In the following papers I propose to construct economic models that incorporate the disastrous effect of conflict. I model conflict theoretically in a Solow growth model and empirically in a GDP per worker growth model, in a civil war onset model and a model for civil war’s severity. The first chapter theoretically and empirically analyzes economic growth with conflict in the context of the Mankiw et al. (1992) adaptation of the Solow growth model and the natural resource growth model by Sachs and Warner (1995). I incorporate a variable of capital destruction in the physical and human capital accumulation equations and derive coherent theoretical and empirical results. The second chapter considers the onset of civil war across all countries and specific subsamples of countries from 1970 to 2007. The onset of war is modeled using economic and financial variables in addition to grievance variables from the political science literature to ascertain the extent to which financial crises and hyperinflation can bring about civil war. I estimate using panel time-series logistic regression techniques and discover the risk of conflict in Africa, Asia, highly-indebted poor countries, and low income countries. Some civil wars are fought for government control and others are fought over local issues - both types of war are controlled for with their own determinants. The third chapter determines factors that significantly affect the severity of civil wars from year to year. I employ the same IV/GMM estimation techniques from Chapter 1 to discover the role of financial crises, hyperinflation, unemployment, and development assistance and aid in the severity of war.

Made available in DSpace on 2014-06-11T19:25:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-02-25Bitstream added on 2014-06-13T19:12:36Z : No. of bitstreams: 1 ferrari_r_me_botfm.pdf: 1633942 bytes, checksum: 661f07a6a0fe1c72e7d870e2a8d1b28b (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Estudos mostram a evolução dos marcadores locais e sistêmicos da doença pulmonar obstrutiva crônica (DPOC) e sua associação com o prognóstico da doença. No entanto, não identificamos estudos prévios avaliando a evolução desses marcadores em pacientes brasileiros com DPOC. Além disso, a associação entre as modificações dos marcadores da doença e a qualidade de vida relacionada à saúde não está clara. O objetivo deste estudo foi verificar a evolução dos marcadores diagnósticos e prognósticos de pacientes com DPOC e a associação destes marcadores com a mortalidade, exacerbação e modificações na qualidade de vida relacionada à saúde no período de três anos. No momento basal foram avaliados 133 pacientes com DPOC leve a muito grave, 15 pacientes (11%) morreram durante o seguimento e 23 pacientes (17%) não foram reavaliados. Portanto, 95 pacientes (72%) foram submetidos às seguintes avaliações no momento basal e após três anos: espirometria, composição corporal, sensação da dispneia por meio da escala Medical Research Council (MRC) e do índice de dispneia basal (BDI), qualidade de vida por meio do Questionário do Hospital Saint George na Doença Respiratória (SGRQ), comorbidades (Índice Charlson), tolerância ao exercício (distância percorrida em seis minutos-DP6) e cálculo do Índice BODE. Após a avaliação inicial, os pacientes ou seus familiares foram contatados a cada três meses para verificar a frequência de exacerbações e óbito. A evolução dos marcadores foi feita por meio do teste T para medidas repetidas. Análise de regressão de Cox foi realizada para identificar os preditores de mortalidade. A associação dos marcadores da doença com a frequência de exacerbação foi avaliada por meio da análise de regressão de Poisson. Análise de regressão logística foi utilizada para avaliar... / Studies show the evolution of local and systemic markers of chronic obstructive pulmonary disease (COPD) and its association with the disease prognosis. However, we did not identify previous studies evaluating the evolution of these markers in Brazilian patients with COPD. In addition, the association between modifications in disease markers and health-related quality of life (HRQL) are unclear. The objective of this study was to verify the evolution of diagnostic and prognostic markers in COPD patients and the association of these markers with mortality, exacerbation and modifications in HRQL over three years. At baseline were evaluated 133 patients with mild to very severe COPD, 15 patients (11%) died and 23 patients (17%) dropped out during the follow-up period. Therefore, 95 patients (72%) underwent following the evaluations at baseline and after three years: spirometry, body composition, dyspnea perception using the Medical Research Council scale (MRC) and the baseline dyspnea index (BDI), quality of life questionnaire by Saint George's Respiratory Questionnaire (SGRQ), comorbidities (Charlson index), exercise tolerance (six-minute walk distance-6MWD) and the calculate BODE index. After the initial assessment, patients or their relatives were contacted every three months to verify the exacerbations frequency and death. The evolution of the markers was evaluated using the paired t-test. Cox regression analysis was performed to identify mortality predictors. Association of disease markers with exacerbation frequency was assessed by Poisson regression analysis. Logistic regression analysis was used to evaluate the predictors of improvement or worsening of HRQL. After three years of study, there was no change in the values of FEV1 (p=0.23) and BMI (p=0.38). There was a significant worsening... (Complete abstract click electronic access below)

