Improvement of management performance in the School System

An increasing awareness of the importance of activating long-term positive relations between scholastic institutions, students, families, governmental authority and other structures of public Administration is crucial for a real autonomy in school management. Few resources, rapid changes of the characteristics that influence educational system, high demand for managerial skill and operational autonomy, impose the capability to optimize performance, transparency of behaviour and results. In this ambit, is critical an effectiveness accountability system as starting point for the improvement of the relations between the schools and their stakeholders. The study propose the sharing and the organization of the information to create a Network of Sustainability Reports as lever for an effectiveness stakeholders engagement. The approach proposed is to optimize performance management cycle of the scholastic institutions and the employment of public resource

School Governance, Accountability and Performance Management

Limited resources, recent reforms of educational system that impose rapid changes in the governance system, high demand for managerial skill and operational autonomy, impose the capability to optimize performance, transparency of behaviour, dialogue with stakeholder to grow results in the school system. It therefore draws attention to the importance of activate long-term positive relations between schools, students, families, governmental authority and other structures of public Administration to improve quality and performance in school management. So is critical an effectiveness accountability system as starting point to develop the quality of relations between the schools and their stakeholders. In this regard, this article proposes the Network Governance as lever to improve an effectiveness stakeholder engagement and to optimize performance in the School System. This study represents a dissertation that aims to raise awareness about the cycle of performance management in schools and for the optimization of the use of public resources

Sustainability in the Higher Education System: An Opportunity to Improve Quality and Image

In view of the increasing importance attributed to social responsibility and stakeholder relationship management, more universities have expanded their research topics and their educational programs through the years. High attention is dedicated to the dominant principles and values of internal and external relations, to the innovation processes designed to ensure an approach to sustainable development. However, less attention is dedicated to the sustainability governance orientation and to the development of a strong institutional culture of sustainability, which is a key success factor to improve the quality and the image. This article observes the sustainability governance orientation, through the analysis of the information on the websites of three fair groups of universities in the international Top 500-ARWU (Academic Ranking of World Universities) 2015 ranking. The aim is to verify if there is a link between the degree of sustainability culture in the management and the positioning of the universities in the international ranking. In addition, the analysis is compared with self-assessment data carried out by the same universities in terms of performance sustainability through the STARS (Sustainability Tracking, Assessment & Rating System) online platform. As principal consideration, we have noted that the best universities in the ranking have a management approach based on a shared vision of sustainability development of their university leaders, who play an essential role affirming and disseminating a sustainability culture. All this opens broader future implications intended to highlight the importance of management sustainability as a quality improvement factor of universities

ESTUDIO DE LA REMODELACIÓN DE LOS CIRCUITOS NEURONALES HIPOTALÁMICOS QUE CONTROLAN EL APETITO ANTE SITUACIONES DE DÉFICIT ENERGÉTICO: ROL DE LA HORMONA GHRELINA

