Le syndrome de détresse respiratoire aiguë (SDRA) se développe suite à une atteinte pulmonaire lésionnelle, induisant un œdème et une inflammation excessive, généralement suivis d’une réparation atypique menant à la fibrose. Malgré de signifiants progrès dans les traitements, la mortalité reste élevée : ~ 40 %. Mon hypothèse de travail est que l’atténuation de l’œdème ou de la réponse inflammatoire pourrait freiner le développement ou la sévérité de la phase exsudative. Nous avons évalué cette hypothèse à l’aide d’un modèle de phase exsudative du SDRA, i.e. instillation intra-trachéale de bléomycine, chez les souris.  La modulation des fluides alvéolaires est étudiée avec des souris transgénique (Tg) pour le canal ENaC, qui sont sensibles à la formation d’un œdème. Cependant, ces souris Tg ne sont pas plus sensibles au développement de la phase exsudative en condition lésionnelle (bléomycine). Nous avons déterminé par une étude électrophysiologique des cellules épithéliales alvéolaires de type II (AT II) que ce n’est pas lié à une inhibition par la bléomycine de la fonction du canal ENaC.  Le traitement de la réponse inflammatoire associée au SDRA par des glucocorticoïdes est une thérapie potentielle mais controversée. Les glucocorticoïdes dans notre modèle murin ne réduisent pas la sévérité des lésions. Nous avons pu déterminé lors d’expériences in vitro que ce serait dû à une réduction de la capacité de réparation des AT II. En résumé :  La modulation du canal ENaC ne modifie pas le développement de la phase exsudative, suggérant que la régulation de l’œdème n’est pas suffisante pour modifier l’évolution du SDRA.  La modulation de l’inflammation par les glucocorticoïdes est ineffective, possiblement à cause d’une altération de la réparation. Mon étude suggère que le traitement de la phase exsudative du SDRA est complexe. En effet, la régulation de l’œdème ou de l’inflammation de façon isolée ne peut pas modifier l’évolution du SDRA. L'hétérogénéité des sources du SDRA et la redondance des mécanismes cellulaires impliqués dans l’évolution des lésions pulmonaires suggèrent que le traitement nécessitera une approche visant plusieurs cibles mécanistiques afin d’en accélérer la résolution. / Although much has been learned about the mechanisms leading to acute respiratory distress syndrome (ARDS), mortality remains high: ~ 40%. This syndrome is associated with lung injury where alveolar edema and excessive inflammatory response can progress to abnormal epithelial repair and fibrosis. The hypothesis of the work presented in this thesis is that attenuation of edema or of the inflammatory response in the initial stage of the acute lung injury would decrease the severity of injury. I evaluated this hypothesis in an ARDS acute phase, modeled by an intratracheal instillation of bleomycin in mice, using two distinct experimental strategies.  The importance of edema clearance was studied in a transgenic (Tg) ENaC mouse, a mouse known to be sensitive to the formation of edema. However, our results show that these Tg mice were not more susceptible to the development of the ARDS acute phase induced by bleomycin. Furthermore, we have been able to show that bleomycin itself did not interfere with the ENaC channel function of alveolar epithelial cells type II (AT II).  The treatment of the inflammatory response associated with ARDS by glucocorticoid therapy is subject to controversy. In our mouse model, glucocorticoids decrease the level of cytokine in the alveolar milieu but did not decrease the severity of lung injury. Using in vitro experiments, we show that this lack of response could be secondary to the impact of the treatment on the epithelial repair capacity of AT II. In summary:  The ENaC channel expression did not have an impact on the development of the exudative phase, suggesting that the regulation of edema is not sufficient to alter the course of ARDS.  The modulation of inflammation by glucocorticoids was ineffective, possibly because of impaired repair of the epithelium. These results suggest that the control of edema or inflammation separately does not modify the evolution of lung injury. The heterogeneity of the ARDS origins and the redundancy of cellular mechanisms involved in lung injury will require therapy aimed at multiple pathophysiological targets to permit the resolution of lung injury.

