Bacterial-induced protection against allergy through a novel multi-component immunoregulatory mechanism

Airborne microbial products have been reported to promote immune responses that suppress asthma, yet how these beneficial effects take place remains controversial and poorly understood. We have found that pulmonary exposure with the bacterium Escherichia coli leads to a suppression of allergic airway inflammation, characterized by reduced airway-hyperresponsiveness, eosinophilia and cytokine production by T cells in the lung. This immune modulation was neither mediated by the induction of a Th1 response nor regulatory T cells; was dependent on TLR-4 but did not involve TLR-desensitization. Dendritic cell migration to the draining lymph nodes and subsequent activation of T cells was unaffected by prior exposure to E.coli indicating that the immunomodulation was limited to the lung environment. In non-treated control mice ovalbumin was primarily presented by airway CD11b+ CD11c+ DCs expressing high levels of MHC class II molecules whilst the DCs in E.coli-treated mice displayed a less activated phenotype and had impaired antigen presentation capacity. Consequently, in situ Th2 cytokine production by ovalbuminspecific effector T cells recruited to the airways was significantly reduced. The suppression of airways hyper responsiveness was mediated through the recruitment of IL-17-producing gd-T cells; however, the suppression of dendritic cells and T cells was mediated through a distinct mechanism that could not be overcome by the local administration of activated dendritic cells, or by the in vivo administration of TNF-alpha. Taken together, these data reveal a novel multi-component immunoregulatory pathway that acts to protect the airways from allergic inflammation.

Endogenous and exogenous regulation of monocyte responses

Mononuclear phagocytes are essential for the innate response to pathogens and for the repair of injured tissue. The cells - which can be broadly divided into circulating monocytes and tissue-resident macrophages and dendritic cells - are selectively equipped to protect the host by mediating pleiotropic and tissue-specific functions. The properties of some mononuclear phagocytes, however, also contribute to the development and the progression of inflammatory diseases. Consequently, current research investigates mononuclear phagocytes into greater detail with the aim to clarify their contributions to pathophysiologic inflammation. Recent studies indicate that circulating monocytes can be divided into distinct populations, which differ in their tissue tropism and functional commitment. Also, tissue macrophages and dendritic cells have been found to adopt context-dependent phenotypes, which can range from "pro-" to "anti-" inflammatory. These findings have markedly contributed to our understanding of the functional heterogeneity of mononuclear phagocyte populations. Yet, in many cases, the factors that control the quantity and/or quality of phagocyte responses in vivo remain largely unknown. The goal of this thesis was to identify cell endogenous and cell exogenous factors that dictate the fate of mononuclear phagocyte populations. To this end we made use of the recent identification of phenotypic markers, which permit to track mononuclear cell types and their lineage precursors. A main approach consisted to define candidate regulatory factors of certain types of mononuclear phagocytes and then to manipulate the expression of these factors in mice so as to address their functions and causal contributions on mononuclear phagocyte lineages in vivo. Human patient material was further used to validate findings. First, we investigated a microRNA and a transcription factor as candidate cell endogenous co- regulators of monocyte subset responses. Second, we studied a tumor-derived hormone as a candidate exogenous factor that amplifies the production of a population of mononuclear phagocytes with tumor-promoting functions. The endogenous and exogenous factors identified in this research appear to act as effective regulators of mononuclear phagocyte responses in vivo and thus may be exploited in future therapeutic approaches to regulate disease-associated inflammation. - Les phagocytes mononucléaires sont essentiels pour la réponse innée aux pathogènes et pour la réparation des tissus lésés. Ces cellules - qui peuvent être largement divisées en deux groupes, les monocytes circulant dans le sang et les macrophages et cellules dendritiques résidant dans les tissus - sont capables de protéger l'hôte en exerçant des fonctions pléiotropiques. Cependant, les propriétés de certains phagocytes mononucléaires contribuent également au développement et à la progression des maladies inflammatoires. Par conséquent, la recherche actuelle étudie les phagocytes mononucléaires plus en détail afin de clarifier leurs contributions à l'inflammation pathophysiologique. Des études récentes indiquent que les monocytes circulants peuvent être divisés en populations distinctes, qui diffèrent dans leur tropisme tissulaire et dans leurs fonctions biologiques. En outre, les macrophages et les cellules dendritiques peuvent adopter des phénotypes dépendants de l'environnement dans lequel ils se trouvent; ces phénotypes peuvent aller du type "pro-" au type "anti-" inflammatoire. Ces récentes découvertes ont contribué à notre compréhension sur l'hétérogénéité fonctionnelle des phagocytes mononucléaires. Pourtant, dans de nombreux cas, les facteurs qui contrôlent la quantité et/ou la qualité des réponses produites par ces cellules restent encore largement inconnus. L'objectif de cette thèse a consisté à identifier de nouveaux facteurs (endogènes ou exogènes) qui contrôlent les phagocytes mononucléaires. Dans ce but, nous avons fait usage de l'identification récente de marqueurs qui permettent d'identifier différents types de phagocytes mononucléaires ainsi que des cellules (souches) dont ils sont issus. Notre approche a consisté à définir des facteurs candidats qui pourraient contrôler certains phagocytes mononucléaires, puis à manipuler l'expression de ces facteurs chez la souris de manière à tester leurs fonctions et leur contributions in vivo. Nous avons également utilisé des échantillons biologiques de patients pour vérifier nos résultats chez l'homme. Tout d'abord, nous avons étudié un microARN et un facteur de transcription pour déterminer si ces deux facteurs opèrent en tant que co-régulateurs d'un certain type de monocytes. Deuxièmement, nous avons considéré une hormone produite par certaines tumeurs afin d'examiner son rôle dans la production d'une population de macrophages qui favorisent la progression des tumeurs. Les facteurs endogènes et exogènes identifiés dans cette recherche semblent agir comme régulateurs dominants de réponses produites par certains phagocytes mononucléaires et pourraient donc être exploités dans de futures approches thérapeutiques afin de contrôler les réponses immunitaires inflammatoires associées a certaines maladies.

