Identidad docente y estrategias de resolución de incidentes críticos en contextos universitarios de alta diversidad sociocultural

Este estudio identifica las estrategias de los profesores cuando se enfrentan a incidentes críticos (IC) en contextos de alta diversidad sociocultural, reconociendo el peso de la identidad y de las emociones en la toma de decisiones, así como la efectividad de las mismas para promover cambios en las prácticas docentes. En el estudio de naturaleza cualitativa, fueron entrevistados 23 profesores universitarios. Los resultados indican que las emociones asociadas a un IC, generan una situación de desequilibrio que puede obstaculizar la actividad cuando son de naturaleza negativa. Al mismo tiempo, en estas situaciones es posible la revision y reconstrución de la propia identidad docente. En cuanto a las estrategias empleadas por los docentes ante los IC, éstas fueron mayoritariamente inmediatas e incidieron en aspectos muy puntuales, lo que derivó en actuaciones reactivas y poco eficaces. Pese a ello, la mayoría de los profesores no modificaron sus posiciones iniciales y fueron excepcionales las situaciones en las que el despliegue de estrategias y la reflexión posterior a un determinado IC permitió cambios estructurales que impactaron en alguna dimension de la identidad del profesor como sus emociones y prácticas

Vacuum extraction and neonatal jaundice

Peer Reviewe

Parasite-mediated nuclear factor kappaB regulation in lymphoproliferation caused by Theileria parva infection.

Infection of cattle with the protozoan Theileria parva results in uncontrolled T lymphocyte proliferation resulting in lesions resembling multicentric lymphoma. Parasitized cells exhibit autocrine growth characterized by persistent translocation of the transcriptional regulatory factor nuclear factor kappaB (NFkappaB) to the nucleus and consequent enhanced expression of interleukin 2 and the interleukin 2 receptor. How T. parva induces persistent NFkappaB activation, required for T cell activation and proliferation, is unknown. We hypothesized that the parasite induces degradation of the IkappaB molecules which normally sequester NFkappaB in the cytoplasm and that continuous degradation requires viable parasites. Using T. parva-infected T cells, we showed that the parasite mediates continuous phosphorylation and proteolysis of IkappaBalpha. However, IkappaBalpha reaccumulated to high levels in parasitized cells, which indicated that T. parva did not alter the normal NFkappaB-mediated positive feedback loop which restores cytoplasmic IkappaBalpha. In contrast, T. parva mediated continuous degradation of IkappaBbeta resulting in persistently low cytoplasmic IkappaBbeta levels. Normal IkappaBbeta levels were only restored following T. parva killing, indicating that viable parasites are required for IkappaBbeta degradation. Treatment of T. parva-infected cells with pyrrolidine dithiocarbamate, a metal chelator, blocked both IkappaB degradation and consequent enhanced expression of NFkappaB dependent genes. However treatment using the antioxidant N-acetylcysteine had no effect on either IkappaB levels or NFkappaB activation, indicating that the parasite subverts the normal IkappaB regulatory pathway downstream of the requirement for reactive oxygen intermediates. Identification of the critical points regulated by T. parva may provide new approaches for disease control as well as increase our understanding of normal T cell function

Parasite-mediated nuclear factor κB regulation in lymphoproliferation caused by Theileria parva infection

Infection of cattle with the protozoan Theileria parva results in uncontrolled T lymphocyte proliferation resulting in lesions resembling multicentric lymphoma. Parasitized cells exhibit autocrine growth characterized by persistent translocation of the transcriptional regulatory factor nuclear factor κB (NFκB) to the nucleus and consequent enhanced expression of interleukin 2 and the interleukin 2 receptor. How T. parva induces persistent NFκB activation, required for T cell activation and proliferation, is unknown. We hypothesized that the parasite induces degradation of the IκB molecules which normally sequester NFκB in the cytoplasm and that continuous degradation requires viable parasites. Using T. parva -infected T cells, we showed that the parasite mediates continuous phosphorylation and proteolysis of IκBα. However, IκBα reaccumulated to high levels in parasitized cells, which indicated that T. parva did not alter the normal NFκB-mediated positive feedback loop which restores cytoplasmic IκBα. In contrast, T. parva mediated continuous degradation of IκBβ resulting in persistently low cytoplasmic IκBβ levels. Normal IκBβ levels were only restored following T. parva killing, indicating that viable parasites are required for IκBβ degradation. Treatment of T. parva -infected cells with pyrrolidine dithiocarbamate, a metal chelator, blocked both IκB degradation and consequent enhanced expression of NFκB dependent genes. However treatment using the antioxidant N- acetylcysteine had no effect on either IκB levels or NFκB activation, indicating that the parasite subverts the normal IκB regulatory pathway downstream of the requirement for reactive oxygen intermediates. Identification of the critical points regulated by T. parva may provide new approaches for disease control as well as increase our understanding of normal T cell function

Prolonged rupture of the fetal membranes and neonatal outcome

Peer Reviewe