Protein Tyrosine Kinase Therapeutic Use
Mostrando 1-4 de 4 artigos, teses e dissertações.
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1. Motivating medical students to learn basic science concepts using chronic myeloid leukemia as an integration theme
Objective: To report on the use of chronic myeloid leukemia as a theme of basic clinical integration for first year medical students to motivate and enable in-depth understanding of the basic sciences of the future physician. Methods: During the past thirteen years we have reviewed and updated the curriculum of the medical school of the Universidade Estadu
Rev. Bras. Hematol. Hemoter.. Publicado em: 2015-02
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2. Hematologic and cytogenetic response in chronic myeloid leukemia patients treated with inhibitor of tyrosine kinase (imatinib) / "Avaliação da resposta clínica e citogenética em portadores de leucemia mielóide crônica, tratados com inibidor da tirosina quinase (imatinib)"
O STI (imatinib, Glivec) é um inibidor da tirosina quinase BCR-ABL, responsável pela patogênese da leucemia mielóide crônica (LMC). Um total de 110 pacientes com LMC na fase crônica (FC) que falharam ou foram intolerantes ao tratamento com interferon, fase acelerada (FA) e crise blástica (CB) foram tratados com imatinibe entre dezembro de 2000 e setem
Publicado em: 2004
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3. Activation of mesangial cells by the phosphatase inhibitor vanadate. Potential implications for diabetic nephropathy.
The metalion vanadate has insulin-like effects and has been advocated for use in humans as a therapeutic modality for diabetes mellitus. However, since vanadate is a tyrosine phosphatase inhibitor, it may result in undesirable activation of target cells. We studied the effect of vanadate on human mesangial cells, an important target in diabetic nephropathy.
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4. N-acetyl-L-cysteine is a pluripotent protector against cell death and enhancer of trophic factor-mediated cell survival in vitro.
We have discovered that N-acetyl-L-cysteine (NAC) protects cells against death induced by exposure to noxious stimuli and against programmed cell death (apoptosis) associated with exposure to inadequate amounts of trophic factors. NAC prevented glutamate-induced death of oligodendrocytes and tumor necrosis factor alpha (TNF-alpha)-induced death of oligodendr