action Newsletter, April 4-17, 2011, Vol. 18, no. 8

Lottery Newsletter for Lottery Retailers