La détérioration de la barrière hémato rétinienne et l'oedème maculaire consécutif est une manifestation cardinale de la rétinopathie diabétique (RD) et la caractéristique clinique la plus étroitement associée à la perte de la vue. Alors que l'oedème maculaire affecte plus de 25% des patients souffrant de diabète, les modalités de traitement actuellement disponibles tels que les corticostéroïdes administrés localement et les thérapies anti-VEGF récemment approuvés présentent plusieurs inconvénients. Bien que le lien entre une rupture de l’unité neuro-vasculaire et la pathogénèse de la RD ait récemment été établi, l’influence de la signalisation neuro-vasculaire sur la vasculopathie oculaire diabetique a jusqu’à présent reçu peu d’attention. Ici, à l’aide d’ètudes humaines et animales, nous fournissons la première preuve du rôle essentiel de la molécule de guidage neuronale classique Sémaphorine 3A dans l’instigation de la perméabilité vasculaire maculaire pathologique dans le diabète de type 1. L’étude de la dynamique d’expression de Sémaphorine 3A révèle que cette dernière est induite dans les phases précoces hyperglycèmiques du diabète dans la rétine neuronale et participe à la rupture initiale de la fonction de barrière endothéliale. En utilisant le modèle de souris streptozotocine pour simuler la rétinopathie diabétique humaine, nous avons démontré par une série d’approches analogue que la neutralisation de Sémaphorine 3A empêche de façon efficace une fuite vasculaire rétinienne. Nos résultats identifient une nouvelle cible thérapeutique pour l’oedème maculaire diabétique en plus de fournir d’autres preuves de communication neuro-vasculaire dans la pathogènese de la RD. / The deterioration of the blood retinal barrier and consequent macular edema is a cardinal manifestation of diabetic retinopathy (DR) and the clinical feature most closely associated with loss of sight. While macular edema affects over 25% of patients suffering from diabetes, currently available treatment modalities such as locally administered corticosteroids and recently approved anti-VEGF therapies, present several drawbacks. Although recent insight on the pathogenesis of DR points to a breakdown in the neurovascular unit, neurovascular cross-talk and its influence on diabetic ocular vasculopathy has thus far received limited attention. Here we provide the first evidence from both human and animal studies for the critical role of the classical neuronal guidance cue Semaphorin3A in instigating pathological macular vascular permeability in type I diabetes. Investigation of the dynamics of expression reveal that Semaphorin3A is induced in the early hyperglycemic phases of diabetes within the neuronal retina and precipitates initial breakdown of endothelial barrier function. Using the streptozotocin mouse model as a proxy for human diabetic retinopathy, we demonstrate by a series of orthogonal approaches (gene silencing or treatment with soluble Neuropilin-1 employed as a Semaphorin3A trap), that neutralization of Semaphorin3A efficiently prevents retinal vascular leakage. Our findings identify a new therapeutic target for DME and provide further evidence for neurovascular cross-talk in pathogenesis of DR.

In this Ph.D. thesis, we study new methods to analyse digital fundus images of diabetic patients. In particular, we concentrate on the development of the algorithmic components of an automatic screening system for diabetic retinopathy. The techniques developed can be categorized in: quality assessment and improvement, lesion segmentation and diagnosis. For the first category, we present a fast algorithm to numerically estimate the quality of a single image by employing vasculature and colour-based features; additionally, we show how it is possible to increase the image quality and remove reflection artefacts by merging information gathered in multiple fundus images (which are captured by changing the stare point of the patient). For the second category, two families of lesion are targeted: exudate and microaneurysms; two new algorithms which work on single fundus images are proposed and compared with existing techniques in order to prove their efficacy; in the microaneurysms case, a new Radon transform-based operator was developed. In the last diagnosis category, we have developed an algorithm that diagnoses diabetic retinopathy and diabetic macular edema based on the lesions segmented; starting from a single unseen image, our algorithm can generate a diabetic retinopathy and ma cular edema diagnosis in _22 seconds on a 1.6 GHz machine with 4 GB of RAM; additionally, we show the first results of a macular edema detection algorithm based on multiple fundus images, which can potentially identify the swelling of the macula even when no lesions are visible.

