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Quality can be defined as the ability of a business to satisfy their customers’ needs and expectations. Total Quality Management is defined as the way to prevent, appraise and improve the entire organization to increase the product quality. In order to systematically increase quality in an organization, there are different quality systems in use. One example is process management, which is to divide the activities of processes. Quality assurance aims to increase revenues and reduce operating expenses. It is therefore essential to identify the costs that arise from poor quality and which do not add value to the customers. In Swedish industries it is estimated that these quality deficiency costs lie between 10 and 30 % of a business' turnover. This study aims to identify costs of poor quality in a manufacturing business. Costs of poor quality are a major part of the organization’s net sales and are therefore important to consider. This study also aims to develop a model with metrics for quality costs. The study is based on a qualitative methodology and empirical data gathered from two observations and seven interviews with representatives from Nordic Waterproofing AB. The empirical material is based on information from three main processes; supplier process, production process and sales process. This study has resulted in a model for survey poor quality costs in a manufacturing business. The total costs of poor quality that could be defined at Nordic Waterproofing AB was estimated to 8 775 000 SEK, which is 2.93 % of the business turnover. This gives a total estimated cost of poor quality around 10-15 % of the business turnover for all the processes. Furthermore, this resulted helped to give Nordic Waterproofing AB an indication of where these cost incurred and recommendations for further work with identify poor costs of quality.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

The Late Devonian-Early Mississippian-age New Albany Shale is both a source rock and reservoir rock for hydrocarbons in the Illinois Basin. Previously suggested models for organic carbon enrichment consider productivity, anoxia, and the interdependent roles of sedimentation, primary production, and microbial metabolism. This study attempts to reconstruct paleoenvironmental conditions during deposition and re-evaluates these models using geochemical data from multiple cores across the eastern edge of the Illinois Basin in west-central Kentucky. Geochemical methods utilizing redox-sensitive major elements (C, S, Fe, P, K, Ti, and Si), trace elements (V and Mo), and ratios (Ni/Co, V/Cr, and V/(V+Ni) are used. Analysis of paleo-redox indicators suggests variable bottom-water conditions during accumulation of the New Albany Shale members including: anoxic to possibly euxinic conditions for the Clegg Creek Member, anoxic to periodically dysoxic conditions for the Camp Run, and dysoxic to oxic (normal marine) for the Morgan Trail and Blocher Members. Variability in redox proxy results suggests that multiple parameters should be utilized in such studies rather than relying on a single proxy. High C/P ratios observed in these members may be controlled by regeneration of P, enhanced productivity, and sequestration of organic carbon (the productivity-anoxia feedback (PAF) mechanism) under anoxic conditions. The lack of correlation between organic carbon content and clastic-influx proxies suggests that organic matter (OM) accumulation was not controlled by sedimentation rate or increased nutrient supply associated with increased sediment influx.

Le PAF (Platelet-Activating Factor) est un médiateur reconnu pour son implication dans plusieurs effets physiologiques et pathologiques, particulièrement les états inflammatoires. À l'instar du PAF, les lymphocytes T Th17 sont aussi reconnus comme exerçant un rôle majeur dans la physiopathologie des maladies auto-immunes. L'objectif de ce projet est de déterminer s'il existe un lien entre ces deux composants. En fait, nous avons émis l'hypothèse que le PAF pourrait provoquer une production de cytokines spécifiques par les cellules présentatrices d'antigène qui elles, interagissant avec les lymphocytes T, pourraient mener ultimement à une différentiation en Th17. En effet, les cellules T ne peuvent interagir directement avec le PAF puisqu'elles n'expriment pas de récepteur pour celui-ci à leur surface. Les cellules T Th17 expriment un facteur de transcription spécifique RORr, nécessitent absolument la sous-unité IL-23p19 pour leur expansion et produisent IL-17. Nous avons donc, dans un premier temps, regardé la capacité d'un type de cellules présentatrices d'antigène, les cellules de Langerhans à produire IL-23p19 en réponse au PAF. Ensuite, nous avons mis en contact ces cellules de Langerhans pré-stimulées au PAF avec des lymphocytes T activés pendant 5 jours pour vérifier l'expression de RORII et la production d'IL-17 dans ces lymphocytes T, plus précisément les lymphocytes T CD4 + . Cette étude nous a permis de mettre en évidence que certains éléments impliqués dans les processus inflammatoires sont possiblement inséparables et interagissent probablement les uns avec les autres pour mener aux séquelles multiples de l'inflammation.

