Division of Tobacco Use prevention and Control 2014-2018 Strategic Plan,

The Division of Tobacco Use Prevention and Control works to reduce tobacco use and the toll of tobacco-caused disease and death by preventing youth from starting, helping Iowans to quit, and preventing exposure to secondhand smoke. Tobacco is the leading preventable cause of death for Iowans, taking the lives of more than 4,400 adults each year. Estimated annual health care costs in Iowa directly related to tobacco use now total $1 billion.

Blue-Green Algae, Iowa Department of Public Health - Division of Environmental Health, September 15, 2011

The Iowa Department of Public Health (IDPH), Division of Environmental Health, Health Assessment Program gives people information about harmful chemicals and organisms in their environment. Blue-green algae are microscopic organisms that are naturally present in lakes and streams. Some blue-green algae produce toxins that could pose a health risk to people and animals when they are exposed to them in large enough quantities. This fact sheet answers questions about blue-green algae.

Annual Report: Division of Acute Disease Prevention, Emergency Response, and Environmental Health 2015 April 25, 2016

This report is a result of the ADPER & EH division management team retreat that was held on July 30 and 31, 2015 where a gap was identified in our communication with customers, especially when it came to sharing information about planning efforts. The purpose of this report is to provide a comprehensive look at what ADPER & EH has accomplished in the past year as well as what we are working on for the future. It also serves as an annual informational resource for stakeholders, local partners, policy makers and the general public.

The role of PLK-1 in asynchronous cell division of two-cell stage "C. elegans" embryos

Summary Acquisition of lineage-specific cell cycle duration is an important feature of metazoan development. In Caenorhabditis a/egans, differences in cell cycle duration are already apparent in two-cell stage embryos, when the larger anterior blastomere AB divides before the smaller posterior blastomere P1. This time difference is under the control of anterior-posterior (A-P) polarity cues set by the PAR proteins. The mechanism by which these cues regulate the cell cycle machinery differentially in AB and P1 are incompletely understood. Previous work established that retardation of P1 cell division is due in part to preferential activation of an ATL1/CHK-1 dependent checkpoint in P1 but how the remaining time difference is controlled was not known at the onset of my work. The principal line of work in this thesis established that differential timing relies also on a mechanism that promotes mitosis onset preferentially in AB. The polo-like kinase PLK-1, a positive regulator of mitotic entry, is distributed in an asymmetric manner in two-cell stage embryos, with more protein present in AB than in P1. We find that PLK-1 asymmetry is regulated by anterior-posterior (A-P) polarity cues through preferential protein retention in the embryo anterior. Importantly, mild inactivation of plk-1 by RNAi delays entry into mitosis in P1 but not in AB, in a manner that is independent of ATL-1/CHK-1. Together, these findings favor a model in which differential timing of mitotic entry in C. elegans embryos relies on two complementary mechanisms: ATL-1/CHK-1 dependent preferential retardation in P1 and PLK-1 dependent preferential promotion in AB, which together couple polarity cues and cell cycle progression during early development. Besides analyzing PLK-1 asymmetry and its role in differential timing of two-cells stage embryos, we also characterized t2190, a mutant that exhibits reduced differential timing between AB and P1. We found this mutant to be a new allele of par-1. Additionally, we analyzed the role of NMY-2 in regulating the asynchrony of two-cell stage embryos, which may be uncoupled from its role in A-P polarity establishment and carried out a preliminary analysis of the mechanism underlying CDC-25 asymmetry between AB and P,. Overall, our works bring new insights into the mechanism controlling cell cycle progression in early C. elegans embryos. As most of the players important in C. elegans are conserved in other organisms, analogous mechanisms may be utilized in polarized cells of other species. Résumé Au cours du développement, les processus de division cellulaire sont régulés dans l'espace et le temps afin d'aboutir à la formation d'un organisme fonctionnel. Chez les Métazoaires, l'un des mécanismes de contrôle s'effectue au niveau de la durée du cycle cellulaire, celle-ci étant specifiée selon la lignée cellulaire. L'embryon du nématode Caenorhabditis elegans apparaît comme un excellent modèle d'étude de la régulation temporelle du cycle cellulaire. En effet, suite à la première division du zygote, l'embryon est alors composé de deux cellules de taille et d'identité différentes, appelées blastomères AB et P1. Ces deux cellules vont ensuite se diviser de manière asynchrone, le grand blastomère antérieur AB se divisant plus rapidement que le petit blastomère postérieur P1. Cette asynchronie de division est sous le contrôle des protéines PAR qui sont impliquées dans l'établissement de l'axe antéro-postérieur de l'embryon. A ce jour, les mécanismes moléculaires gouvernant ce processus d'asynchronie ne sont que partiellement compris. Des études menées précédemment ont établit que le retard de division observé dans le petit blastomère postérieur P1 était dû, en partie, à l'activation préférentielle dans cette cellule de ATL-1/CHK-1, protéines contrôlant la réponse à des erreurs dans le processus de réplication de l'ADN. L'analyse des autres mécanismes responsables de la différence temporelle d'entrée en mitose des deux cellules a été entreprise au cours de cette thèse. Nous avons considéré la possibilité que l'asynchronie de division était du à l'entrée préférentielle en mitose du grand blastomère AB. Nous avons établi que la protéine kinase PLK-1 (polo-like kinase 1), impliquée dans la régulation positive de la mitose, était distribuée de manière asymétrique dans l'embryon deux cellules. PLK-1 est en effet enrichi dans le blastomère AB. Cette localisation asymétrique de PLK-1 est sous le contrôle des protéines PAR et semble établie via une rétention de PLK-1 dans la cellule AB. Par ailleurs, nous avons démontré que l'inactivation partielle de plk-7 par interférence à ARN (RNAi) conduit à un délai de l'entrée en mitose de la cellule P1 spécifiquement, indépendamment des protéines régulatrices ATL-1/CHK-1. En conclusion, nous proposons un modèle de régulation temporelle de l'entrée en mitose dans l'embryon deux cellules de C. elegans basé sur deux mécanismes complémentaires. Le premier implique l'activation préférentielle des protéines ATL-1/CHK-1, et conduit à un retard d'entrée en mitose spécifiquement dans la cellule P1. Le second est basé sur la localisation asymétrique de la protéine kinase PLK-1 dans la cellule AB et induit une entrée précoce en mitose de cette cellule. Par ailleurs, nous avons étudié un mutant appelé t2190 qui réduit la différence temporelle d'entrée en mitose entre les cellules AB et P1. Nous avons démontré que ce mutant correspondait à un nouvel allèle du Bene par-1. De plus, nous avons analysé le rôle de NMY-2, une protéine myosine qui agit comme moteur moléculaire sur les filaments d'active; dans la régulation de l'asynchronie de division des blastomères AB et P1, indépendamment de sa fonction dans l'établissement de l'axe antéro-postérieur. Par ailleurs, nous avons commencé l'étude du mécanisme moléculaire régulant la localisation asymétrique entre les cellules AB et P1 de la protéine phosphatase CDC25, qui est également un important régulateur de l'entrée en mitose. En conclusion, ce travail de thèse a permis une meilleure compréhension des mécanismes gouvernant la progression du cycle cellulaire dans l'embryon précoce de C. elegans. Etant donné que la plupart des protéines impliquées dans ces processus sont conservées chez d'autres organismes multicellulaires, il apparaît probable que les mécanismes moléculaires révélés dans cette étude soit aussi utilisés chez ceux-ci.