Thesis (doctoral)--Uppsala University, 1982. / Includes bibliographical references (p. 35-39).

Un dysfonctionnement du métabolisme cérébral est observé au décours d'un traumatisme crânien (TC). L’œdème cérébral et l’hypoxie cérébrale post-traumatiques sont des acteurs principaux de l’apparition des lésions ischémiques secondaires responsables en partie de la défaillance énergétique. Cette hypoxie tissulaire résulte de troubles macrocirculatoires, de troubles de la microcirculation et/ou de troubles de la diffusion de l’oxygène des capillaires sanguins aux tissus. La baisse de la consommation en oxygène est également liée à une dysfonction mitochondriale post traumatique de la chaine respiratoire. Ces phénomènes ischémiques ou hypoxiques aboutissent ainsi à une élévation de lactate endogène en condition anaérobie. Cependant, l'élévation de lactate endogène post traumatique est liée majoritairement à une crise métabolique conduisant à une hyperglycolyse en dehors de tout phénomène hypoxique ou ischémique. L'objectif de notre étude était donc d’étudier l'œdème cérébral, l'oxygénation cérébrale, la défaillance mitochondriale post traumatique et le métabolisme cérébral dans un modèle expérimental de traumatisme crânien diffus par impact accélération chez l'animal. Nous avons étudié les effets de différents neuroprotecteurs sur le métabolisme cérébral à l'aide d'un monitorage multimodal. Les effets de la rhEpo (5000UI/Kg), du mannitol (1g/kg) et du lactate de sodium molaire (1.5 ml/Kg soit 3mOsm/kg) ont été étudiés sur l'œdème cérébral (IRM, microscopie électronique), sur l'hypoxie cérébrale tissulaire (IRM BOLD, mesure de la pression tissulaire en O2, saturation veineuse en O2 du sinus longitudinal supérieur), sur le métabolisme cérébral (spectroRMN) et sur la mitochondrie (analyse de la capacité de rétention calcique, de la chaine respiratoire, microscopie électronique et mesure du calcium intramitochondrial) chez des rats wistar mâles. Notre hypothèse était que l’injection de différents neuroprotecteurs permettrait d’améliorer le métabolisme cérébral post traumatique par des effets bénéfiques sur l’hémodynamique cérébrale et l'œdème cérébral, sur l'hypoxie tissulaire ou sur la dysfonction mitochondriale post TC. Nos résultats ont démontré que la rhEpo avait un effet bénéfique sur l'hypoxie cérébrale post traumatique par le biais d'une diminution de l'œdème cérébral péri capillaire en phase aigue associée à une diminution de la dysfonction mitochondriale proapoptotique. Le mannitol améliore l'hypoxie cérébrale post traumatique en jouant sur la microvascularisation cérébrale perturbée par l'œdème astrocytaire péri capillaire. Enfin, le lactate de sodium molaire avait des effets bénéfiques anti œdémateux et sur la dysfonction mitochondriale post TC améliorant ainsi la crise métabolique post traumatique. Ces résultats permettent d'améliorer la compréhension de la physiopathologie des lésions survenant au décours du traumatisme crânien ainsi que les mécanismes d'action de différentes molécules neuroprotectrices. / Cerebral metabolism is impaired after a Traumatic Brain Injury (TBI). Post traumatic cerebral edema and hypoxia are mainly responsible of the development of secondary ischemic lesions after TBI leading to metabolic impairment. Tissular hypoxia can result from disorders in macro and microcirculation and/or disturbance in the diffusion of oxygen from the blood capillaries to tissue. The decrease in oxygen consumption observed after brain injury is also related to a post traumatic dysfunction of the mitochondrial respiratory chain. These ischemic or hypoxic phenomena may be responsible for metabolic disorders leading to elevated level of endogenous lactate under anaerobic conditions. However, the elevation of endogenous lactate is mainly the consequence of a metabolic crisis that led to a state of hyperglycolysis without cerebral hypoxia or ischemia after TBI. The aim of our study was to investigate cerebral edema, cerebral oxygenation, mitochondrial and metabolic impairment post TBI in an experimental model of impact acceleration diffuse brain injury in rats. We also analyzed the effects of various neuroprotective agents on cerebral metabolism using a multimodal monitoring. The effects of rhEpo (5000UI/Kg), mannitol (1g/Kg) and of molar sodium lactate (1.5 ml/Kg or 3mOsm/kg) were investigated on brain edema (MRI, electronic microscopy), on brain tissue hypoxia (BOLD MRI, measurement of the tissular pressure of O2, venous O2 saturation of the upper longitudinal sinus), on brain metabolism (Magnetic Resonance Spectroscopy) and on mitochondria (study of the calcium retention capacity, of the respiratory chain, morphological analysis with electronic microscopy and measurement of intramitochondrial calcium) in male wistar rats. We