abstract: Bicyclist and pedestrian safety is a growing concern in San Francisco, CA, especially given the increasing numbers of residents choosing to bike and walk. Sharing the roads with automobiles, these alternative road users are particularly vulnerable to sustain serious injuries. With this in mind, it is important to identify the factors that influence the severity of bicyclist and pedestrian injuries in automobile collisions. This study uses traffic collision data gathered from California Highway Patrol’s Statewide Integrated Traffic Records System (SWITRS) to predict the most important determinants of injury severity, given that a collision has occurred. Multivariate binomial logistic regression models were created for both pedestrian and bicyclist collisions, with bicyclist/pedestrian/driver characteristics and built environment characteristics used as the independent variables. Results suggest that bicycle infrastructure is not an important predictor of bicyclist injury severity, but instead bicyclist age, race, sobriety, and speed played significant roles. Pedestrian injuries were influenced by pedestrian and driver age and sobriety, crosswalk use, speed limit, and the type of vehicle at fault in the collision. Understanding these key determinants that lead to severe and fatal injuries can help local communities implement appropriate safety measures for their most susceptible road users. / Dissertation/Thesis / Masters Thesis Sustainability 2016

Analisa a importÃncia de reduzir o nÃmero de acidentes de trÃnsito atravÃs da instalaÃÃo de Redutores EletrÃnicos de Velocidade (REV), nos cruzamentos na cidade de Fortaleza. Com a utilizaÃÃo da tecnologia cada dia mais avanÃada, os REVâs estÃo presente em muitas cidades do paÃs no controle de velocidade dos veÃculos em locais considerados crÃticos, registrando a velocidade dos veÃculos à distancia, a placa, identificando infratores. Para esta anÃlise utiliza-se o Ãndice de severidade denominado Unidade PadrÃo de Severidade (UPS), uma das tÃcnicas que identifica os locais crÃticos a partir da gravidade dos acidentes, associando a cada situaÃÃo (com vÃtima fatal, com ferido e com danos materiais) um determinado peso, dando prioridade aqueles acidentes cujo resultado foi mais severo em termos de vÃtimas. Apresenta resultados obtidos com a tÃcnica utilizada.

