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1.
Praxis (Bern 1994) ; 110(1): 30-36, 2021 Jan.
Artigo em Alemão | MEDLINE | ID: mdl-33406929

RESUMO

Entrustable Professional Activities in Graduate Medical Education in Psychiatry: A Promising Concept Abstract. Entrustable Professional Activities (EPAs) are competency-based learning goals derived from observable clinical activities. In undergraduate medical education, they have now been adopted throughout Switzerland as part of the so-called PROFILES catalog (Principal Relevant Objectives and Framework for Integrated Learning and Education in Switzerland). The nine core EPAs to be mastered in undergraduate medical education can serve as a basis for introducing EPAs in graduate medical education as well. We will discuss this approach in the context of graduate medical education in psychiatry and psychotherapy from the perspective of different training contexts and a pilot example. In this position paper, we describe a promising opportunity to improve graduate medical training through the implementation of EPAs, both in terms of the quality of training and thus of patient care, as well as in terms of the attractiveness of the specialty for future residents.


Assuntos
Educação de Graduação em Medicina , Internato e Residência , Psiquiatria , Competência Clínica , Educação Baseada em Competências , Educação de Pós-Graduação em Medicina , Avaliação Educacional , Humanos , Suíça
2.
Matrix Biol ; 24(3): 198-207, 2005 May.
Artigo em Inglês | MEDLINE | ID: mdl-15905080

RESUMO

Hepatic stellate cells (HSC) cultured on plastic spontaneously transdifferentiate to a myofibroblast-like cell type (MFB). This model system of hepatic fibrogenesis is characterized by phenotypic changes of the cells and increased matrix synthesis. Here, we analyzed if transdifferentiation-dependent induction of ECM components, e.g., collagen type I and thrombospondin-2 (TSP-2), and phenotypic changes are coregulated events and if both processes are mediated via TGF-beta pathway(s). Blocking the TGF-beta-dependent p38 MAPK pathway in HSC with the specific inhibitor SB203580 strongly reduces collagen I and TSP-2 mRNA expression without inhibiting upregulation of the typical MFB-marker, alpha-smooth-muscle actin (alpha-SMA). Similarly, interference with the Smad2/3/4 pathway using dexamethasone also heavily decreased expression of collagen type I and TSP-2 whereas transdifferentiation of HSC to the typical morphology of MFB with loss of fat droplets and increasing alpha-SMA was unchanged. Further, p38 MAPK mediated induction of collagen I and TSP-2 expression by TGF-beta1 was still achieved in the presence of dexamethasone, showing that dexamethasone does not block p38 while it delays Smad2 phosphorylation and antagonizes stimulation of a Smad3/Smad4 dependent TGF-beta reporter construct. Interestingly, in contrast to SB203580 and dexamethasone, overexpression of the TGF-beta antagonist Smad7 reduced ECM expression and simultaneously inhibited morphologic transdifferentiation, indicating that Smad7 fulfills additional features in HSC. In conclusion, our data show that phenotypic changes of transdifferentiating HSC and induction of matrix synthesis are independent processes, the latter being stimulated by both, Smad dependent and MAPK dependent TGF-beta signaling.


Assuntos
Actinas/metabolismo , Colágeno Tipo I/metabolismo , Fígado/citologia , Fígado/metabolismo , Músculo Liso/metabolismo , Trombospondinas/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Animais , Diferenciação Celular/fisiologia , Colágeno Tipo I/antagonistas & inibidores , Proteínas de Ligação a DNA/metabolismo , Dexametasona/farmacologia , Matriz Extracelular/metabolismo , Fibroblastos/citologia , Fibroblastos/metabolismo , Glucocorticoides/farmacologia , Humanos , Sistema de Sinalização das MAP Quinases/fisiologia , Masculino , Miócitos de Músculo Liso/citologia , Miócitos de Músculo Liso/metabolismo , Fosforilação/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Proteína Smad2 , Trombospondinas/antagonistas & inibidores , Transativadores/metabolismo , Fator de Crescimento Transformador beta/fisiologia , Fator de Crescimento Transformador beta1 , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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