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The field of hematology involves the analysis of blood and its components like platelets, red blood cells, white blood cells. The outcome of this analysis can be vital in determining the condition of the human body and it is important to obtain accurate results. A deep learning algorithm scans over the given input data for unique features and learns them. Then it identifies these features and correlates them to give the result. This can save a significant amount of time and manual work. In contrast, a traditional machine learning algorithm requires the developer to carry-out the feature engineering. This thesis involves the analysis of white blood cells (WBC) using deep learning techniques. In collaboration with a hematology company HemoCue AB based in Angelholm, we will be developing deep learning algorithms for the analysis of white blood cells in the HemoCue R WBC DIFF System. Predominantly, there are two stages in this thesis. The first stage is white blood cell identification, which is used to calculate the number of white blood cells in the given blood sample. The next stage is to identify the different types of white blood cells with which the concentration of each type of WBC in the given blood sample is calculated. We have explored different classification approaches like ’one vs all’ and ’4-class classifier’, and have developed two CNN architectural designs i.e. ’multi-input’ and ’multi-channel’. On comparing the performance of all these design approaches, a final integrated model is put forth for the analysis of WBCs in the company’s device. The proposed ’one vs all’ classification approach combined with a 3-class CNN classifier has yielded very promising results with a combined accuracy 95.45% in WBC identification and 90.49% in WBC differential classification.

Human cells from acute myeloid leukemia (AML) patients are frequently transplanted into immune-compromised mouse strains to provide an in vivo environment for studies on the biology of the disease. Since frequencies of leukemia re-initiating cells are low and a unique cell surface phenotype that includes all tumor re-initiating activity remains unknown, the underlying mechanisms leading to limitations in the xenotransplantation assay need to be understood and overcome to obtain robust engraftment of AML-containing samples. We report here that in the NSG xenotransplantation assay, the large majority of mononucleated cells from patients with AML fail to establish a reproducible myeloid engraftment despite high donor chimerism. Instead, donor-derived cells mainly consist of polyclonal disease-unrelated expanded co-transplanted human T lymphocytes that induce xenogeneic graft versus host disease and mask the engraftment of human AML in mice. Engraftment of mainly myeloid cell types can be enforced by the prevention of T cell expansion through the depletion of lymphocytes from the graft prior transplantation.

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Made available in DSpace on 2014-08-20T13:49:19Z (GMT). No. of bitstreams: 1 CatiaFLeite.pdf: 1303895 bytes, checksum: f2a907bfd8b3da1ab25067969c014119 (MD5) Previous issue date: 2011-03-24 / Fatigue can be caused by depletion of carbohydrates and by the action of reactive oxygen species. Thus, carbohydrates are recognized as important to improve performance, minimize the decline in immune activity and reduce oxidative stress. Objective: To assess the occurrence of oxidative damage and abnormal levels of blood leukocytes in trained and sedentary rats supplemented with maltodextrina or water. Methods: Male Wistar rats (60 days) were divided into six groups: sedentary non-supplemented (n = 12) and supplemented (n = 12), trained in EEML - Maximum Lactate Steady State - not supplemented (n = 11) and supplemented (n = 11), trained at high intensity non-supplemented (n = 12) and supplemented (n = 11). The training protocol consisted of 8 weeks of swimming in a continuous pattern in EEML (60min.day-1) or intermittent (two periods of 30 minutes, with an interval of 10min), with loads corresponding to 5% and 10% of body weight,respectively. During 37 days the animals were supplemented with a daily dose of 0.48 g.kg-1 maltodextrin dissolved in water or pure water. Concentrations of blood lactate, hepatic glycogen content and muscle lipid peroxidation, protein oxidation and total and differential leukocytes were measured. Results: Despite the lack of statistical significance in malondialdehyde concentration and total and differential count of leukocytes between the groups, both exercise models have resulted in increases in protein carbonyl (p˂0.001). Aerobic exercise and supplementation with maltodextrin resulted in increased muscle glycogen content when compared to sedentary groups receiving water (p=0.007) or maltodextrin (p=0.008). Conclusions: The exercise did not cause damage to the lipid layers or abnormal levels of circulating leukocytes, however, both standards of training provided important protein loss. Maltodextrin supplementation was effective in sparing muscle glycogen stores during aerobic exercise. / A fadiga pode ser causada pela acidose metabólica, a depleção de substratos e a ação das espécies reativas de oxigênio (EROs). A hipoglicemia, por exemplo, também resulta em imunossupressão. Sendo o carboidrato um nutriente importante para retardar a acidose metabólica, melhorar o desempenho esportivo, minimizar a queda na atividade imunológica e reduzir a ocorrência de estresse oxidativo, além de haver uma escassez de estudos nesta área se reforçam a necessidade de novos estudos. Objetivo: verificar a ocorrência de dano oxidativo e alterações nas concentrações de leucócitos sanguíneos em ratos treinados e suplementados ou não com maltodextrina. Materiais e Métodos: Ratos machos (69 no total), Wistar, com 60 dias serão divididos em seis grupos experimentais: SN (sedentário não suplementado, n=12), SS (sedentário suplementado, n=12), TEN (treinado em EEML - Estado Estável Máximo de Lactato - não suplementado, n=11), TES (treinado em EEML suplementado, n=11), TAN (treinado em alta intensidade não suplementado, n=12) e TAS (treinado em alta intensidade suplementado, n=11). O protocolo de treinamento consistirá de oito semanas de exercícios de natação em padrão contínuo em EEML (60min.dia-1) ou intermitente (2 períodos de 30min, com intervalo de 10min), com sobrecargas correspondentes a 5% e 10% do peso corporal, respectivamente. Os animais serão suplementados por oito semanas com uma dose diária de 0,48g.kg-1 de maltodextrina dissolvida em água ou receberão somente água pura. As concentrações de lactato sanguíneo, conteúdo de glicogênio hepático e muscular, peroxidação lipídica através de TBARS, oxidação de proteínas e contagem total e diferencial de leucócitos serão analisadas

Human cells from acute myeloid leukemia (AML) patients are frequently transplanted into immune-compromised mouse strains to provide an in vivo environment for studies on the biology of the disease. Since frequencies of leukemia re-initiating cells are low and a unique cell surface phenotype that includes all tumor re-initiating activity remains unknown, the underlying mechanisms leading to limitations in the xenotransplantation assay need to be understood and overcome to obtain robust engraftment of AML-containing samples. We report here that in the NSG xenotransplantation assay, the large majority of mononucleated cells from patients with AML fail to establish a reproducible myeloid engraftment despite high donor chimerism. Instead, donor-derived cells mainly consist of polyclonal disease-unrelated expanded co-transplanted human T lymphocytes that induce xenogeneic graft versus host disease and mask the engraftment of human AML in mice. Engraftment of mainly myeloid cell types can be enforced by the prevention of T cell expansion through the depletion of lymphocytes from the graft prior transplantation.

The cellular prion protein (PrPc) is essential for pathogenesis of fatal neurodegenerative prion diseases. Recently reported four cases of vCJD transmission by blood transfusion raise concerns about the safety of blood products. Proper understanding of PrPc in blood is necessary for development of currently unavailable blood screening tests for prion diseases. Flow cytometry is an attractive method for prion detection, however, the reports on the quantity of PrPc on human blood cells are contradictory. We showed that the majority of PrPc in resting platelets is present in the intracellular pool and is localized in α-granules. We demostrated that both, human platelets and red blood cells (RBC) express significant amount of PrPc and thus may play an important role in the transmission of prions by blood transfusion. Our results suggest a unique modification of PrPc on human RBC. Such modification of pathological prion protein could distort the results of blood screening tests for prions. Further we showed that the storage of blood prior to analysis and the choice of anti-prion antibody greatly affect the detection of PrPc by flow cytometry and we identified platelet satellitism as a factor contributing to the heterogeneity of PrPc detection in blood cells. Moreover, we demonstrated existence of...