L’accident vasculaire cérébral (AVC) ischémique est une principale cause de décès et d’handicap en Europe. L’éthanol est une drogue largement consommée et la consommation chronique d’éthanol est un facteur participant à la survenue d’AVC ischémique (Reynolds et al., 2003). La consommation chronique et excessive d’éthanol est associée à un risque accru de mortalité et de morbidité suite à un AVC ischémique (Zhang et al., 2014). Ce facteur aggraverait les lésions ischémiques cérébrales dans les modèles animaux (Zhao et la 2010 ; Lemarchand et al., 2015). Le stress oxydatif et l’excitotoxicité glutamatergique peuvent jouer un rôle important dans l’exacerbation de l’infarctus cérébral après une consommation chronique et excessive d’éthanol (Zhao et la 2010 ; Zhao et la 2011). Le premier objectif de la thèse est de vérifier que la consommation chronique et excessive d’éthanol aggrave les dommages cérébraux ischémiques chez les patients et dans un modèle animal d’ischémie cérébrale. Le deuxième objectif est d'étudier l'inflammation post-ischémique dans le cerveau et dans le foie à court et moyen termes. Des rats mâles Wistar ont été soumis à l'administration chronique d'éthanol (10% ou 35% v/v, 5 ml / kg, deux fois par jour, quatre semaines avant l'opération) ou d’eau (vehicule), suivie d’une occlusion de l'artère cérébrale moyenne (OACM). Nous avons déterminé les effets de l'ingestion d’éthanol sur le volume de l'infarctus, des déficits neurologiques et moteurs, à 24 heures (J1) et à 7 jours (J7) de reperfusion sanguine. Nous avons quantifié le nombre de microglies activées dans l'hémisphère ipsilatéral. Nous avons mesuré le nombre de neutrophiles et les taux d’ARNm d’ICAM-1 et de VCAM-1 dans l'hémisphère ipsilatéral et dans le foie. Nous avons examiné la stéatose et l'état inflammatoire dans le foie des rats non ischémiés, pour évaluer l'état physiologique hépatique dans les 3 groupes à J1 et J7. Nous avons recruté 435 patients ayant eu une ischémie cérébrale supratentorielle dans les 48 heures après l'apparition des symptômes. La consommation excessive et chronique d’éthanol est définie par une prise hebdomadaire ≥300 g d'éthanol et les AVC ischémiques sévères par un score National Institutes of Health Stroke Scale (NIHSS) ≥6. Le score NIHSS a été évalué dans les 48 heures. Nous avons effectué des mesures des taux de transferrine déficiente en carbohydrates (CDT, biomarqueur de la consommation chronique excessive d'éthanol) et de marqueurs inflammatoires. Être un consommateur excessif et avoir un taux plasmatique élevé de neutrophiles étaient indépendamment associés à des déficits neurologiques plus sévères chez les patients ayant subi un AVC ischémique ou accident ischémique transitoire, dans les 48 heures. La consommation excessive et chronique d'éthanol chez le rat non ischémié a induit une stéatose hépatique et une augmentation d'un état inflammatoire dans le cortex, le striatum et le foie par l'intermédiaire d'augmentation de l'expression de protéines d'adhésion. Toutefois, aucune infiltration des neutrophiles n’a été notée dans le foie ou dans le cerveau. Dans le modèle OACM, la consommation chronique d’éthanol 35 ° aggravait le volume des lésions de l'AVC ischémique et les déficits moteurs, comparativement aux rats non exposés à l’éthanol. L'aggravation des déficits neurologiques et fonctionnels a été expliquée par une augmentation de l'inflammation post-ischémique dans le foie et le cerveau, via l'activation de la microglie, l’infiltration des neutrophiles, et l’expression des protéines d’adhésion leucocytaire à court et moyen termes. / Ischaemic stroke is a major cause of disability and death in Europe. Ethanol is a widely consumed drug and chronic ethanol consumption is a participating factor in ischaemic stroke (Reynolds et al., 2003). Chronic and excessive ethanol consumption is associated with an increased risk of mortality and morbidity from ischaemic stroke (Zhang et al., 2014). It may increase consequences of ischaemic brain injury in animals (Zhao et al., 2010, Lemarchand et al., 2015). Oxidative stress and glutamatergic excitotoxicity may play an important role in exacerbating ischaemic damage following chronic consumption of ethanol (Zhao et al., 2010; Zhao et al., 2011). The primary aim of my thesis was to assess whether chronic excessive ethanol consumption has a deleterious effect on ischaemic brain damage both in human and in a rat model. The secondary aim was to study the post-ischaemic inflammation in the brain and in the liver at short and intermediate terms. Wistar male rats were subjected to chronic administration of ethanol (10% or 35% v/v, 5ml/kg, twice per day, 4 weeks prior operation) or water (vehicle), followed by middle cerebral artery occlusion (OACM). The effects of ethanol ingestion on infarct volume, neurologic and motor deficits were determined at 24 hours (J1) and at 7 days (J7) of reperfusion. We quantified the number of activated microglia in the ipsilateral hemisphere and additionally measured the number of neutrophils and levels of ICAM-1 and VCAM-1 mRNA in the ipsilateral hemisphere and liver. Further, we examined the steatosis by comparing oil-red coloration of J1, J7 and non-ischemic rats to assess the physiologic liver status in the 3 groups. Patients with supratentorial cerebral ischaemia were recruited within 48 hours of symptom onset. Heavy drinkers were defined by a weekly consumption of ≥300 g ethanol and severe ischaemic strokes (score≥6 according to the National Institutes of Health Stroke Scale, NIHSS). The NIHSS score was evaluated within 48 hours. We performed measurements of carbohydrate-deficient transferrin (CDT, biomarker of chronic excessive ethanol consumption) and inflammatory markers plasmatic levels. Being a heavy drinker and having a higher plasma level of neutrophils were independently associated with a higher baseline severity of the neurological deficit in patients with supratentorial ischemic stroke or transient ischemic attack within 48 hours. Excessive and chronic ethanol consumption in non-ischaemic rats conferred an increased hepatic steatosis and an inflammatory condition in the cortex, the striatum and the liver, observed as increased expression of adhesion proteins. However, neutrophil infiltration was not observed in the liver or in the brain. In the OACM model, chronic consumption of 35% ethanol worsened ischemic stroke lesions and motor deficits, compared to non-ethanol-exposed rats. Neutrophil infiltration and the mRNA levels of VCAM-1 and ICAM-1 are increased in the brain and in the liver of ischaemic rats exposed to 35% ethanol, compared to control ischaemic rats, at J1 and J7. The aggravation of neurologic and functional deficits was associated with increased post-ischaemic inflammation in both the liver and brain, as observed by microglial activation, neutrophil infiltration and leukocyte adhesion at short and intermediate terms.