No description available.

Background: Globally, there are 10 million new cases of tuberculosis (TB) disease annually and 95% of cases occur in low- and middle-income countries (LMIC). More than 1 billion people use tobacco, and 80% of tobacco users reside in LMIC. Smoking approximately doubles the risk of TB disease and is associated with excess mortality during TB treatment. We aimed to estimate the proportion of annual incident TB cases and TB mortality attributable to tobacco smoking in high burden TB countries. Methods: To estimate population attributable fractions (PAF), we obtained country specific estimates of TB incidence and TB mortality rates from the WHO 2015 Global TB Report. Country specific smoking prevalence was estimated from WHO 2015 tobacco surveillance reports and the Tobacco Atlas. Risk ratios for the effect of smoking on TB incidence and TB mortality were obtained from previously published meta-analyses. Country specific PAF of smoking for TB disease were age and sex adjusted. Results: In high burden countries during 2014, an estimated 4.5 million adults developed TB disease and 163,000 people died from TB. An estimated 740 million adult smokers lived in those high burden countries in 2014. We estimated that tobacco smoking was attributable for 17.7% (95% confidence interval [CI] 8.6-21.9%) of TB cases and 15.0% (95% CI 1.9-31.6%) of TB mortality. Of the high burden countries, Russia had the highest proportion of smoking attributable TB disease (31.8%, 95% CI 16.0-37.8%) and death (28.1%, 95% CI 3.8-51.3%). India had the greatest absolute number of TB cases (233,000) and TB deaths (7,400) attributable to smoking. Men (30.5%, 95% CI 14.9%-36.9%) had a greater proportion of TB cases attributable to smoking than women (4.7%, 95% CI 1.9%-6.2%). Conclusion: In high-burden TB countries, nearly one-sixth of all TB cases and TB deaths were attributable to smoking. Our findings highlight the need for tobacco control in high TB burden regions and specifically among patients with TB. Reaching key populations and integrating smoking cessation efforts into TB programs will be essential to achieve global TB control goals.

El shock es una situación clínica que se ha venido observando durante cientos de años y cuya presencia ha ido asociada con procesos que culminaban casi siempre con la muerte. El estudio de estos procesos ha permitido llegar a la conclusión de que el shock tiene un componente multifactorial y multietiológico. La cascada de eventos que tienen lugar en un estado de shock parece demasiado compleja como para que la actuación terapéutica sobre uno solo de estos pasos sea suficiente como para bloquear el shock en su conjunto. Sin embargo, desde hace años se vienen estudiando diferentes aproximaciones terapéuticas entre las que se encuentra el antagonismo del factor activador de ls plaquetas (PAF). Los diferentes trabajos desarrollados en esta tesis pretenden ser una aportación al estudio del papel del PAF y de sus antagonistas en el shock. Para ello se han recogido una serie de modelos experimentales, tanto in vitro como in vivo , con el antagonista del PAF UR-12460. Los modelos estudiados son: shock anafiláctico, shock por isquemia-reperfusión esplácnica y coronaria, shock endotóxico y shock hemorrágico. El UR-12460 presenta actividad en modelos de shock anafiláctico activo, tanto en cobayo como en ratón. Además, para una serie de antagonistas del PAF estudiados, se demuestra una buena correlación entre la inhibición de la mortalidad inducida por PAF y la inhibición de la mortalidad inducida por shock anafiláctico activo en ratón, lo cual indica que el PAF está implicado en estos procesos. La ineficacia del UR-12460 en procesos de shock pasivo sugiere una menor importancia relativa del PAF con respecto a otros mediadores como la histamina. Por otra parte, en modelos de shock por isquemia-reperfusión esplácnica en rata, el UR-12460 se ha mostrado parcialmente efectivo, inhibiendo la mortalidad y la trombocitopenia producidas por el shock. Otro modelo de isquemia-reperfusión, pero a nivel miocárdico en este caso, ha sido extensamente estudiado en la rata. La oclusión durante 6 minutos de la arteria coronaria izquierda en la rata anestesiada, y posterior reperfusión durante 10 minutos, produce una serie de alteraciones del ritmo cardíaco que son inhibidas por el UR-12460. Dicho compuesto disminuye la incidencia de taquicardias ventriculares durante la oclusión, y disminuye la aparición de fibrilación ventricular en la reperfusión. Esto apoya el papel del PAF en la arritmogénesis por isquemia-reperfusión. Las pruebas de isquemia-reperfusión en corazón aislado de rata, por el método de Langendorff, combinadas con la incubación posterior del tejido cardíaco con cloruro de trifeniltetrazolio, permiten