Rol del terapeuta ocupacional en la evaluación y tratamiento de prematuros en las unidades de cuidados intensivos neonatales. Revisión sistemática

Objective: To know the different occupational therapist duties in neonatal intensive care units in the evaluation and treatment of premature infants with birth weight under 1500g. Methods: A bibliographic review was carried out using 3 databases selecting only those studies answering the study question, that is, occupational therapy’s role in neonatal units throughout the last 15 years. Results: Sixteen studies were evaluated in which an occupational therapist was included as part of the intensive care unit, emphasizing their role as the health care professional in charge of implementing the techniques and processes which allow infants to continue their growth and neurological development. Conclusions: Further studies are necessary in order to prove the need of occupational therapy practitioners in neonatal units.Objetivos: conocer las diferentes funciones del o de la terapeuta ocupacional en las Unidades de Cuidados de Neonatología en la evaluación y tratamiento de prematuros menores de 1500g. Métodos: se realizó una revisión bibliográfica utilizando 3 bases de datos donde fueron seleccionados los artículos que daban respuesta a la pregunta de estudio para conocer el trabajo de la persona profesional terapeuta ocupacional en las unidades neonatales durante los últimos 15 años. Resultados: fueron evaluados un total de dieciseis estudios en los que se incluye al terapeuta ocupacional como profesional de las unidades UCI, donde se resalta que el es el que debe llevar a cabo técnicas y procesos, que permitan continuar con su crecimiento y desarrollo neurológico. Conclusiones: se concluye que, sería conveniente llevar a cabo más estudios para demostrar la necesidad de terapia ocupacional en unidades de neonatología

Infection exposure promotes ETV6-RUNX1 precursor B-cell leukemia via impaired H3K4 demethylases

ETV6-RUNX1 is associated with the most common subtype of childhood leukemia. As few ETV6-RUNX1 carriers develop precursor B-cell acute lymphocytic leukemia (pB-ALL), the underlying genetic basis for development of full-blown leukemia remains to be identified, but the appearance of leukemia cases in time-space clusters keeps infection as a potential causal factor. Here, we present in vivo genetic evidence mechanistically connecting preleukemic ETV6-RUNX1 expression in hematopoetic stem cells/precursor cells (HSC/PC) and postnatal infections for human-like pB-ALL. In our model, ETV6-RUNX1 conferred a low risk of developing pB-ALL after exposure to common pathogens, corroborating the low incidence observed in humans. Murine preleukemic ETV6-RUNX1 pro/preB cells showed high Rag1/2 expression, known for human ETV6-RUNX1 pB-ALL. Murine and human ETV6-RUNX1 pB-ALL revealed recurrent genomic alterations, with a relevant proportion affecting genes of the lysine demethylase (KDM) family. KDM5C loss of function resulted in increased levels of H3K4me3, which coprecipitated with RAG2 in a human cell line model, laying the molecular basis for recombination activity. We conclude that alterations of KDM family members represent a disease-driving mechanism and an explanation for RAG off-target cleavage observed in humans. Our results explain the genetic basis for clonal evolution of an ETV6-RUNX1 preleukemic clone to pB-ALL after infection exposure and offer the possibility of novel therapeutic approaches.J. Hauer has been supported by the German Children's Cancer Foundation, DJCLS 02R/2016, KKS A2016/07 and from the “Forschungskommission” of the medical faculty of the Heinrich Heine University. M. Müschen is an HHMI Faculty Scholar (HHMI-55108547) and supported by NIH/NCI through an Outstanding Investigator Award (R35CA197628) to M. Müschen, a Wellcome Trust Senior Investigator Award, the Leukemia and Lymphoma Society, the California Institute for Regenerative Medicine, the William Lawrence and Blanche Hughes Foundation. A. Borkhardt has been supported by the German Children's Cancer Foundation and the Federal Ministry of Education and Research, Bonn, Germany. Research in I. Sánchez-García's group is partially supported by FEDER and by MINECO (SAF2012-32810, SAF2015-64420-R and Red de Excelencia Consolider OncoBIOSAF2014-57791-REDC), Instituto de Salud Carlos III (PIE14/00066), ISCIII- Plan de Ayudas IBSAL 2015 Proyectos Integrados (IBY15/00003), by Junta de Castilla y León (BIO/SA51/15, CSI001U14, UIC-017, and CSI001U16), Fundacion Inocente Inocente and by the ARIMMORA project (European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreement no. 282891). I. Sánchez-García's lab is a member of the EuroSyStem and the DECIDE Network funded by the European Union under the FP7 program. A. Borkhardt and I. Sánchez-García have been supported by the German Carreras Foundation (DJCLS R13/26). Research in C. Vicente-Dueñas' group is partially supported by a “Miguel Servet” grant (CP14/00082-AES 2013-2016-FEDER) from the Instituto de Salud Carlos III (Ministerio de Economía y Competitividad) and by the Lady Tata International Award for Research in Leukaemia 2016–2017. A. Martín-Lorenzo and G. Rodríguez-Hernández were supported by FSE-Conserjería de Educación de la Junta de Castilla y León (CSI001-13 and CSI001-15, respectively).Peer Reviewe