hypothesized that the injection of various neuroprotective agents would improve posttraumatic cerebral metabolism by restoring a better cerebral hemodynamic status, by improving cerebral edema, tissular oxygenation and/or mitochondrial function. On the early phase of TBI, we demonstrated that rhEpo had a beneficial effect on post traumatic cerebral hypoxia by decreasing post-traumatic cerebral capillaries collapse due to astrocytic end-foot swelling. This effect was associated with an improvement in cellular apoptosis induced by mitochondrial pathways. Mannitol improved brain hypoxia by decreasing peri vascular astrocytic edema. Sodium lactate had benefic effects on cerebral hypoxia by decreasing cerebral edema and improved mitochondrial and metabolic impairments after TBI. These results help understanding physiopathological events after TBI and the various effects of neuroprotective agents that can be used in future clinical research.

A infestação de pastagens por populações de Pteridium arachnoideum é um problema que afeta a pecuária, em diversas partes do mundo. Os efeitos deletérios da infestação pela planta sobre a bovinocultura são manifestados na forma de mortalidades e de redução das áreas de pastagens, assim como de perdas produtivas. Devido à importância dessas perdas na produção de bovinos, foi proposto o acompanhamento de uma propriedade do Rio Grande do Sul com problemas decorrentes da infestação pela planta em sua casuística e métodos de controle empregados. Adicionalmente, realizou-se teste da viabilidade de ovinos como ferramenta de controle biológico. Dos casos de intoxicação naturais acompanhados na propriedade, observou-se a ocorrência de quadro agudo de diátese hemorrágica e de quadro crônico de carcinomas do trato digestório superior. Observou-se que quando expostos a fatores predisponentes, como a introdução em áreas recentemente roçadas, os bovinos podem consumir altas doses da planta e assim desenvolver a enfermidade aguda em forma de surtos. Em diversos bovinos jovens com quadro de diátese hemorrágica, além das hemorragias disseminadas e infartos múltiplos, observou-se acentuado edema laríngeo, que cursava clinicamente com dispneia e estertores respiratórios característicos. Os carcinomas do trato digestório superior, apesar de menos frequentes, causaram expressivas perdas devido a mortalidades anuais de matrizes. A tentativa de controle pelo pastejo por ovinos não foi eficiente, devido ao consumo pouco expressivo na lotação praticada. Mortalidade de ovinos, no entanto, decorrente do consumo da planta não foi registrada. O método de combate à planta aplicado na propriedade combinava ou associava a roçagem em áreas densamente povoadas com o uso de herbicidas, nomeadamente metilsulfuron-metil e picloram, em todos os piquetes. A redução da cobertura da P. arachnoideum foi variada em diferentes piquetes; entretanto, possibilitou a recuperação de algumas áreas de pastejo. / The infestation of pastured areas by Pteridium arachnoideum populations has been a considerable and global problem to the livestock production. The deleterious effects of the plant infestation on cattle are manifested as animal mortality and pasture coverage reduction. Given the importance of P. arachnoideum in cattle production, it has been proposed to monitor a beef cattle farm in Rio Grande do Sul, to assess some of the losses associated with the plant consumption apart of the methods employed for controlling the plant. In addition, the viability of sheep’s grazing as a biological control tool was tested. Cases of natural poisoning observed in the farm included the acute form, known as hemorrhagic diathesis as well as the chronic form, consisting in digestive carcinomas. When cattle were exposed to any predisposing factor, such as being moved to newly mowed areas, it was noted that the amount of plant consumed can readily lead to an outbreak of acute poisoning. Several cases of hemorrhagic diathesis in young cattle went along with marked laryngeal edema, which was clinically manifested as dyspnea and roaring, in addition to the classic pathological changes of widespread hemorrhages and infarcts. Even though less frequent, carcinomas of the upper digestive tract caused significant losses, due to annual mortality of mature cows. The attempt through grazing by sheep wasn’t efficient to control P. aquilinum, due to the low consumption of the plant seen in the actual stocking. However, sheep mortality, by P. arachnoideum consumption was not recorded. The plant control method applied at the farm combined mowing of densely populated areas with herbicide applications, namely metilsulfuron-methyl and picloram, in all paddocks. The reduction of P. arachnoideum coverage was varied in different paddocks; however, allowed the recovery of some grazing areas.