La ghrelina, producida principalmente por el tracto digestivo, es un péptido de 28 residuos y esterificado con un ácido n-octanoico en la ser3. La ghrelina se destaca por sus efectos estimulantes sobre la secreción de la hormona de crecimiento, la regulación de la respuesta al estrés y la ingesta de alimento. Los valores plasmáticos de ghrelina aumentan en condiciones de balance energético negativo, como ayuno o restricción calórica, donde la hormona es esencial para aumentar el apetito y activar mecanismos neuroendocrinos hiper-glucemiantes. La ghrelina actúa a través del receptor secretagogo de la hormona de crecimiento (GHSR, por sus siglas en inglés), el cual se expresa en la mayoría de los núcleos importantes en el control del apetito y de los ejes neuroendocrinos. Una de las características más importantes de GHSR es su alta actividad constitutiva, la cual causa señalización intracelular en ausencia de ghrelina. Dicha actividad constitutiva de GHSR podría también cumplir un rol en situaciones de balance energético negativo, cuando la expresión del receptor en el cerebro aumenta. Recientemente el grupo de Neurofisiología del IMBICE describió que la ghrelina posee, además, un efecto neurotrófico, es decir que controlaría el crecimiento, desarrollo y diferenciación neuronal. Uno de los principales blancos neuronales de la ghrelina son las neuronas del núcleo arcuato (ARC) hipotalámico que producen el péptido relacionado al gen agouti (AgRP) (o neuronas ARC-AgRP), las cuales expresan elevados niveles de GHSR y son necesarias para que la ghrelina aumente el apetito. El grupo de Neurofisiología descubrió que las proyecciones de ARC-AgRP al núcleo paraventricular hipotalámico (PVH) se remodelan en ratones adultos ayunados de una manera dependiente de GHSR. Dentro del hipotálamo, las neuronas ARC-AgRP no solo inervan el PVH, sino también el área hipotalámica lateral (AHL), la cual cumple un rol importante articulando los componentes homeostáticos y hedónicos de la ingesta de alimento. Estudios recientes de resonancia magnética de difusión combinada con tractografía probabilística mostraron que la conectividad del ARC y del AHL se altera en pacientes que sufren de anorexia nerviosa, quienes se encuentran en un déficit energético crónico. Por este motivo, el objetivo general de este proyecto es estudiar el proceso de remodelación de los circuitos neuronales hipotalámicos que controlan el apetito en ratones adultos sometidos a situaciones de déficit energético y el rol de la hormona ghrelina sobre este fenómeno. Para esto estudiaremos si la acción de ghrelina es requerida, utilizando modelos con bloqueo farmacológico o genético de la señalización de GHSR y también investigaremos si la acción de ghrelina es suficiente para que ocurra esta remodelación. A su vez evaluaremos si la activación mediante fármaco-genética de las neuronas ARC-AgRP es suficiente para que ocurran estos cambios

The ups and downs of growth hormone secretagogue receptor signaling

The growth hormone secretagogue receptor (GHSR) has emerged as one of the most fascinating molecules from the perspective of neuroendocrine control. GHSR is mainly expressed in the pituitary and the brain, and plays key roles regulating not only growth hormone secretion but also food intake, adiposity, body weight, glucose homeostasis and other complex functions. Quite atypically, GHSR signaling displays a basal constitutive activity that can be up- or downregulated by two digestive system-derived hormones: the octanoylated-peptide ghrelin and the liver-expressed antimicrobial peptide 2 (LEAP2), which was recently recognized as an endogenous GHSR ligand. The existence of two ligands with contrary actions indicates that GHSR activity can be tightly regulated and that the receptor displays the capability to integrate such opposing inputs in order to provide a balanced intracellular signal. This article provides a summary of the current understanding of the biology of ghrelin, LEAP2 and GHSR and discusses the reconceptualization of the cellular and physiological implications of the ligand-regulated GHSR signaling, based on the latest findings.Fil: Cornejo, María Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Mustafá, Emilio Román. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Cassano, Daniela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Banères, Jean Louis. Université Montpellier II; FranciaFil: Raingo, Jesica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Perello, Mario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentin

Localization of Magic-F1 Transgene, Involved in Muscular Hypertrophy, during Early Myogenesis

We recently showed that Magic-F1 (Met-activating genetically improved chimeric factor 1), a human recombinant protein derived from hepatocyte growth factor/scatter factor (HGF/SF) induces muscle cell hypertrophy but not progenitor cell proliferation, both in vitro and in vivo. Here, we examined the temporal and spatial expression pattern of Magic-F1 in comparison with Pax3 (paired box gene 3) transcription factor during embryogenesis. Ranging from 9.5 to 17.5 dpc (days post coitum) mouse embryos were analyzed by in situ hybridization using whole mounts during early stages of development (9.5–10.5–11.5 dpc) and cryostat sections for later stages (11.5–13.5–15.5–17.5 dpc). We found that Magic-F1 is expressed in developing organs and tissues of mesenchymal origin, where Pax3 signal appears to be downregulated respect to the wt embryos. These data suggest that Magic-F1 could be responsible of muscular hypertrophy, cooperating with Pax3 signal pathway in skeletal muscle precursor cells

Growth hormone secretagogue receptor in dopamine neurons controls appetitive and consummatory behaviors towards high-fat diet in ad-libitum fed mice