Effects of the PPAR-beta agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelination.

BACKGROUND: Brain inflammation plays a central role in numerous brain pathologies, including multiple sclerosis (MS). Microglial cells and astrocytes are the effector cells of neuroinflammation. They can be activated also by agents such as interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor (PPAR) pathways are involved in the control of the inflammatory processes, and PPAR-beta seems to play an important role in the regulation of central inflammation. In addition, PPAR-beta agonists were shown to have trophic effects on oligodendrocytes in vitro, and to confer partial protection in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In the present work, a three-dimensional brain cell culture system was used as in vitro model to study antibody-induced demyelination and inflammatory responses. GW 501516, a specific PPAR-beta agonist, was examined for its capacity to protect from antibody-mediated demyelination and to prevent inflammatory responses induced by IFN-gamma and LPS. METHODS: Aggregating brain cells cultures were prepared from embryonal rat brain, and used to study the inflammatory responses triggered by IFN-gamma and LPS and by antibody-mediated demyelination induced by antibodies directed against myelin-oligodendrocyte glycoprotein (MOG). The effects of GW 501516 on cellular responses were characterized by the quantification of the mRNA expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), inducible NO synthase (i-NOS), PPAR-beta, PPAR-gamma, glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), and high molecular weight neurofilament protein (NF-H). GFAP expression was also examined by immunocytochemistry, and microglial cells were visualized by isolectin B4 (IB4) and ED1 labeling. RESULTS: GW 501516 decreased the IFN-gamma-induced up-regulation of TNF-alpha and iNOS in accord with the proposed anti-inflammatory effects of this PPAR-beta agonist. However, it increased IL-6 m-RNA expression. In demyelinating cultures, reactivity of both microglial cells and astrocytes was observed, while the expression of the inflammatory cytokines and iNOS remained unaffected. Furthermore, GW 501516 did not protect against the demyelination-induced changes in gene expression. CONCLUSION: Although GW 501516 showed anti-inflammatory activity, it did not protect against antibody-mediated demyelination. This suggests that the protective effects of PPAR-beta agonists observed in vivo can be attributed to their anti-inflammatory properties rather than to a direct protective or trophic effect on oligodendrocytes.

