Assuntos
Hematoma/diagnóstico , Hemofilia A/complicações , Hemofilia A/diagnóstico , Doenças da Bexiga Urinária/diagnóstico , Neoplasias da Bexiga Urinária/diagnóstico , Pré-Escolar , Diagnóstico Diferencial , Fator VIII/uso terapêutico , Seguimentos , Hematoma/tratamento farmacológico , Hematúria/etiologia , Hemofilia A/tratamento farmacológico , Humanos , Lactente , Recém-Nascido , Assistência de Longa Duração , Masculino , Ultrassonografia , Doenças da Bexiga Urinária/tratamento farmacológico , Neoplasias da Bexiga Urinária/tratamento farmacológicoAssuntos
Hemofilia A/complicações , Hemofilia A/diagnóstico , Degeneração Hepatolenticular/complicações , Degeneração Hepatolenticular/diagnóstico , Adenosina Trifosfatases/genética , Proteínas de Transporte de Cátions/genética , Deleção Cromossômica , Inversão Cromossômica , ATPases Transportadoras de Cobre , Análise Mutacional de DNA , Diagnóstico Precoce , Fator VIII/genética , Fator VIII/uso terapêutico , Triagem de Portadores Genéticos , Hemofilia A/genética , Hemofilia A/terapia , Degeneração Hepatolenticular/genética , Degeneração Hepatolenticular/terapia , Humanos , Íntrons , Testes de Função Hepática , Masculino , Penicilamina/uso terapêutico , Ultrassonografia , Vitamina B 6/uso terapêuticoRESUMO
Early manifestations of posttransplant lymphoproliferative disorders (PTLD) are mainly associated with a primary Epstein-Barr virus (EBV) infection. Rapid increases in peripheral blood EBV DNA load are supposed to reliably predict PTLD. We report a boy who 6 months after living-related kidney transplantation presented with an extranodal esophageal manifestation of PTLD. Despite a primary EBV infection with tonsillitis, the peripheral blood EBV DNA remained low, hiding the progression to PTLD.
Assuntos
Neoplasias Esofágicas/diagnóstico , Transplante de Rim/efeitos adversos , Transplante de Rim/imunologia , Transtornos Linfoproliferativos/diagnóstico , Adulto , Criança , Neoplasias Esofágicas/patologia , Herpesvirus Humano 4/isolamento & purificação , Teste de Histocompatibilidade , Humanos , Transtornos Linfoproliferativos/fisiopatologia , Imageamento por Ressonância Magnética , Masculino , Complicações Pós-Operatórias/imunologiaRESUMO
Several aryl substituted C-fucopeptides have been developed as sialyl Lewis X mimetics. Although the compounds have a much simpler structure compared to SLe(x), up to 3-times higher binding affinity toward E-selectin and > 1000 times toward P-selectin was observed. Furthermore, a convenient strategy for generating a number of analogues from a SLe(x) mimetic template at a very late stage of the synthesis was introduced, using a ruthenium catalyzed cross olefin metathesis under benchtop conditions.
Assuntos
Fucose/química , Oligossacarídeos/síntese química , Oligossacarídeos/farmacologia , Peptídeos/química , Sequência de Carboidratos , Desenho de Fármacos , Concentração Inibidora 50 , Modelos Químicos , Dados de Sequência Molecular , Selectinas/metabolismo , Antígeno Sialil Lewis XRESUMO
Two series of C-linked fucosides as mimetics for the tetrasaccharide sialyl Lewis X have been synthesized and tested as inhibitors of E-Selectin. The fucopeptides have been prepared from three key intermediates, including alpha-C-allyl fucose, natural and unnatural amino acids bearing hydroxyl groups and an alpha, omega-diacid moiety for the imitation of the essential three parts of SLex, i.e., the Fuc, Gal, and NeuAc. The nature and distance of the linkage of the fucose moiety to the amino acids as well as the distance between the amino acids and the terminal carboxylic acid group turned out to be crucial for the biological activity. In addition the necessity of both OH groups (4- and 6-OH) in the Gal part could be confirmed. Conformational NMR study of the most active mimetic supports the structure-activity relationship. A second series of mimetics was prepared, where Fuc and Gal moieties were purely C-linked. In the synthesis of beta-C-allyl galactose an intramolecular 1,2-hydride shift led to an interesting side product. However, the substituted glycosidic oxygens led to a substantial loss of conformational constrain, which could not be compensated and resulted in low activity.