8 research outputs found

    The European Hematology Association Roadmap for European Hematology Research: a consensus document

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    The European Hematology Association (EHA) Roadmap for European Hematology Research highlights major achievements in diagnosis and treatment of blood disorders and identifies the greatest unmet clinical and scientific needs in those areas to enable better funded, more focused European hematology research. Initiated by the EHA, around 300 experts contributed to the consensus document, which will help European policy makers, research funders, research organizations, researchers, and patient groups make better informed decisions on hematology research. It also aims to raise public awareness of the burden of blood disorders on European society, which purely in economic terms is estimated at €23 billion per year, a level of cost that is not matched in current European hematology research funding. In recent decades, hematology research has improved our fundamental understanding of the biology of blood disorders, and has improved diagnostics and treatments, sometimes in revolutionary ways. This progress highlights the potential of focused basic research programs such as this EHA Roadmap. The EHA Roadmap identifies nine ‘sections’ in hematology: normal hematopoiesis, malignant lymphoid and myeloid diseases, anemias and related diseases, platelet disorders, blood coagulation and hemostatic disorders, transfusion medicine, infections in hematology, and hematopoietic stem cell transplantation. These sections span 60 smaller groups of diseases or disorders. The EHA Roadmap identifies priorities and needs across the field of hematology, including those to develop targeted therapies based on genomic profiling and chemical biology, to eradicate minimal residual malignant disease, and to develop cellular immunotherapies, combination treatments, gene therapies, hematopoietic stem cell treatments, and treatments that are better tolerated by elderly patients

    Myelo peroxidase as an Indicator of Oxidative Stress in Metabolic Syndrome

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    Background: Increased myeloperoxidase (MPO) activity would be the link between the rise of the inflammatory response and oxidative stress (OS) in metabolic syndrome (MS). Objective: The aim of this study was to determine the enzymatic activity of MPO associated with OS in animals with MS and establish their relationship with probable cardiovascular injury. Methods: Male Wistar rats were divided into two groups: Group A, control (n=12) and Group B, induced MS (n=12). Metabolic syndrome was produced by 6-week administration of 10% fructose diluted in the drinking water. Insulin (mU/ml), glucose (mg/dl), lipid panel (mg/dl), HOMA (homeostatic model assessment), MPO (IU/ml) and superoxide dismutase (SOD) activity (U/ml) were measured. Light microscopy was used for the histological study of the heart and thoracic aorta. Results: Group B showed significantly increased levels of plasma glucose (176±17.3 mg/dl), insulin (29.5±4.52 mU/ml), HOMA (11±1.3), total cholesterol (133±9.6 mg/dl) and triglycerides (75±12.9 mg/dl) compared with Group A: plasma glucose (115±1.1 mg/dl), insulin (4±0.82 mU/ml), HOMA (3±0.38), total cholesterol (69.7±1.6 mg/dl) and triglycerides (46.2±6 mg/dl), (p<0.001 for all variables). A significant decrease in HDL (28.3±1.14 mg/dl) in Group B vs. Group A (61±1.0 mg/dl) (p<0.001) validated the experimental MS model. Myeloperoxidase activity increased significantly in Group B (181.3±15.7 IU/ml) vs. Group A (116.07±4.2 IU/ml) (p<0.001). A similar behavior was seen with SOD antioxidant activity in Group B (181±6 U/ml) vs. Group A (138±3.6 U/ml) (p <0.01). Light microscopy of the heart and thoracic aorta revealed histopathological changes in animals with induced MS. Conclusion: Increased MPO and SOD in Group B would indicate the presence of OS in MS, with consequences at the vascular level.Introducción: Los incrementos en la actividad de la mieloperoxidasa (MPO) serían el nexo entre el aumento de la respuesta inflamatoria y el estrés oxidativo (EO) en el síndrome metabólico (SM). Objetivo: Determinar la actividad de la enzima MPO asociada con EO en animales con SM y establecer su relación con las probables lesiones cardiovasculares. Material y métodos: Se utilizaron ratas macho de la cepa Wistar, que se dividieron en: Grupo A, control (n = 12) y Grupo B, inducción de SM (n = 12). El SM se indujo con la administración de fructosa al 10% diluida en agua de bebida durante 6 semanas. Se cuantificaron insulina (mU/ml), glucemia (mg/dl), perfil lipídico (mg/dl), HOMA (homeostatic model assessment), MPO (UI/ml) y actividad de la superóxido dismutasa (SOD) (U/ml). Se estudió la histología de la aorta torácica y el corazón por microscopia óptica. Resultados: Se observaron niveles de glucemia (176 ± 17,3 mg/dl), insulina (29,5 ± 4,52 mU/ml), HOMA (11 ± 1,3), colesterol total (133 ± 9,6 mg/dl) y triglicéridos (75 ± 12,9 mg/dl) incrementados significativamente en el Grupo B en comparación con el Grupo A: glucemia (115 ± 1,1 mg/dl), insulina (4 ± 0,82 mU/ml), HOMA (3 ± 0,38), colesterol total (69,7 ± 1,6 mg/dl) y triglicéridos (46,2 ± 6 mg/dl) (p < 0,001 para todas las variables); se verificó disminución significativa de los valores de HDL (28,3 ± 1,14 mg/dl) en el Grupo B en comparación con el Grupo A (61 ± 1,01 mg/dl) (p < 0,001), validando así el modelo experimental de SM. La actividad de la MPO se incrementó significativamente en el Grupo B (181,3 ± 15,7 UI/ml) respecto del Grupo A (116,07 ± 4,2 UI/ml) (p < 0,001). Similar comportamiento presentó la actividad antioxidante de la SOD en el Grupo B (181 ± 6 U/ml) respecto del Grupo A (138 ± 3,6 U/ml) (p < 0,01). Las microscopias ópticas de corazón y de aorta torácica evidenciaron cambios histopatológicos en los animales con SM inducido. Conclusión: Los incrementos de la MPO y la SOD en el Grupo B demostrarían la presencia de EO, con repercusión a nivel vascular en el SM

    Proceedings Of The 23Rd Paediatric Rheumatology European Society Congress: Part Two

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    Proceedings of the 23rd Paediatric Rheumatology European Society Congress: part one

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