Using flow cytometry for in situ monitoring of antimicrobial compound production in the biocontrol bacterium Pseudomonas fluorescens CHA0

Pseudomonas fluorescens strain CHA0 is able to protect plants against a variety of pathogens, notably by producing the two antimicrobial compounds 2,4-diacetylphloroglucinol (DAPG) and pyoluteorin (PLT). The regulation of the expression of these compounds is affected by many biotic factors, such as fungal pathogens, rhizosphere bacteria as well as plant species. Therefore, the influence of some plant phenolic compounds on the expression of DAPG and PLT biosynthetic genes has been tested using GFP-based reporter, monitored by standard fluometry and flow cytometry. In situ experiments were also performed with cucumber plants. We found that several plant metabolites such as IAA and umbelliferone are able to modify significantly the expression of DAPG and PLT. The use of flow cytometry with autofluorescents proteins seems to be a promising method to study rhizobacteria-plant interactions.

Peroxynitrite cytotoxicity on bovine retinal pigmented epithelial cells in culture.

Peroxynitrite induced in vitro a dose dependent toxicity on retinal pigmented epithelial (RPE) cells. Cell death was partially mediated by apoptosis as demonstrated by nuclear fragmentation and TdT-mediated dUTP nick-end labeling assay. Peroxynitrite-induced tyrosine nitration was revealed by immunocytochemistry, both in the cytoplasm and in the nucleus of the cells. Nitration was not observed in RPE cells, producing nitric oxide (NO) after stimulation by lipopolysacharide and interferon-g (IFN-gamma), suggesting that peroxynitrite was not formed in vitro in such conditions. Peroxynitrite could be responsible for the retinal damages observed in pathological conditions in which NO has been demonstrated to be involved. In this context, EGb761, identified as a free radical scavenger, was showed herein to protect RPE cells against peroxynitrite injury.

Financial crisis: theory and practice

In the last 50 years, we have had approximately 40 events with characteristics related to financial crisis. The most severe crisis was in 1929, when the financial markets plummet and the US gross domestic product decline in more than 30 percent. Recently some years ago, a new crisis developed in the United States, but instantly caused consequences and effects in the rest of the world.This new economic and financial crisis has increased the interest and motivation for the academic community, professors and researchers, to understand the causes and effects of the crisis, to learn from it. This is the one of the main reasons for the compilation of this book, which begins with a meeting of a group of IAFI researchers from the University of Barcelona, where researchers form Mexico and Spain, explain causes and consequences of the crisis of 2007.For that reason, we believed this set of chapters related to methodologies, applications and theories, would conveniently explained the characteristics and events of the past and future financial crisisThis book consists in 3 main sections, the first one called "State of the Art and current situation", the second named "Econometric applications to estimate crisis time periods" , and the third one "Solutions to diminish the effects of the crisis". The first section explains the current point of view of many research papers related to financial crisis, it has 2 chapters. In the first one, it describe and analyzes the models that historically have been used to explain financial crisis, furthermore, it proposes to used alternative methodologies such as Fuzzy Cognitive Maps. On the other hand , Chapter 2 , explains the characteristics and details of the 2007 crisis from the US perspective and its comparison to 1929 crisis, presenting some effects in Mexico and Latin America.The second section presents two econometric applications to estimate possible crisis periods. For this matter, Chapter 3, studies 3 Latin-American countries: Argentina, Brazil and Peru in the 1994 crisis and estimates the multifractal characteristics to identify financial and economic distress.Chapter 4 explains the crisis situations in Argentina (2001), Mexico (1994) and the recent one in the United States (2007) and its effects in other countries through a financial series methodology related to the stock market.The last section shows an alternative to prevent the effects of the crisis. The first chapter explains the financial stability effects through the financial system regulation and some globalization standards. Chapter 6, study the benefits of the Investor activism and a way to protect personal and national wealth to face the financial crisis risks.

Executive Order Number Eighty August 20, 2012

This order when adopting regulations to protect the healthy, safety and welfare of the people of the State of Iowa, state agencies should seek to achieve statutory goals as effectively and efficiently as possible without imposing unnecessary burdens.

