Reframed teacher leadership: A narrative inquiry

Teacher leadership has been in schools from the time teachers rang the school bells. Three waves of teacher leadership have been examined. The first wave focused on formal managerial positions such as department chairs, the second wave focused on curriculum and staff development, and the third wave focused on daily acts of collaboration to solve problems and provide professional development activities for staffs. This study explored the third wave practice of teacher leaders in a qualitative study focusing on the narratives of 11 teacher leaders. A narrative of lives format was used to study leadership experiences. A pilot study was conducted with three teacher leaders in two school districts. The teachers in the research study were purposely selected from a pool of graduates from a master\u27s degree program focusing on teacher leadership. The teacher leaders shared their stories and their present philosophy and acts of teacher leadership in semi-structured interviews. The study explored the relationship of teachers\u27 personal and professional experiences on their construct of teacher leadership. A number of factors influenced leadership development including childhood experiences, serendipity and happenstance experiences, and mentors who encouraged teachers to get involved in leadership. Families influenced leadership activity and timing. Characteristics of meaningful site-based professional development and university-school professional development programs were examined. Principals either promoted or discouraged teacher leadership. The study describes implications for teachers, principals, and professional development programs and activities

Stress Resistance Screen in a Human Primary Cell Line Identifies Small Molecules That Affect Aging Pathways and Extend Caenorhabditis elegans' Lifespan.

Increased resistance to environmental stress at the cellular level is correlated with the longevity of long-lived mutants and wild-animal species. Moreover, in experimental organisms, screens for increased stress resistance have yielded mutants that are long-lived. To find entry points for small molecules that might extend healthy longevity in humans, we screened ∼100,000 small molecules in a human primary-fibroblast cell line and identified a set that increased oxidative-stress resistance. Some of the hits fell into structurally related chemical groups, suggesting that they may act on common targets. Two small molecules increased C. elegans' stress resistance, and at least 9 extended their lifespan by ∼10-50%. We further evaluated a chalcone that produced relatively large effects on lifespan and were able to implicate the activity of two, stress-response regulators, NRF2/skn-1 and SESN/sesn-1, in its mechanism of action. Our findings suggest that screening for increased stress resistance in human cells can enrich for compounds with promising pro-longevity effects. Further characterization of these compounds may reveal new ways to extend healthy human lifespan

New Genes Tied to Endocrine, Metabolic, and Dietary Regulation of Lifespan from a Caenorhabditis elegans Genomic RNAi Screen

Most of our knowledge about the regulation of aging comes from mutants originally isolated for other phenotypes. To ask whether our current view of aging has been affected by selection bias, and to deepen our understanding of known longevity pathways, we screened a genomic Caenorhabditis elegans RNAi library for clones that extend lifespan. We identified 23 new longevity genes affecting signal transduction, the stress response, gene expression, and metabolism and assigned these genes to specific longevity pathways. Our most important findings are (i) that dietary restriction extends C. elegans' lifespan by down-regulating expression of key genes, including a gene required for methylation of many macromolecules, (ii) that integrin signaling is likely to play a general, evolutionarily conserved role in lifespan regulation, and (iii) that specific lipophilic hormones may influence lifespan in a DAF-16/FOXO-dependent fashion. Surprisingly, of the new genes that have conserved sequence domains, only one could not be associated with a known longevity pathway. Thus, our current view of the genetics of aging has probably not been distorted substantially by selection bias

A Role for Autophagy in the Extension of Lifespan by Dietary Restriction in C. elegans

In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles. In this study, we asked whether autophagy might contribute to the lifespan extension induced by dietary restriction in C. elegans. We find that dietary restriction and TOR inhibition produce an autophagic phenotype and that inhibiting genes required for autophagy prevents dietary restriction and TOR inhibition from extending lifespan. The longevity response to dietary restriction in C. elegans requires the PHA-4 transcription factor. We find that the autophagic response to dietary restriction also requires PHA-4 activity, indicating that autophagy is a transcriptionally regulated response to food limitation. In spite of the rejuvenating effect that autophagy is predicted to have on cells, our findings suggest that autophagy is not sufficient to extend lifespan. Long-lived daf-2 insulin/IGF-1 receptor mutants require both autophagy and the transcription factor DAF-16/FOXO for their longevity, but we find that autophagy takes place in the absence of DAF-16. Perhaps autophagy is not sufficient for lifespan extension because although it provides raw material for new macromolecular synthesis, DAF-16/FOXO must program the cells to recycle this raw material into cell-protective longevity proteins

Pediatric Emergency Care Capacity in a Low-Resource Setting: An assessment of district hospitals in Rwanda