BACKGROUND: Osteoarthritis is a leading cause of disability in people of 65 and older. Researches have shown several possible factors leading to knee osteoarthritis development. Patellofemoral joint maltracking has been thought to be associated with or caused edema in the knee; which is thought to be the early signs of osteoarthritis. Hoffa's fat pad is an intra-articular component of knee located under the kneecap. It has also been suggested as one marker for osteoarthritis, when MRI shows a presence of edema in it. Recently, edema in the superolateral region of Hoffa's fat pad has been hypothesized as a distinct signal than the edema on other regions. There is an interest in finding the relation of this superolateral edema with other factors of osteoarthritis development. OBJECTIVE: This thesis research project is aimed to assess the relation of kneecap-thighbone (patellofemoral) joint alignment, femoral trochlea morphology, and patellar height to edema in the superolateral region of Hoffa’s fat pad especially in the population with average age above 65 years old. The hypothesis is that the flatter trochlear morphology and abnormal patella alignment will have higher risk of superolateral edema. METHODS: This is a cross-sectional study using a subset data from Multicenter Osteoarthritis (MOST) study, specifically at 60-month visit. This study measured the patellofemoral measurements (sulcus angle, lateral and medial trochlear inclination angle, trochlear angle, Insall-Salvati ratio, patellar tilt angle, and bisect offset) as the predictor variables, and semiquantitative scoring of MRI edema in superolateral Hoffa’s fat pad as the outcome variable. Logistic regression analyses were performed to find the strongly associated patellofemoral measurements to superolateral Hoffa’s fat pad edema. RESULTS: From the logistic regression analysis, trochlear angle, Insall-Salvati ratio, and bisect offset were highly associated with the superolateral edema. A further analysis, by categorizing the measurements to quartiles, was found that only the highest quartiles of both bisect offset and trochlear angle are associated with superolateral Hoffa’s fat pad edema when compared to the reference quartile. All quartiles of Insall-Salvati ratio are strongly associated with superolateral edema when compared to the reference quartile. CONCLUSION: Current study presents that people above 65 years old with high trochlear angle, extreme lateral patellar translation or bisect offset, and high patella riding have high risk of having superolateral Hoffa’s fat pad edema.