aunar en un mismo experimento y bajo las mismas condiciones, la valoración macroscópica del área de infarto y la alteración funcional del corazón. En este modelo los corazones se perfunden con sangre diluida en líquido de Krebs y se comparan con corazones que reciben sólo el diluyente. Las marcadas diferencias entre los corazones isquémicos que han recibido sangre diluida y los que no, sugieren que las células sanguíneas son pieza clave en la génesis de los infartos y en el deterioro del funcionalismo cardíaco. Por otra parte, la ausencia de una relación directa entre el tiempo de isquemia-reperfusión y la gravedad del infarto, en ausencia de sangre, sugiere que la situación de anoxia no es un factor determinante en la génesis del infarto. Sí existe relación entre el tiempo de isquemia-reperfusión y las alteraciones de la función mecánica. La presencia de células sanguíneas podría representar un sistema de amplificación del daño causado por la anoxia. Los resultados obtenidos en este modelo con el compuesto UR-12460 y el antioxidante mercaptopropionilglicina sugieren que tanto el antagonismo del PAF como la captación de radicales libres pueden ser útiles en la disminución del infarto y, en general, en la mejoría de la función miocárdica durante la reperfusión y en la disminución de las arritmias. Otro importante modelo es el shock endotóxico, inducido en la rata por la administración de lipopolisacárido (LPS) de E. coli de diversos serotipos. El serotipo 0111:B4 produce un característico efecto bifásico de hipotensión arterial. El UR-12460 no inhibe la profunda e inmediata fase de hipotensión pero sí la segunda fase, más lenta y progresiva. Utilizando el serotipo 0127:B8 se ha estudiado el aumento de permeabilidad vascular en la rata. Se ha comprobado que sólo algunos órganos resultan afectados significativamente y que el aumento de permeabilidad se aprecia a partir de los 15 minutos de administrado el LPS. Por otra parte, hay una buena correlación entre la inhibición de la mortalidad inducida por PAF y la inducida por LPS en ratón, lo que refuerza la participación del PAF como mediador clave en la cascada de acontecimientos que producen la mortalidad por LPS. Este papel queda reforzado por la eficacia mostrada por el UR-12460 al atenuar las alteraciones bioquímicas y enzimáticas inducidas por LPS en rata. La inhibición del aumento del tiempo parcial de tromboplastina activada indica que el PAF puede estar también implicado en los mecanismos que conducen al síndrome de coagulación intravascular diseminada en la rata. El último modelo estudiado es el shock hipovolémico hemorrágico, en el cual la eficacia de los antagonistas probados no se ha demostrado. Es posible que su administración sólo sea beneficiosa en fases iniciales de la hemorragia, cuando el shock no se ha hecho todavía progresivo o no se han liberado otros mediadores.En resumen, puede decirse que el UR-12460 se ha mostrado activo, al menos parcialmente, en varios modelos de shock, reforzando la idea de la participación importante del PAF en estos procesos de tan diversa etiología. Sin embargo, el hecho de que este compuesto no tenga efecto sobre algunos de los marcadores del shock estudiados hace pensar que el futuro de un posible tratamiento del shock pasaría por la administración conjunta de diferentes sustancias, dirigidas cada una a los diferentes mediadores del shock que, además del PAF, intervienen en mayor o menor grado en su etiopatogenia. / Shock is a clinical situation that has been observed for centuries and whose presence has been associated to processes leading usually to death. The study of these processes has allowed to reach the conclusion that shock is a multifactorial and multietiological component syndrome. Since the cascade of events that take place during shock is very complex, it seems unlikely that acting on a single of its steps may be sufficient to block the shock state in its entirety. Nevertheless, in the last years different therapeutic approaches are being studied, among them the antagonism of platelet activating factor (PAF). The different studies carried out in this thesis intend to be a contribution to the study of the role of PAF and of its antagonists in shock. With a view to this we have performed several experimental models, both in vitro and in vivo, using UR-12460, a potent and selective PAF antagonist. The studied models are: anaphylactic shock, splachnic and coronary ischemia-reperfusion-induced shock, endotoxic shock and hemorrhagic shock. UR-12460 was found to be effective in active anaphylactic shock models, both in guinea pigs and mice. Furthermore, for a series of PAF antagonists, we have observed a good correlation between the inhibition of PAF-induced mortality and of active anaphylactic shock -induced