BACKGROUND: Health system strengthening is crucial to improving infant and child health outcomes in low-resource countries. While the knowledge related to improving newborn and child survival has advanced remarkably over the past few decades, many healthcare systems in such settings remain unable to effectively deliver pediatric advance life support management. With the introduction of the Emergency Triage, Assessment and Treatment plus Admission care (ETAT+)-a locally adapted pediatric advanced life support management program-in Rwandan district hospitals, we undertook this study to assess the extent to which these hospitals are prepared to provide this pediatric advanced life support management. The results of the study will shed light on the resources and support that are currently available to implement ETAT+, which aims to improve care for severely ill infants and children. METHODS: A cross-sectional survey was undertaken in eight district hospitals across Rwanda focusing on the availability of physical and human resources, as well as hospital services organizations to provide emergency triage, assessment and treatment plus admission care for severely ill infants and children. RESULTS: Many of essential resources deemed necessary for the provision of emergency care for severely ill infants and children were readily available (e.g. drugs and laboratory services). However, only 4/8 hospitals had BVM for newborns; while nebulizer and MDI were not available in 2/8 hospitals. Only 3/8 hospitals had F-75 and ReSoMal. Moreover, there was no adequate triage system across any of the hospitals evaluated. Further, guidelines for neonatal resuscitation and management of malaria were available in 5/8 and in 7/8 hospitals, respectively; while those for child resuscitation and management of sepsis, pneumonia, dehydration and severe malnutrition were available in less than half of the hospitals evaluated. CONCLUSIONS: Our assessment provides evidence to inform new strategies to enhance the capacity of Rwandan district hospitals to provide pediatric advanced life support management. Identifying key gaps in the health care system is required in order to facilitate the implementation and scale up of ETAT+ in Rwanda. These findings also highlight a need to establish an outreach/mentoring program, embedded within the ongoing ETAT+ program, to promote cross-hospital learning exchanges

Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans

Several hundred proteins become insoluble and aggregation-prone as a consequence of aging in Caenorhabditis elegans. The data indicate that these proteins influence disease-related protein aggregation and toxicity

Developing and implementing a novel mentorship model (4+ 1) for maternal, newborn and child health in Rwanda

BACKGROUND: There are a number of factors that may contribute to high mortality and morbidity of women and newborns in low-income countries. These include a shortage of competent health care providers (HCP) and a lack of sufficient continuous professional development (CPD) opportunities. Strengthening the skills and building the capacity of HCP involved in the provision of maternal, newborn and child health (MNCH) is essential to ensure quality care for mothers, newborns and children. To address this challenge in Rwanda, mentorship of HCPs was identified as an approach that could help build capacity, improve the provision of care and accelerate the reduction in maternal and neonatal mortality and morbidity. In this paper, we describe the development and implementation of a novel mentorship model named Four plus One (4 METHODS: The mentorship model built on the basis of inter-professional collaboration (IPC) was developed in early 2017 through consultations with different key actors. The design phase included refresher courses in specific skills and training course on mentoring. Field visits were conducted in 10 hospitals from June 2017 to February 2020. Hospital management teams (MT) were involved in the development and implementation of this mentorship model to ensure ownership of the program. RESULTS: Upon completion of planned visits to each hospital, a total of 218 HCPs were involved in the process. Reports prepared by mentors upon each mentorship visit and compiled by Training Support and Access Model (TSAM) for MNCH\u27CPD team, highlighted the mothers and newborns who were saved by both mentors and mentees. Also, different logbooks of mentees showed how the capacity of staff was strengthened, thereby suggesting effectiveness of the model. Through different mentorship coordination meetings, the model was much appreciated by the MTs of hospitals, especially the IPC component of the model and confirmed the program \u27effectiveness. CONCLUSION: The initiation of a mentorship model built on IPC together with the involvement of the leadership of the hospital may be the cause effect of reduction of specific mortality and improve MNCH in low resource settings even when there are a limited number of specialists in the health facilities

The first long-lived mutants: discovery of the insulin/IGF-1 pathway for ageing

Inhibiting insulin/IGF-1 signalling extends lifespan and delays age-related disease in species throughout the animal kingdom. This life-extension pathway, the first to be defined, was discovered through genetic studies in the small roundworm Caenorhabditis elegans. This discovery is described here

Reviewer Form Induction, Multiplication, and Acclimatization of Red Betel Plant (Piper Crocatum Ruiz and Pav.) By in Vitro Organogenesis

Animals have many ways of protecting themselves against stress; for example, they can induce animal-wide, stress-protective pathways and they can kill damaged cells via apoptosis. We have discovered an unexpected regulatory relationship between these two types of stress responses. We find that C. elegans mutations blocking the normal course of programmed cell death and clearance confer animal-wide resistance to a specific set of environmental stressors; namely, ER, heat and osmotic stress. Remarkably, this pattern of stress resistance is induced by mutations that affect cell death in different ways, including ced-3 (cell death defective) mutations, which block programmed cell death, ced-1 and ced-2 mutations, which prevent the engulfment of dying cells, and progranulin (pgrn-1) mutations, which accelerate the clearance of apoptotic cells. Stress resistance conferred by ced and pgrn-1 mutations is not additive and these mutants share altered patterns of gene expression, suggesting that they may act within the same pathway to achieve stress resistance. Together, our findings demonstrate that programmed cell death effectors influence the degree to which C. elegans tolerates environmental stress. While the mechanism is not entirely clear, it is intriguing that animals lacking the ability to efficiently and correctly remove dying cells should switch to a more global animal-wide system of stress resistance

The Somatic Reproductive Tissues of C. elegans Promote Longevity through Steroid Hormone Signaling

Removal of the germ cells of C. elegans extends lifespan in part because signals from the somatic reproductive tissues activate the nuclear hormone receptor DAF-12