Bacillus anthracis, agent de la maladie du charbon, est aussi un agent majeur de la menace biologique. Sa virulence est liée à deux principaux facteurs : une capsule et deux toxines, la toxine oedémateuse (ET = EF + PA) et la toxine létale (LT = LF + PA). EF est une adénylate cyclase, calcium et calmoduline dépendante, produisant une élévation de la concentration en AMPc intracellulaire tandis que LF est une métalloprotéase à zinc clivant la majorité des Mitogen Activated Protein Kinase Kinases. Les toxines jouent un rôle central dans la pathogénie de la maladie du charbon et dans la dérégulation des fonctions des cellules du système immunitaire. Le cytosquelette d'actine participe activement aux fonctions de phagocytose et de migration des macrophages et des cellules dendritiques.Cependant, peu d'études analysent l'implication du cytosquelette d'actine des cellules immunitaires dans la physiopathologie des toxines. ET induit une rétraction temps-dépendant des cellules dendritiques et des macrophages normalisés sur des micropatterns de fibronectine, s'accompagnant d'une dépolymérisation de l'actine et d'une perte des points d'ancrage des cellules dendritiques. Précocement, ET active la cofiline par l'activation de la voie de signalisation AMPc – PKA – Protéines phosphatases. Malgré ces altérations du cytosquelette d'actine, ET n'induit pas de modification des capacités phagocytaires des cellules dendritiques, à l'exception d'une dérégulation de la maturation des phagosomes. ET conduit également à une augmentation de la migration des cellules dendritiques in vitro par activation et expression de CCR7 et CXCR4 à la surface des cellules dendritiques.A l'inverse, LT conduit à un étalement temps-dépendant des cellules dendritiques normalisées, accompagné d'une dérégulation de la dynamique de l'actine provoquant des regroupements anormaux d'actine filament. LT active les myosines phosphatases via la voie RhoA-ROCK pour déphosphoryler les myosines II. A la différence de ET, LT inhibe les capacités phagocytaires des cellules dendritiques mais ne conduit pas à une modification de la migration des cellules dendritiques in vitro. / Bacillus anthracis, the agent of anthrax, is also a major agent of biological warfare threat. Its virulence is caused by two main factors : the capsule and two toxins, edema toxin (ET = PA + EF) and lethal toxin (LT = LF + PA). EF is a calcium and calmodulin-dependent adenylate cyclase, producing a rise in intracellular cAMP concentration, while LF is a zinc metalloprotease cleaving the majority of Mitogen Activated Protein Kinase Kinases. The toxins play a central role in the pathogenesis of the disease and the deregulation of the functions of immune cells. The actin cytoskeleton is actively participating in the phagocytosis and the migration of macrophages and dendritic cells.However, few studies analyze the involvement of the actin cytoskeleton of immune cells in the pathogenesis of toxins. ET induces a time-dependent retraction of dendritic cells and macrophages on fibronectin micropatterns, accompanied by actin depolymerization and a loss of the anchor points of dendritic cells. ET early activates cofilin by activating the cAMP - PKA - Protein phosphatases signaling pathway. Despite these alterations of the actin cytoskeleton, ET does not induce any change in the phagocytic capacity of dendritic cells, except for a deregulation of the phagosomes maturation. ET also leads to an increase in the migration of dendritic cells in vitro by activation and expression of CCR7 and CXCR4 on the surface of dendritic cells.In contrast, LT results in a time-dependent spreading of micropatterned dendritic cells, accompanied by a dysregulation of actin dynamics causing abnormal combinations of actin filament. LT activates myosin phosphatase via the RhoA-ROCK pathway to dephosphorylate myosin II. Unlike ET, LT inhibits the dendritic cells phagocytosis but does not lead to a change in dendritic cells migration in vitro.

Submitted by Jos? Henrique Henrique (jose.neves@ufvjm.edu.br) on 2017-02-14T16:13:27Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) thiago_cesar_lima.pdf: 1162775 bytes, checksum: 1299abb85838ff2827416270126f508d (MD5) / Approved for entry into archive by Rodrigo Martins Cruz (rodrigo.cruz@ufvjm.edu.br) on 2017-03-06T12:23:26Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) thiago_cesar_lima.pdf: 1162775 bytes, checksum: 1299abb85838ff2827416270126f508d (MD5) / Made available in DSpace on 2017-03-06T12:23:26Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) thiago_cesar_lima.pdf: 1162775 bytes, checksum: 1299abb85838ff2827416270126f508d (MD5) Previous issue date: 2016 / A remo??o de terceiros molares inferiores retidos ? um procedimento invasivo com extenso trauma tecidual e resposta inflamat?ria p?s-operat?ria consider?vel. O