Teacher induction in North Carolina: relationships to retention

Support for beginning teachers in North Carolina is mandated by the State Board of Education and supported through legislative mandates and. Teacher induction programs have been developed to help support and guide new teachers toward a successful career; however each Local Educational Agency (LEA) has the flexibility to establish the induction program in their district, creating a variety of models of induction across the state supporting beginning teachers (BTs). The goal of this research was to better understand the impact of induction programs in North Carolina on beginning teachers' retention. This mixed-methods study examined the current state of induction in 11 of North Carolina's LEAs in order to better understand how varying models of induction impact beginning teachers and to gather the LEAs' and BTs' perspectives about induction. The research questions investigate how the components of induction programs are implemented in North Carolina's LEAs and the perceptions of both the LEAs and BTs about the importance of these components in influencing teacher retention. This study focused on several components of LEA's induction programs (e.g., orientation, mentoring, professional development, and other resources) and explored the impact of these programs by examining the relationships between the components of induction and beginning teacher retention. The study used quantitative and qualitative data collection and analysis to document, describe and compare approaches to induction and BT perception about them. The results indicated that a wide variety of induction components are used across the 11 participating North Carolina LEAs, including various types of orientation, mentoring, and professional development. All 11 participating LEAs reported that their induction programs were beneficial in supporting their beginning teachers. However, the 378 participating BTs provided varying reports about their perceptions of the induction components offered in their districts. Overwhelmingly, BTs acknowledged that their mentor and/or resources were the most induction beneficial component

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction

ReConceptualising the Possible Narratives of Adolescence

This paper explores a range of epistemological paradigms available to understand, interpret and semiotically depict young people. These paradigms all draw upon a metadiscourse of developmental age and stage (e.g. Hall 1914) and then work from particular epistemological views of the world to cast young people in different lights. Using strategic essentialism (Spivak 1996), the paper offers descriptions of four existing paradigms, including biomedical (Erikson 1980), psychological (e.g. Piaget 1973), critical (e.g. Giroux & MacLaren 1982) and postmodern (e.g. Kenway & Bullen 2001). While some of these paradigms have been more distinct in particular cultural, historical and political contexts, they have overlapped and informing each other. Each paradigm carries unique consequences for the role of the learner, the teacher and the curriculum. The paper explores contemporary manifestations of the paradigms. From this investigation, a potential new space using concepts of subjectivity (Grosz 1994) for conceptualising young people is offered

Aligning school reform and teacher education reform in The Middle Years: An Australian case study

This paper discusses the development of a new Bachelor of Education (Middle Years of Schooling) at The University of Queensland, Australia. The middle years of schooling have increasingly been the focus of education reform initiatives in Australia, but this has not been accompanied by significant increases in the number of teacher education institutions offering specialised middle schooling-level teacher preparation programmes. Considering the rapidly changing social and economic context and the emergent state of middle schooling in Australia, the programme represented a conceptual and practical opportunity and challenge for The University of Queensland team. Working collaboratively, the team sought to design a teacher education preservice programme that was both responsive and generative: that is, responsive to local school contexts and to current education research and reform at national and international levels; and generative of cutting-edge theories and practices associated with middle schooling, teachers' work, and teacher education. This paper focuses on one component of the Middle Years of Schooling Teacher Education programme at The University of Queensland; namely, the practicum. We first present the underlying principles of the practicum programme and then examine "dilemmas" that emerged early in the practicum. These issues and tensions were associated with the ideals of "middle years" philosophy and the pragmatics of school reform associated with that approach. Within this context, we explore what it means to be both responsive and generative, and describe how we as teacher educators negotiated the extremes these terms implied

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure underpinning obesity

Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, non-coding variants from which pinpointing causal genes remains challenging. Here, we combined data from 718,734 individuals to discover rare and low-frequency (MAF<5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which eight in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2, ZNF169) newly implicated in human obesity, two (MC4R, KSR2) previously observed in extreme obesity, and two variants in GIPR. Effect sizes of rare variants are ~10 times larger than of common variants, with the largest effect observed in carriers of an MC4R stop-codon (p.Tyr35Ter, MAF=0.01%), weighing ~7kg more than non-carriers. Pathway analyses confirmed enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically-supported therapeutic targets to treat obesity

Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity

In the HTML version of this article initially published, the author groups ‘CHD Exome+ Consortium’, ‘EPIC-CVD Consortium’, ‘ExomeBP Consortium’, ‘Global Lipids Genetic Consortium’, ‘GoT2D Genes Consortium’, ‘EPIC InterAct Consortium’, ‘INTERVAL Study’, ‘ReproGen Consortium’, ‘T2D-Genes Consortium’, ‘The MAGIC Investigators’ and ‘Understanding Society Scientific Group’ appeared at the end of the author list but should have appeared earlier in the list, after author Krina T. Zondervan. The errors have been corrected in the HTML version of the article

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity

Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, noncoding variants from which pinpointing causal genes remains challenging. Here we combined data from 718,734 individuals to discover rare and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which 8 variants were in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previously observed to be mutated in extreme obesity and 2 variants were in GIPR. The effect sizes of rare variants are ~10 times larger than those of common variants, with the largest effect observed in carriers of an MC4R mutation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed ~7 kg more than non-carriers. Pathway analyses based on the variants associated with BMI confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, noncoding variants from which pinpointing causal genes remains challenging. Here we combined data from 718,734 individuals to discover rare and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which 8 variants were in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previously observed to be mutated in extreme obesity and 2 variants were in GIPR. The effect sizes of rare variants are ~10 times larger than those of common variants, with the largest effect observed in carriers of an MC4R mutation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed ~7 kg more than non-carriers. Pathway analyses based on the variants associated with BMI confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity