Algunes reflexions sobre la psicoteràpia centrada en la persona

Aquest escrit pretén fer una breu presentació de l'Enfocament Centrat en la Persona com una proposta, bastant desconeguda a casa nostra, que arreu del món es fa servir en el camp ampli de les relacions d'ajuda, i destacar-ne les diferents aplicacions rellevants en psicoteràpia i en alguns àmbits de les ciències humanes. A més, informem que des de la Unitat d'Investigació Centrada en la Persona de la Universitat de València es treballa en el desenvolupament d'aquesta perspectiva

Resolución de conflictos e interacción social desde una comunidad social de investigación. Una propuesta formativa desde la unidad de investigación centrada en la persona

La investigación científica para la Resolución de Conflictos se ha enriquecido con los nuevos planteamientos epistemológicos que las ciencias sociales y el Enfoque Centrado en la Persona en particular han realizado a este respecto. Una innovación investigadora que incluye la interdisciplinariedad basada en la confianza y la integración paradigmática. Dar la prioridad a la necesidad de conciliar los conocimientos, de unificar sin destruir la diversidad (E. Vinyamata, 2004). El diálogo y el encuentro, el reconocimiento del otro, las comunidades investigadoras, etc. son el centro de relevantes propuestas para la validación de los conocimientos. La Unidad de Investigación Centrada en la Persona (OTRI-UV-0160), adscrita al Departamento MIDE de la Universitat de València, aglutina investigadores de distintas disciplinas y ha obtenido la favorable disposición de otros agentes sociales interesados, todos ellos, en colaborar en el desarrollo de esta experiencia innovadora que pretende aportar conocimiento sobre cómo se puede humanizar la ciencia a partir de la práctica del diálogo para el entendimiento y la convivencia ciudadana

BCR-ABL induces the expression of Skp2 through the PI3K pathway to promote p27Kip1 degradation and proliferation of chronic myelogenous leukemia cells

Chronic myelogenous leukemia (CML) is characterized by the expression of the BCR-ABL tyrosine kinase, which results in increased cell proliferation and inhibition of apoptosis. In this study, we show in both BCR-ABL cells (Mo7e-p210 and BaF/3-p210) and primary CML CD34+ cells that STI571 inhibition of BCR-ABL tyrosine kinase activity results in a G(1) cell cycle arrest mediated by the PI3K pathway. This arrest is associated with a nuclear accumulation of p27(Kip1) and down-regulation of cyclins D and E. As a result, there is a reduction of the cyclin E/Cdk2 kinase activity and of the retinoblastoma protein phosphorylation. By quantitative reverse transcription-PCR we show that BCR-ABL/PI3K regulates the expression of p27(Kip1) at the level of transcription. We further show that BCR-ABL also regulates p27(Kip1) protein levels by increasing its degradation by the proteasome. This degradation depends on the ubiquitinylation of p27(Kip1) by Skp2-containing SFC complexes: silencing the expression of Skp2 with a small interfering RNA results in the accumulation of p27(Kip1). We also demonstrate that BCR-ABL cells show transcriptional up-regulation of Skp2. Finally, expression of a p27(Kip1) mutant unable of being recognized by Skp2 results in inhibition of proliferation of BCR-ABL cells, indicating that the degradation of p27(Kip1) contributes to the pathogenesis of CML. In conclusion, these results suggest that BCR-ABL regulates cell cycle in CML cells at least in part by inducing proteasome-mediated degradation of the cell cycle inhibitor p27(Kip1) and provide a rationale for the use of inhibitors of the proteasome in patients with BCR-ABL leukemias

BCR-ABL induces the expression of Skp2 through the PI3K pathway to promote p27Kip1 degradation and proliferation of chronic myelogenous leukemia cells

Chronic myelogenous leukemia (CML) is characterized by the expression of the BCR-ABL tyrosine kinase, which results in increased cell proliferation and inhibition of apoptosis. In this study, we show in both BCR-ABL cells (Mo7e-p210 and BaF/3-p210) and primary CML CD34+ cells that STI571 inhibition of BCR-ABL tyrosine kinase activity results in a G(1) cell cycle arrest mediated by the PI3K pathway. This arrest is associated with a nuclear accumulation of p27(Kip1) and down-regulation of cyclins D and E. As a result, there is a reduction of the cyclin E/Cdk2 kinase activity and of the retinoblastoma protein phosphorylation. By quantitative reverse transcription-PCR we show that BCR-ABL/PI3K regulates the expression of p27(Kip1) at the level of transcription. We further show that BCR-ABL also regulates p27(Kip1) protein levels by increasing its degradation by the proteasome. This degradation depends on the ubiquitinylation of p27(Kip1) by Skp2-containing SFC complexes: silencing the expression of Skp2 with a small interfering RNA results in the accumulation of p27(Kip1). We also demonstrate that BCR-ABL cells show transcriptional up-regulation of Skp2. Finally, expression of a p27(Kip1) mutant unable of being recognized by Skp2 results in inhibition of proliferation of BCR-ABL cells, indicating that the degradation of p27(Kip1) contributes to the pathogenesis of CML. In conclusion, these results suggest that BCR-ABL regulates cell cycle in CML cells at least in part by inducing proteasome-mediated degradation of the cell cycle inhibitor p27(Kip1) and provide a rationale for the use of inhibitors of the proteasome in patients with BCR-ABL leukemias