Renal tumor ablation using radiofrequency: results in 28 patient. Exposition scientifique: Radiologie interventionnelle

Objectifs: To describe the technique and results of radiofrequency ablation (RFA) of small renal tumors.Matériels et méthodes: 28 patients with median age 79 years were treated with RFA for small renal exophytic tumor (median size 20 mm). Most patients were poor operative candidatesbecause of associated morbidity. Four patients were treated for biopsy proven papillary tumor, 7 for clear cell carcinoma, 2 for oncocytoma and one for renalhepatocellular metastasis. No biopsy sample was obtained for the others because of a typical radiological aspect of RCC.Résultats: All patients but one were treated successfully in one session under combined ultrasound and CT guidance using either Radionics 2000 cool-tip or Bostonscientific expandable needles, one was treated in two sessions. One Splenic, 3 colic and 1 pancreatic displacement with CO2 injection and one injection of G5%solution in the costo-phrenic recessus were done in order to protect adjacent organs. Two complications were observed, one splenic iatrogenic lesion treated byembolization and one renal pelvis stenosis treated with JJ stent. After a mean follow-up of 20 months, no patient developped local recurrence on MRI follow-up.Conclusion: RFA is a simple and efficient technique pending on strict selected criteria (small size < 3 cm and exophytic lesion). Long local control is obtained with minimalmorbidity.

Evaluation of Safety Treatments for Roadside Culverts: TR-517, April 24, 2009

Roadside cross-drainage culverts have been found to impact vehicle accident injury levels. Designers have commonly used three safety treatments to protect errant drivers from culvert accidents. These treatments have included: culvert extension, guardrail installation and grating. In order to define which safety treatment is the most appropriate, benefit-cost analysis has used accident cost reduction to estimate societal gains earned by using any safety treatment. The purpose of this study was to estimate accident costs for a wide range of roadway and roadside characteristics so that designers can calculate benefit/cost ratios for culvert safety treatment options under any particular scenario. This study began with conducting a parametric study in order to find variables which have significant impact on accident cost changes. The study proceeded with highway scenario modeling which included scenarios with different values for combinations of roadway and roadside variables. These variables were chosen based upon findings from the parametric study and their values were assigned based upon highway classification. This study shows that the use of different culvert safety treatments should be flexible to roadway and roadside characteristics. It also shows that culvert extension and grating were the safety treatments found to produce the lowest accident costs for all highway scenarios modeled. Therefore, it is believed that the expanded adoption of culvert extension and culvert grates can improve overall highway safety.

Monnaie, citoyenneté et globalisation financière. Les citoyens entre protection sociale et promesses de la capitalisation boursière