objetivo deste estudo foi comparar o efeito da dexametasona 8mg (grupo controle) com o diclofenaco s?dico 50mg associados com fosfato de code?na 50mg (grupo experimental) para o controle da dor, edema e trismo, ap?s a exodontia dos terceiros molares inferiores impactados. Trinta terceiros molares inferiores de quinze pacientes saud?veis, com idade m?dia de 22,8 anos (desvio padr?o 12,62) receberam dose oral e ?nica de um dos f?rmacos uma hora antes de cada procedimento cir?rgico (dentes do lado esquerdo ou direito). Ap?s a cirurgia o edema foi aferido em 24, 48, 72 horas e 7 dias, sendo determinado por medidas lineares sobre o rosto, o trismo foi determinado pela abertura m?xima de boca. A dor p?s-operat?ria foi determinada pelo paciente atrav?s de uma escala visual de anal?gica, em intervalos de 24 horas, dentro de um per?odo total de 72 horas. A an?lise dos dados envolveu estat?stica descritiva, teste de Shapiro-Wilk, Wilcoxon, e teste T emparelhado (P<0,05). A dexametasona obteve melhores resultados nas an?lises de dor (p = 0,016) e edema (p = 0,08) no per?odo de 48 horas. N?o houve diferen?as estatisticamente significativas entre as drogas em rela??o ao trismo e ao n?mero de analg?sicos consumidos. Em conclus?o, a administra??o preventiva da dexametasona 8mg apresentou melhor controle da dor e edema nas exodontias bilaterais de terceiros molares inferiores impactados. / Disserta??o (Mestrado) ? Programa de P?s-Gradua??o em Odontologia, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2016. / Removing third retained molars is an invasive procedure with extensive tissue trauma and considerable postoperative inflammatory response. The aim of this study was to compare the effect of dexamethasone 8mg (control group) with diclofenac sodium 50mg associated with codeine phosphate 50 mg (experimental group) to control pain, swelling and trismus after extraction of third molars impacted. Thirty third molars fifteen healthy subjects with a mean age of 22.8 years (standard deviation 12.62) and received oral single dose of one of the drugs an hour before each surgery (teeth on the left or right). After surgery the edema was measured at 24, 48, 72 hours and 7 days, being determined by linear measurements on the face, trismus was determined by the maximum mouth opening. Postoperative pain was determined by the patient using a visual analogue scale at intervals of 24 hours, within a total period of 72 hours. The data analysis involved descriptive statistics, Shapiro-Wilk test, Wilcoxon test, and paired t-test (P <0.05). Dexamethasone better results in pain analysis (p = 0.016) and edema (p = 0.08) within 48 hours. There were no statistically significant differences between the drug relative to trismus, and the number of analgesics consumed. In conclusion, the preventive administration of dexamethasone 8mg showed better control of pain and edema in bilateral extractions of third molars impacted.

Através das imagens de fundo do olho, os especialistas em oftalmologia podem detectar possíveis complicações relacionadas ao Diabetes como a diminuição ou até a perda da capacidade de visão. O Edema Macular Diabético (EMD) é uma das complicações que lideram os casos de danos à visão em pessoas em idade de trabalho. Sendo assim, esta tese apresenta métodos para automaticamente identificar os diferentes níveis de gravidade do Edema Macular Diabético visando auxiliar o especialista no diagnóstico dessa patologia. Como resultado final, propõe-se automaticamente e rapidamente identificar, a partir da imagem, se o paciente possui o EMD leve, moderado ou grave. Utilizando imagens de fundo do olho de um banco de dados livremente disponível na internet (ou seja, o DIARETDB1), o método proposto para a identificação automática do EMD obteve uma precisão de 94,29%. Alguns métodos intermediários necessários para a solução desse problema foram propostos e os resultados publicados na literatura científica. / Through color eye fundus images, the eye care specialists can detect possible complications related to diabetes as the vision impairment or vision loss. The Diabetic Macular Edema (DME) is the most common cause of vision damage in working-age people. Therefore, this thesis presents an approach to automatically identify the different levels of severity of diabetic macular edema aiming to assist the expert in the diagnosis of this pathology. As a final result, a methodology to automatically and quickly identify, from the eye fundus image, if a patient has the EMD mild, moderate or severe EMD is proposed. In a preliminary evaluation of our DME grading scheme using publicly available eye fundus images (i.e., DIARETDB1 image database), an accuracy of 94.29% was obtained. Some intermediate methods needed to solve this problem have been proposed and the results published in scientific literature.