mortality in mice, which indicates that PAF is involved in these processes. The ineffectiveness of UR-12460 in passive shock processes suggests a minor relative importance of PAF with respect to other mediators such as histamine. On the other hand, in splachnic ischemia-reperfusion (ischemia-reperfusion) shock models in the rat, UR-12460 has been shown partially effective, inhibiting the mortality and thrombocytopenia induced by shock. Another model of ischemia-reperfusion, but at myocardial level in this case, has been extensively studied in the rat. The occlusion during 6 minutes of the left coronary artery in the anesthetized rat, and subsequent reperfusion during 10 minutes, produces a number of disturbances in cardiac rhythm that are inhibited by UR-12460. This compound reduces the incidence of ventricular tachycardia during the occlusion phase as well as the onset of ventricular fibrillation in the reperfusion. This finding supports the role of PAF in the arrhythmogenesis by ischemia-reperfusion. The ischemia-reperfusion tests in isolated rat heart using the Langendorff method, combined with the subsequent incubation of the cardiac tissue with triphenyltetrazolium chloride, allow to combine in a single experiment, and under identical conditions, the macroscopic assessment of the infarcted area and the functional alterations of the heart. In this model, hearts are perfused with blood diluted with Krebs solution and are compared with hearts receiving only Krebs. The marked differences observed between the ischemic hearts that have received diluted blood and those that have not suggest that blood cells are a key factor in the genesis of infarction and in the impairment of cardiac function. On the other hand, the absence of a direct relationship between the time of ischemia-reperfusion and the severity of the infarction in the absence of blood suggests that the situation of anoxia is not a relevant factor in the genesis of infarction. There is indeed a relationship between the time of ischemia-reperfusion and the impairment of the mechanical function. The presence of blood cells may represent an amplification system of the damage caused by the anoxia. The results obtained in this model with the compound UR-12460 and the antioxidant mercaptopropionylglycine suggest that both PAF antagonism and free radical scavenging may be useful to reduce infarction and, in general, to improve the myocardial function during reperfusion and to reduce arrhythmias.Another important model is the endotoxic shock, which is induced in the rat by the administration of E. coli lipopolysaccharide (LPS) of different serotypes. Serotype 0111:B4 produces a characteristic biphasic effect of arterial hypotension. UR-12460, although not able to inhibit the steep and immediate phase of hypotension, clearly inhibits the second phase, which is slower and more progressive. The increase in vascular permeability has been studied in the rat using serotype 0127:B8. We have observed that only some organs are significantly affected and that the increase in permeability is noticeable from 15 minutes post-administration of LPS. UR-12460 has been shown to inhibit extravasation in the trachea and seminal vesicle. On the other hand, we have observed a good correlation between the inhibition of the mortality induced by PAF and that induced by LPS in the mouse, which fact reinforces the involvement of PAF as a key mediator in the cascade of events that cause the mortality by LPS. This is additionally supported by the ability shown by UR-12460 to reduce the biochemical and enzymatic alterations induced by LPS in the rat. The inhibition of the increase in the activated partial thromboplastin time shows that PAF may also be involved in the mechanisms leading to disseminated intravascular coagulation syndrome in the rat. The last shock model we have studied is the hemorrhagic hypovolemic shock, where none of the antagonists tested has proved effective. It is possible that their administration may only be beneficial in the initial stages of hemorrhage, when shock has not yet become progressive or other mediators have not yet been released. To sum up, it can be said that UR-12460 has proved effective, at least partially, in several models of shock, reinforcing the theory that PAF has a key role in these processes of such diverse etiology. However, the fact that this compound has no effect on some of the shock markers studied in this thesis brings us to think that the future of a possible treatment for shock requires the administration of different substances, directed to each one of the different mediators of shock that, in addition to PAF, are involved to a greater or lesser extent in its etiopathogenesis.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.