La monnaie a été étudiée par des économistes hétérodoxes, des sociologues et des historiens qui ont souligné ses rapports à l'ordre collectif, mais elle n'est que rarement analysée sous l'angle de la citoyenneté. Notre thèse propose une réflexion théorique sur quatre types de fonctions (politique, symbolique, socioéconomique et psychoaffective) qui permettent à la monnaie de jouer un rôle de médiation de la citoyenneté. A partir d'une perspective qui combine les apports de l'économie politique internationale et de l'école de la régulation, nous montrons que cette médiation ne mobilise pas seulement des mécanismes sociopolitiques nationaux, mais aussi des mécanismes internationaux qui rétroagissent sur la sphère domestique des États et affectent leur capacité à définir leur régime de citoyenneté. Cette relation est analysée dans le contexte de l'institutionnalisation du système monétaire international de Bretton Woods (1944) et du développement de la globalisation financière depuis les années 1970. Si la monnaie a été mise au service d'un principe de protection des droits sociaux des citoyens contre les pressions financières extérieures après la Seconde guerre mondiale, elle contribue aujourd'hui à l'ouverture de la sphère domestique des Etats aux flux de capitaux transnationaux et à la création d'un ordre politique et juridique favorable aux droits des investisseurs. Cette dynamique est impulsée par l'essor de nouveaux intermédiaires financiers (notamment les agences de notation et les investisseurs institutionnels) et l'émergence concomitante d'une nouvelle forme d'Etat légitimée à partir d'un discours politique néolibéral insistant sur la quête de compétitivité, la réduction de la protection sociale et la responsabilisation individuelle. Elle se traduit par la privatisation des régimes de retraite et le développement des politiques d'éducation financière qui incitent les citoyens à se comporter en « preneurs de risques » actifs et responsables, assurant eux-mêmes leur sécurité économique à travers le placement de leur épargne retraite sur les marchés financiers. Nous soulignons toutefois les difficultés institutionnelles, cognitives et socioéconomiques qui rendent cette transformation de la citoyenneté contradictoire et problématique. Money has been studied by heterodox economists, sociologists and historians who stressed its relationship to collective order. However, it has hardly been analysed from the viewpoint of its relationship to citizenship. We propose a theoretical account of four types of functions (political, symbolic, socioeconomic and psychoaffective) enabling money to operate as a mediation of citizenship. From a perspective that combines the contributions of international political economy and the regulation school, we show that this mediation mobilises not only national sociopolitical mechanisms, but also international mechanisms which feed back on the domestic sphere of states and affect their capacity to define their regime of citizenship. This relationship is analysed in the context of the institutionalisation of the international monetary system of Bretton Woods (1944) and the development of financial globalization since the 1970s. If money has served to protect the social rights of citizens against external financial pressures after the Second World War, today it contributes to the opening of the domestic sphere of states to transnational capital flows and to the creation of a political and legal order favorable to the rights of investors. This dynamic is driven by the rise of new financial intermediaries (in particular rating agencies and institutional investisors) and the simultaneous emergence of a new form of state legitimized from a neoliberal political discourse emphasizing the quest for competitiveness, reduced social protection and individual responsibilization. It results in the privatization of pension systems and the development of policies of financial education that encourage citizens to behave as active and responsible « risk takers », ensuring their own economic security through the investment of their savings retirement on financial markets. However, we emphasize the institutional, cognitive and socioeconomic difficulties that make this transformation of citizenship contradictory and problematic. - Money has been studied by heterodox economists, sociologists and historians who stressed its relationship to collective order. However, it has hardly been analysed from the viewpoint of its relationship to citizenship. We propose a theoretical account of four types of functions (political, symbolic, socioeconomic and psychoaffective) enabling money to operate as a mediation of citizenship. From a perspective that combines the contributions of international political economy and the regulation school, we show that this mediation mobilises not only national sociopolitical mechanisms, but also international mechanisms which feed back on the domestic sphere of states and affect their capacity to define their regime of citizenship. This relationship is analysed in the context of the institutionalisation of the international monetary system of Bretton Woods (1944) and the development of financial globalization since the 1970s. If money has served to protect the social rights of citizens against external financial pressures after the Second World War, today it contributes to the opening of the domestic sphere of states to transnational capital flows and to the creation of a political and legal order favorable to the rights of investors. This dynamic is driven by the rise of new financial intermediaries (in particular rating agencies and institutional investisors) and the simultaneous emergence of a new form of state legitimized from a neoliberal political discourse emphasizing the quest for competitiveness, reduced social protection and individual responsibilization. It results in the privatization of pension systems and the development of policies of financial education that encourage citizens to behave as active and responsible « risk takers », ensuring their own economic security through the investment of their savings retirement on financial markets. However, we emphasize the institutional, cognitive and socioeconomic difficulties that make this transformation of citizenship problematic.