Growth hormone secretagogue receptor (GHSR), the receptor for ghrelin, is expressed in key brain nuclei that regulate food intake. The dopamine (DA) pathways have long been recognized to play key roles mediating GHSR effects on feeding behaviors. Here, we aimed to determine the role of GHSR in DA neurons controlling appetitive and consummatory behaviors towards high fat (HF) diet. For this purpose, we crossed reactivable GHSR-deficient mice with DA transporter (DAT)-Cre mice, which express Cre recombinase under the DAT promoter that is active exclusively in DA neurons, to generate mice with GHSR expression limited to DA neurons (DAT-GHSR mice). We found that DAT-GHSR mice show an increase of c-Fos levels in brain areas containing DA neurons after ghrelin treatment, in a similar fashion as seen in wild-type mice; however, they did not increase food intake or locomotor activity in response to systemically- or centrally-administered ghrelin. In addition, we found that satiated DAT-GHSR mice displayed both anticipatory activity to scheduled HF diet exposure and HF intake in a binge-like eating protocol similar to those in wild-type mice, whereas GHSR-deficient mice displayed impaired responses. We conclude that GHSR expression in DA neurons is sufficient to both mediate increased anticipatory activity to a scheduled HF diet exposure and fully orchestrate binge-like HF intake, but it is insufficient to restore the acute orexigenic or locomotor effects of ghrelin treatment. Thus, GHSR in DA neurons affects appetitive and consummatory behaviors towards HF diet that take place in the absence of caloric needs.Fil: Cornejo, María Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Barrile, Franco. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Cassano, Daniela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Aguggia, Julieta Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Garcia Romero, Guadalupe. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Reynaldo, Mirta Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Andreoli, Maria Florencia. Provincia de Buenos Aires. Ministerio de Salud. Hospital de Niños "Sor María Ludovica" de La Plata. Instituto de Desarrollo e Investigaciones Pediátricas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: de Francesco, Pablo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Perello, Mario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentin

Guide cells support muscle regeneration and affect neuro-muscular junction organization

Muscular regeneration is a complex biological process that occurs during acute injury and chronic degeneration, implicating several cell types. One of the earliest events of muscle regeneration is the inflammatory response, followed by the activation and differentiation of muscle progenitor cells. However, the process of novel neuromuscular junction formation during muscle regeneration is still largely unexplored. Here, we identify by single-cell RNA sequencing and isolate a subset of vessel-associated cells able to improve myogenic differentiation. We termed them 'guide' cells because of their remarkable ability to improve myogenesis without fusing with the newly formed fibers. In vitro, these cells showed a marked mobility and ability to contact the forming myotubes. We found that these cells are characterized by CD44 and CD34 surface markers and the expression of Ng2 and Ncam2. In addition, in a murine model of acute muscle injury and regeneration, injection of guide cells correlated with increased numbers of newly formed neuromuscular junctions. Thus, we propose that guide cells modulate de novo generation of neuromuscular junctions in regenerating myofibers. Further studies are necessary to investigate the origin of those cells and the extent to which they are required for terminal specification of regenerating myofibers

Magic-F1 transgene cooperates with Pax 3 during early myogenesis to induce muscular hypertrophy

Met-Activating Genetically Improved Chimeric Factor-1 (Magic-F1) is a human recombinant protein derived from hepatocyte growth factor/scatter factor (HGF/ SF) and consists in two Met-binding domains repeated in tandem and separated by an artificial linker. It has a reduced affinity for Met and, in contrast to HGF, it elicits activation of the AKT but not the ERK signaling pathway. We recently showed that Magic-F1 induces muscle cell hypertrophy but not progenitor cell proliferation, both in vitro and in vivo where a transgenic mouse express the recombinant protein exclusively in skeletal muscle tissue [1]. Here, we examined the temporal and spatial expression pattern of Magic-F1 in comparison with Pax3 (paired box gene 3) transcription factor during embryogenesis [2]. Ranging from 9.5 to 17.5 dpc (days post coitum) mouse embryos were analyzed by in situ hybridization using whole mounts during early stages of development (9.5-10.5-11.5 dpc) and cryostat sections for later stages (11.5-13.5-15.5-17.5 dpc). We found that Magic-F1 is expressed in developing organs and tissues of mesenchymal origin, where Pax3 signal appears to be downregulated respect to the wt embryos. These data suggest that Magic-F1 could be responsible of muscular hypertrophy, cooperating with Pax3 signal pathway in skeletal muscle precursor cells