Foi demonstrado que a L-prolina é fundamental para o metabolismo das formas intracelulares de T.cruzi e está envolvida em processos de resistência a diferentes condições de estresse. O ácido L-tiazolidina-4-carboxílico (T4C) age como inibidor competitivo do transporte de prolina para o interior do parasita, desta forma, pode-se assumir que, quando aplicado como agente terapêutico simula uma situação de hipoprolinemia no hospedeiro mamífero. Sobre esta base, propomos que a prolinemia poderia estar relacionada com a severidade da infecção pelo T. cruzi, portanto, decidimos inverter o racional e obter nesse trabalho um modelo de hiperprolinemia. Inicialmente foi estabelecido um modelo murino de hiperprolinemia transiente. Camundongos da linhagem BALB/c que foram tratados com prolina, por via intraperitonial (i.p), em 30 minutos já apresentaram concentrações plasmáticas de 1,359 ± 0,121 mM, porém, após 3 horas seus níveis plasmáticos retornaram ao normal, 0,4361 ± 0,03496. Utilizando este modelo, foi avaliado o efeito da hiperprolinemia transiente em camundongos infectados pelo T.cruzi. Em três ensaios de um total de seis foi observado um aumento significativo da parasitemia em camundongos tratados, sem nenhuma diferença na mortalidade e na carga parasitária de diversos tecidos. Essa inconsistência observada no perfil da parasitemia redirecionou os experimentos para um modelo de hiperprolinemia hereditário previamente estabelecido. Interessantemente, foram observados diminuições na parasitemia, porém, a mortalidade foi aumentada. Foi hipotetizado que, diferentemente do que acontece com a hiperprolinemia transiente, com os níveis plasmáticos aumentados de maneira estável, as formas intracelulares de T.cruzi teriam acesso ao aminoácido em quantidades e tempo maiores. No entanto, não se pode descartar como hipótese complementar, que a hiperprolinemia possa afetar a resposta imune e por sua vez, imunossuprimir ou imunoestimular o hospedeiro mamífero. Por esse motivo, avaliaram-se alguns parâmetros da resposta imune ex vivo. Ensaios ex vivo mostraram que tratamento com prolina diminui a produção de NO sob ativação por LPS, no entanto quando células peritoneais não ativadas por LPS são infectadas por T. cruzi, o tratamento com prolina não altera o perfil de NO. A expressão gênica da óxido nítrico sintase induzível (iNOS) das células peritoneais diminui quando elas são cultivadas na presença de prolina, confirmando esses resultados. Mostrou-se dessa maneira que a hiperprolinemia pode interferir com a resposta imune do hospedeiro, o que levaria a uma eventual imunossupressão. Observou-se que, tanto células peritoneais infectadas como não infectados tratadas com prolina apresentam redução de seu volume celular o que poderia ser indício de sinal apoptótico. Ensaios de infecção (ex vivo) em células peritoneais de camundongos BALB/c com tripomastigotas da cepa MJL superexpressando o transportador de prolina apresentaram aumento da taxa de infecção enquanto que as infectadas por tripomastigotas da cepa Y superexpressando o mesmo transportador de prolina apresentaram diminuição da taxa de infeçção, quando comparadas aos controles, mostrando que a reposta de redução ou aumento da taxa de infecção ao tratamento com prolina é determinada também pela cepa de T. cruzi. Análises da prolinemia em soro de pacientes com sintomas de cardiopatia chagásica severa mostraram menores níveis de prolina sérica quando comparados aos controles (pacientes não infectados). Juntos, todos esses resultados colocam a prolina como um fator de severidade na infecção pelo T. cruzi. / It was shown that L-proline is essential for the metabolism of the intracellular forms of T. cruzi and is involved in resistance to different stress conditions. L-thiazolidine-4-carboxylic acid (T4C) acts as a competitive inhibitor of the proline transport to the inside of parasite, thus it can be assumed that when T4C is applied as a therapeutic agent simulates a hipoprolinemia situation in the mammalian host. On this basis, we propose that prolinemia could be related to the severity of T. cruzi infection, then, in this work we decided to reverse the rational and obtain a hyperprolinemia model. As a starting point, it was established a mouse transient hyperprolinemia model. BALB/c mice were intraperitoneally injected with proline showed an increased proline levels in sera after 30 min (1,359 ± 0,121 mM). However, these increased levels were diminished to normal levels after 3 h (0,4361 ± 0,03496 mM). Once established this model, was initially used to evaluate the effect of transient hyperprolinemia in mice infected by T.cruzi. In three out of six experiments an increase in parasitemia but not in mortality or in tissue parasite loads was observed. In the remaining three experiments no differences were detected. These inconsistencies directed the work to the search to a previously established hereditary model of mouse hyperprolinemia model. Interestingly, in this new model, a diminished parasitemia was recorded, however, mortality was higher. From this information it was hypothesized that, differently to what happens in the transient hyperprolinemia, a permanent hyperprolinemia exposes the T. cruzi infected cells (and so, the intracellular parasites) to higher concentrations of proline as well as for longer times. In addition, it cannot be disregarded the complementary hypothesis that hyperprolinemia could be affecting the immune response and, at the same time of its action on the parasite, it could be immunosupresing or immunostimulating the mammalian host. This possibility led us to evaluate some parameters of the immune response both, in vivo and ex vivo. Ex vivo assays showed that proline-treated LPS-activated peritoneal cells had a diminished production of NO while proline-treatment of T. cruzi infected, non-LPS-activated peritoneal cells did not affect their NO production. This data showed that hyperprolinemia could interfer the immune response leading the host to an eventual immunosupresion. In addition, both, infected and non-infected macrophages had their cellular volume diminished when treated with proline, which could be attributed to the iniciation of an apoptotic process. Infection assays (ex vivo) of perioneal cells from BALB/c mice with MJL strain trypomastigotes overexpressing a proline transporter had an increased infection rate, while the same type of cells infected with Y strain trypomastigotes overexpressing the same proline transporter showed a diminution in the infection rate. These results show that changes in the infection rate as a function of intracellular proline availability depends on T. cruzi strain. The analysis of prolinemia in patients serum with symptoms of Severe Chronic Chagasic Cardiopathy showed tat proline levels were diminished in comparison to control (non-infected patients). Taken together, these results prompt proline as a factor modulating the severity of T. cruzi infection.