Annual Review of the European Football Players' Labour Market / Etude annuelle du marché du travail européen des footballeurs

The key reference on the labour market and the logics of squad formation in the five main European leagues. One hundred richly coloured pages, illustrated by graphics, maps, rankings, statistical models and analysis in French and English which... - inform managers about potential strategies to put their clubs on the road to success - help managers of federations and players' unions to understand current trends and to take decisions - suggest to journalists new lines of investigation likely to interest the general public - allow researchers and students to benefit from reliable and comparable sources, developed with the greatest possible rigour - give fans the possibility to understand in detail the dynamics at work in their favourite sport and club Demographic Study of Footballers in Europe The Demographic Study of European Footballers is an annual publication destined for anyone who wishes to acquire a scientific understanding of the European football players' labour market. It presents the dynamics at work in 36 first division leagues in UEFA member countries. This edition covers our biggest ever survey comprising more than 520 clubs and 13,000 footballers. Statistical indicators relative to nine thematics (morphology, age, experience training, origin, etc.) allow the comparison of player profiles and squad compositions at league and club level. Through easily-understable regression analyses, the Study brings to light the principle differences between clubs and leagues according to economic and sporting level of championships. The final part presents the list of the most promising players under 23 years of age by league and position

Political centralization and government accountability

This paper studies fiscal federalism when regions differ in voters' ability to monitor publicofficials. We develop a model of political agency in which rent-seeking politicians providepublic goods to win support from heterogeneously informed voters. In equilibrium, voterinformation increases government accountability but displays decreasing returns. Therefore,political centralization reduces aggregate rent extraction when voter information varies acrossregions. It increases welfare as long as the central government is required to provide publicgoods uniformly across regions. The need for uniformity implies an endogenous trade off between reducing rents through centralization and matching idiosyncratic preferences throughdecentralization. We find that a federal structure with overlapping levels of government canbe optimal only if regional differences in accountability are sufficiently large. The modelpredicts that less informed regions should reap greater benefits when the central governmentsets a uniform policy. Consistent with our theory, we present empirical evidence that lessinformed states enjoyed faster declines in pollution after the 1970 Clean Air Act centralizedenvironmental policy at the federal level.