Missouri River Flood Coordination Task Force Report, September 25, 2011

The Missouri River floods of 2011 will go down in history as the longest duration flooding event this state has seen to date. The combination of above normal snowfall in the upper Missouri River basin followed by the equivalent of nearly one year’s worth of rainfall in May created an above normal runoff situation which filled the Missouri River and the six main reservoirs within the basin. Compounding this problem was colder than normal temperatures which kept much of the snowpack in the upper basin on the ground longer into the spring, setting the stage for this historic event. The U.S. Army Corps of Engineers (USACE) began increasing the outflow at Gavin’s Point, near Yankton, South Dakota in May. On June 14, 2011, the outflow reached a record rate of over 160,000 cubic feet per second (cfs), over twice the previous record outflow set in 1997. This increased output from Gavin’s Point caused the Missouri River to flow out of its banks covering over 283,000 acres of land in Iowa, forcing hundreds of evacuations, damaging 255,000 acres of cropland and significantly impacting the levee system on the Missouri River basin. Over the course of the summer, approximately 64 miles of primary roads closed due to Missouri River flooding, including 54 miles of Interstate Highway. Many county secondary roads were closed by high water or overburdened due to the numerous detours and road closures in this area. As the Missouri River levels began to increase, municipalities and counties aided by State and Federal agencies began preparing for a sustained flood event. Citizens, businesses, state agencies, local governments and non‐profits made substantial preparations, in some cases expending millions of dollars on emergency protective measures to protect their facilities from the impending flood. Levee monitors detected weak spots in the levee system in all affected counties, with several levees being identified as at risk levees that could potentially fail. Of particular concern was the 28 miles of levees protecting Council Bluffs. Based on this concern, Council Bluffs prepared an evacuation plan for the approximately 30,000 residents that resided in the protected area. On May 25, 2011, Governor Branstad directed the execution of the Iowa Emergency Response Plan in accordance with Section 401 of the Stafford Act. On May 31, 2011, HSEMD Administrator, Brigadier General J. Derek Hill, formally requested the USACE to provide technical assistance and advanced measures for the communities along the Missouri River basin. On June 2, 2011 Governor Branstad issued a State of Iowa Proclamation of Disaster Emergency for Fremont, Harrison, Mills, Monona, Pottawattamie, and Woodbury counties. The length of this flood event created a unique set of challenges for Federal, State and local entities. In many cases, these organizations were conducting response and recovery operations simultaneously. Due to the length of this entire event, the State Emergency Operations Center and the local Emergency Operations Centers remained open for an extended period of time, putting additional strain on many organizations and resources. In response to this disaster, Governor Branstad created the Missouri River Recovery Coordination Task Force to oversee the State’s recovery efforts. The Governor announced the creation of this Task Force on October 17, 2011 and appointed Brigadier General J. Derek Hill, HSEMD Administrator as the chairman. This Task Force would be a temporary group of State agency representatives and interested stakeholders brought together to support the recovery efforts of the Iowa communities impacted by the Missouri River Flood. Collectively, this group would analyze and share damage assessment data, coordinate assistance across various stakeholders, monitor progress, capture best practices and identify lessons learned.

Excitotoxicity-induced endocytosis mediates neuroprotection by TAT-peptide-linked JNK inhibitor.

ABSTRACT: Excitotoxicity and cerebral ischemia induce strong endocytosis in neurons, and we here investigate its functional role in neuroprotection by a functional transactivator of transcription (TAT)-peptide, the c-Jun N-terminal kinase (JNK) inhibitor D-JNKI1, against NMDA-excitotoxicity in vitro and neonatal ischemic stroke in P12 Sprague-Dawley rats. In both situations, the neuroprotective efficacy of D-JNKI1 was confirmed, but excessively high doses were counterproductive. Importantly, the induced endocytosis was necessary for neuroprotection, which required that the TAT-peptide be administered at a time when induced endocytosis was occurring. Uptake by other routes failed to protect, and even promoted cell death at high doses. Blocking the induced endocytosis of D-JNKI1 with heparin or with an excess of D-TAT-peptide eliminated the neuroprotection. We conclude that excitotoxicity-induced endocytosis is a basic property of stressed neurons that can target neuroprotective TAT-peptides into the neurons that need protection. Furthermore, it is the main mediator of neuroprotection by D-JNKI1. This may explain promising reports of strong neuroprotection by TAT-peptides without apparent side effects, and warns that the timing of peptide administration is crucial.

Commissioner’s Planning Guidance, 2013

As technology evolves, vital resources shift, and the state’s population diversifies, Public Safety will have a unique opportunity to show our integrity, values, and worth to the citizens of Iowa. To take advantage of this unique moment in history, and will remain committed to, proactive and on-going strategic mapping. This strategic work will always be guided by Public Safety’s mission and core values, as well as by our responsibility to support local Police Departments and Sheriff’s Offices.

Performance Evaluation Of Iowa Bridge Decks Constructed With Epoxy-Coated Reinforcing Bars, RB06-011, 2011

Epoxy coatings have been used on the embedded reinforcing bars of bridge decks since the mid-1970s to mitigate deterioration caused by chloride-induced corrosion. The use of chloride-based deicers became common in the early 1960s and caused corrosion of conventional uncoated bars in bridge decks within 5 to 10 years of commencement of deicer applications. In response to this rapid deterioration, the National Bureau of Standards researched coatings to protect the reinforcement (National Bureau of Standards, 1975), resulting in the development of epoxy-coated reinforcing bars, which were used in bridge decks beginning in 1973. While corrosion-related deterioration has been prevalent on bridge decks with uncoated reinforcing bars in northern climates where the use of deicing salts is common, bridge decks constructed after 1973 with epoxy-coated reinforcing have shown good corrosion resistance with only limited exceptions. On the whole, previous laboratory and field studies regarding the performance of epoxy-coated reinforcing bars are very promising; however, some laboratory and field studies have yielded differing results. In recent years, maintenance personnel for the Iowa Department of Transportation (Iowa DOT) have reportedly performed patch repairs to some bridge decks reinforced with epoxy-coated bars. At one such bridge, the southbound US 65 bridge (Bridge No. 7788.5L065) over the Union Pacific Railroad near Bondurant in Polk County, Iowa, deck repairs were performed by Iowa DOT maintenance personnel in the Spring of 2010, based on our communications regarding this topic with Mr. Gordon Port of the Iowa DOT. These repairs were observed by engineers from the Iowa DOT Office of Bridges and Structures, who reported that significant corrosion was found at a number of epoxy-coated reinforcing bars uncovered during this patch work. These repairs were reportedly performed at spalls and delaminated areas corresponding to cracks over transverse reinforcing bars, and involved careful removal of the concrete from over the bars. Figures 1 through 4 contain photographs provided by Iowa DOT personnel showing the removal process (Figure 1), the conditions encountered (Figures 2 and 3), and close-up views of the corroded reinforcing (Figure 4). As a result of these observations, the Iowa Department of Transportation has requested this study to gain further understanding of the long-term performance of bridge decks reinforced with epoxy-coated bars. The two main objectives of this study are to determine the long-term effectiveness of the epoxy coatings and to determine the potential causes for the deterioration at locations where corrosion has occurred. Wiss, Janney, Elstner Associates, Inc. (WJE) and the Iowa DOT identified eight different bridge decks across Iowa for this study that were constructed using epoxy-coated reinforcing bars. A field investigation consisting of visual inspections, a delamination survey, a concrete cover survey, electrical testing for susceptibility to corrosion, and concrete sampling was conducted within a survey area deemed to be representative of the condition of each bridge deck. Laboratory testing, including chloride ion content testing, characterization of the extracted bars, petrographic examination of the concrete, and carbonation testing, was conducted on the core samples taken from each bridge deck.

Assessment of Weathering Steel Bridge Performance in Iowa and Development of Inspection and Maintenance Techniques, RB17-012, 2013

Weathering steel is commonly used as a cost-effective alternative for bridge superstructures, as the costs and environmental impacts associated with the maintenance/replacement of paint coatings are theoretically eliminated. The performance of weathering steel depends on the proper formation of a surface patina, which consists of a dense layer of corrosion product used to protect the steel from further atmospheric corrosion. The development of the weathering steel patina may be hindered by environmental factors such as humid environments, wetting/drying cycles, sheltering, exposure to de-icing chlorides, and design details that permit water to pond on steel surfaces. Weathering steel bridges constructed over or adjacent to other roadways could be subjected to sufficient salt spray that would impede the development of an adequate patina. Addressing areas of corrosion on a weathering steel bridge superstructure where a protective patina has not formed is often costly and negates the anticipated cost savings for this type of steel superstructure. Early detection of weathering steel corrosion is important to extending the service life of the bridge structure; however, written inspection procedures are not available for inspectors to evaluate the performance or quality of the patina. This project focused on the evaluation of weathering steel bridge structures, including possible methods to assess the quality of the weathering steel patina and to properly maintain the quality of the patina. The objectives of this project are summarized as follows:  Identify weathering steel bridge structures that would be most vulnerable to chloride contamination, based on location, exposure, environment, and other factors.  Identify locations on an individual weathering steel bridge structure that would be most susceptible to chloride contamination, such as below joints, splash/spray zones, and areas of ponding water or debris.  Identify possible testing methods and/or inspection techniques for inspectors to evaluate the quality of the weathering steel patina at locations discussed above.  Identify possible methods to measure and evaluate the level of chloride contamination at the locations discussed above.  Evaluate the effectiveness of water washing on removing chlorides from the weathering steel patina.  Develop a general prioritization for the washing of bridge structures based on the structure’s location, environment, inspection observations, patina evaluation findings, and chloride test results.