No description available.

Portugal is one of the Mediterranean countries that besides its natural condition to occur forest fires, has had an increase of forest fires during the last decades and has a consequence the increase of the burned surface and the costs associated, economic, social and environmental. This study case took place in Serra da Freita, a mountain region in the north of Portugal in the Aveiro District. The aim of this case study was to establish a relation between forest fires, erosion and social consequences for the region. For this purpose, a mixed approach was used with Remote sensing to acquire burn severity (dNBR) by comparing the areas before and after forest fires, soil analyses, and with a questionnaire to the local community to comprehend how they are affected. The results obtained permits to understand that not only the forest fires have a direct impact on the soil erosion, but also affect the local community by promoting the abandonment of the area.

No description available.

Ligia J. Zarate College of Nursing Master of Science Peripheral catheter-related phlebitis is the inflammation of a superficial vein that can lead to infection or thrombus formation if untreated. About 150 million peripheral intravenous catheters (PIVC) are inserted in the United States each year with phlebitis rates reported between 5% and 70%. Many PIVCs are started on trauma patients, but the rate of phlebitis in trauma patients whether the PIVC is started outside the emergency department (ED) or inside the ED is unknown. Therefore, the purpose of this pilot study was to determine phlebitis rates in trauma patients when PIVC's are started inside or outside the emergency department. Variables investigated, which may influence phlebitis rates were duration of time the catheter was in place, the anatomical placement site of the PIVC, the catheter gauge, where the PIVC initially was placed (inside or outside the ED), and the injury severity score (ISS). This was a prospective descriptive design. Results indicated 432 catheters were placed inside or outside the ED in trauma patients that met the inclusion criteria. The overall phlebitis rate was 5.79 %. The rate of phlebitis when the PIVC was started inside the ED was 2.92%. The rate of phlebitis when the PIVC was started outside the ED was 6.94%. If the PIVC was started outside the ED by EMTs the rate was 6.09%. When the PIVC was started outside the ED by paramedics the rate was 7.78%. There was no significant difference in rates of phlebitis according to where the PIVC was started when a Chi Square analysis was performed. No variables predicted phlebitis no matter where the PIVC was started when regression analyses were conducted. The rate of phlebitis in PIVCs started in the ED, or by EMTs or Paramedics outside the ED in this study was similar to and low according to the literature. The Center for Disease Control and Prevention (CDC) suggests removal of the PIVC within 48 hours if placed under emergency situations. However in this study, phlebitis rates of trauma patients meet the benchmark of best practice and perhaps removal of the PIVC within 48 hours should be reconsidered. Complete documentation of medical records was 87.4%. However, best practice of recording information and patient response to treatment should be higher.