Teacher Knowledge Part 1: Unstopping the Dam

Research on teachers and their teaching aims at understanding what it means to teach. Such research is conducted in a variety of ways. Major users of its findings are teacher educators. It is hoped that the research findings will provide a knowledge base for teacher education programmes often characterised as being more whimsical than rational. There are two basic views of the process of becoming a teacher: master the model or model the master (Stones, 1972). Both views stress institutional conformity, draw upon institutionalised knowledge and aim at developing technical skill rather than professional competency. The intention of this paper is to suggest a theory, and accompanying methodology, which could be used to explore and develop a model of teacher development more in keeping with institutional and personal freedom: to explore the process of becoming a.teacher as proposed by Fielding (1983)

Teacher Knowledge Part 2: Personal Construct Theory as the Basis of a Methodology to Study Teaching

In the previous paper, Teacher Knowledge Part 1; Unstopping the Dam, the suggestion was made that a methodology based on Personal Construct Theory (PCT) could be used to explore and develop a new model of teacher professional development prepared by Fielding (1983). Two questions were asked. What is this methodology? How can it be used to explore and develop Fielding\u27s model? The second question was dealt with in the earlier paper. The first is the subject of this paper. The intention here is threefold; firstly, to describe the theory of personal constructs, originated by Kelly (1955) and elaborated by Fransella and Bannister (1971) second to discuss the preparation and analysis of repertory grids, a procedure stemming from the theory conceived by Kelly (1955, 1961) and again elaborated by Fransella and Bannister (1977); finally to consider some of the measures used in and interpretations made of repertory grid analyses

The Personal Construction of Teaching and Mathematics Teacher Education

With the expansion of schooling in the 1950s and 1960s there was a consequent flurry of curriculum activity. More pupils stayed longer at school and schools had to cater for a wider range of abilities and interests. New curricula were developed, old curricula revised to provide educational programmes for the changing clientele, and many curriculum projects initiated, covering all aspects of schooling. By the 1970s these curriculum projects had been evaluated and the evaluations provided new insights into the whole curriculum process. One insight of particular interest concerned the role of the teacher. What the teacher did in the classroom was central to the whole curriculum process; no curriculum was teacher-proof. In particular, what were the teacher\u27s views on, and beliefs about, teaching in general and teaching specific subjects in particular? (Howson, 1976; Fey, 1979)

Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette smoke-induced lung inflammation in mice

Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) is a pivotal cytokine that regulates lung immunity and inflammation. The aim of this study was to investigate how IL-17A regulates CS-induced lung inflammation in vivo . IL-17A KO mice and neutralisation of IL-17A in WT mice reduced macrophage and neutrophil recruitment and CCL2, CCL3 and MMP-12 mRNA expression in response to acute CS exposure. IL-17A expression was increased in NOD SCID mice with non-functional B and T cells over a 4 week CS exposure period, where macrophages accumulated to the same extent as WT mice. Gene expression analysis by QPCR of isolated immune cell subsets detected increased levels of IL-17A transcript in macrophages, neutrophils and NK/NKT cells in the lungs of CS-exposed mice. In order to further explore the relative contribution of innate immune cellular sources, intracellular IL-17A staining was performed. Here, we demonstrate that CS exposure primes NK, NKT and γδ T cells to produce more IL-17A protein and CS alone increased the frequency of IL17+ γδ T cells in the lung, whereas IL-17A protein was not detected in macrophages and neutrophils. Our data suggest that activation of innate cellular sources of IL-17A is an essential mediator of macrophage accumulation in CS-exposed lungs. Targeting non-conventional T cell sources of IL-17A may offer an alternative strategy to reduce pathogenic macrophages in COPD

Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice

There is emerging epidemiological data to suggest that upper respiratory tract bacterial colonisation in infancy may increase the risk of developing respiratory dysfunction later in life, and respiratory viruses are known to precipitate persistent colonisation. This study utilized a neonatal mouse model of Streptococcus pneumonia (SP) and influenza A virus (IAV) co-infection, where bronchoalveolar leukocyte infiltration had resolved by adulthood. Only co-infection resulted in persistent nasopharyngeal colonisation over 40 days and a significant increase in airway resistance in response to in vivo methacholine challenge. A significant increase in hysteresivity was also observed in IAV and co-infected mice, consistent with ventilatory heterogeneity and structural changes in the adult lung. Airway hyper-responsiveness was not associated with a detectable increase in goblet cell transdifferentiation, peribronchial smooth muscle bulk or collagen deposition in regions surrounding the airways. Increased reactivity was not observed in precision cut lung slices challenged with methacholine in vitro. Histologically, the airway epithelium appeared normal and expression of epithelial integrity markers (ZO-1, occludin-1 and E-cadherin) were not altered. In summary, neonatal co-infection led to persistent nasopharyngeal colonisation and increased airway responsiveness that was not associated with detectable smooth muscle or mucosal epithelial abnormalities, however increased hysteresivity may reflect ventilation heterogeneity

Granulocyte Macrophage Colony-Stimulating Factor: A New Putative Therapeutic Target in Multiple Sclerosis

Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, can be induced by immunization with a number of myelin antigens. In particular, myelin oligodendrocyte glycoprotein, a central nervous system (CNS)-specific antigen expressed on the myelin surface, is able to induce a paralytic MS-like disease with extensive CNS inflammation and demyelination in several strains of animals. Although not well understood, the egress of immune cells into the CNS in EAE is governed by a complex interplay between pro and antiinflammatory cytokines and chemokines. The hematopoietic growth factor, granulocyte macrophage colony-stimulating factor (GM-CSF), is considered to play a central role in maintaining chronic inflammation. The present study was designed to investigate the previously unexplored role of GM-CSF in autoimmune-mediated demyelination. GM-CSF−/− mice are resistant to EAE, display decreased antigen-specific proliferation of splenocytes, and fail to sustain immune cell infiltrates in the CNS, thus revealing key activities for GM-CSF in the development of inflammatory demyelinating lesions and control of migration and/or proliferation of leukocytes within the CNS. These results hold implications for the pathogenesis of inflammatory and demyelinating diseases and may provide the basis for more effective therapies for inflammatory diseases, and more specifically for multiple sclerosis

EAE mediated by a non-IFN-Γ/non-IL-17 pathway

Previous studies have shown that EAE can be elicited by the adoptive transfer of either IFN-Γ-producing (Th1) or IL-17-producing (Th17) myelin-specific CD4 + T-cell lines. Paradoxically, mice deficient in either IFN-Γ or IL-17 remain susceptible to EAE following immunization with myelin antigens in CFA. These observations raise questions about the redundancy of IFN-Γ and IL-17 in autoimmune demyelinating disease mediated by a diverse, polyclonal population of autoreactive T cells. In this study, we show that an atypical form of EAE, induced in C57BL/6 mice by the adoptive transfer of IFN-Γ-deficient effector T cells, required IL-17 signaling for the development of brainstem infiltrates. In contrast, classical EAE, characterized by predominant spinal cord inflammation, occurred in the combined absence of IFN-Γ and IL-17 signaling, but was dependent on GM-CSF and CXCR2. Our findings contribute to a growing body of data, indicating that individual cytokines vary in their importance across different models of CNS autoimmunity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/77956/1/2340_ftp.pd

Thymic crosstalk restrains the pool of cortical thymic epithelial cells with progenitor properties

Cortical (cTEC) and medullary (mTEC) thymic epithelial cells establish key microenvironments for T-cell differentiation and arise from thymic epithelial cell progenitors (TEP). However, the nature of TEPs and the mechanism controlling their stemness in the postnatal thymus remain poorly defined. Using TEC clonogenic assays as a surrogate to survey TEP activity, we found that a fraction of cTECs generates specialized clonal-derived colonies, which contain cells with sustained colony-forming capacity (ClonoTECs). These ClonoTECs are EpCAM+MHCII-Foxn1lo cells that lack traits of mature cTECs or mTECs but co-express stem-cell markers, including CD24 and Sca-1. Supportive of their progenitor identity, ClonoTECs reintegrate within native thymic microenvironments and generate cTECs or mTECs in vivo. Strikingly, the frequency of cTECs with the potential to generate ClonoTECs wanes between the postnatal and young adult immunocompetent thymus, but it is sustained in alymphoid Rag2-/-Il2rg-/- counterparts. Conversely, transplantation of wild-type bone marrow hematopoietic progenitors into Rag2-/-Il2rg-/- mice and consequent restoration of thymocyte-mediated TEC differentiation diminishes the frequency of colony-forming units within cTECs. Our findings provide evidence that the cortical epithelium contains a reservoir of epithelial progenitors whose abundance is dynamically controlled by continual interactions with developing thymocytes across lifespan.This work has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement No 637843 - TEC_Pro), from FEDER - Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020 - Operacional Programme for Competitiveness and Internationalisation (POCI), Portugal 2020, and by Portuguese funds through FCT - Fundacao para a Ciencia e a Tecnologia/Ministerio da Ciencia, Tecnologia e Ensino Superior in the framework of the project "Institute for Research and Innovation in Health Sciences" (POCI-01-0145-FEDER-007274) and FEDER funds through the Operational Competitiveness Programme - COMPETE and by National Funds through FCT - Fundacao para a Ciencia e a Tecnologia under the project FCOMP-01-0124-FEDER-021075 (PTDC/SAU-IMU/117057/2010). N.L.A., P.M.R., A.R.R., C.M., and R.D.P. are supported by the Investigator program, Post-doctoral and PhD fellowships from FCT (Portugal)

Deriving C4 photosynthetic parameters from combined gas exchange and chlorophyll fluorescence using an Excel tool: theory and practice

The higher photosynthetic potential of C4 plants has led to extensive research over the past 50 years, including C4-dominated natural biomes, crops such as maize, or for evaluating the transfer of C4 traits into C3 lineages. Photosynthetic gas exchange can be measured in air or in a 2% Oxygen mixture using readily available commercial gas exchange and modulated PSII fluorescence systems. Interpretation of these data, however, requires an understanding (or the development) of various modelling approaches, which limit the use by non-specialists. In this paper we present an accessible summary of the theory behind the analysis and derivation of C4 photosynthetic parameters, and provide a freely available Excel Fitting Tool (EFT), making rigorous C4 data analysis accessible to a broader audience. Outputs include those defining C4 photochemical and biochemical efficiency, the rate of photorespiration, bundle sheath conductance to CO2 diffusion and the in vivo biochemical constants for PEP carboxylase. The EFT compares several methodological variants proposed by different investigators, allowing users to choose the level of complexity required to interpret data. We provide a complete analysis of gas exchange data on maize (as a model C4 organism and key global crop) to illustrate the approaches, their analysis and interpretation