The contribution of Teacher education to universities:a case study for international teacher educators

This paper reports on the initial stage of a research project which aims to develop deeper understanding of the contribution teacher education, as a sub-discipline within Education, makes to Higher Education in England. The study is located in the intersection between the domains of teacher education and higher education scholarship, which in England represents a contested and ambiguous professional space. Tensions between competing accountability measures, pulling away from university-based to exclusively school-based teacher education, are exacerbated by proposed policy changes arising from the government's recent market review. Findings drawn from analysis of qualitative data from a national survey are discussed in the context of Elizabeth Povinelli's critique of late liberalism and previous scholarship on the nature of teacher educators’ work. Evidence from the study demonstrates numerous benefits to higher education of hosting teacher education departments, including contributions to standard metrics, regional development and knowledge exchange within a strategic social justice agenda. However, teacher educators themselves may find articulating these benefits difficult, because of marginalisation from the dominant ways of achieving and accounting for excellence in the modern university. These findings offer a cautionary tale to international colleagues whose governments may be embarking on equivalent paths of teacher education reform.<br/

ATL9, a RING Zinc Finger Protein with E3 Ubiquitin Ligase Activity Implicated in Chitin- and NADPH Oxidase-Mediated Defense Responses

Pathogen associated molecular patterns (PAMPs) are signals detected by plants that activate basal defenses. One of these PAMPs is chitin, a carbohydrate present in the cell walls of fungi and in insect exoskeletons. Previous work has shown that chitin treatment of Arabidopsis thaliana induced defense-related genes in the absence of a pathogen and that the response was independent of the salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) signaling pathways. One of these genes is ATL9 ( = ATL2G), which encodes a RING zinc-finger like protein. In the current work we demonstrate that ATL9 has E3 ubiquitin ligase activity and is localized to the endoplasmic reticulum. The expression pattern of ATL9 is positively correlated with basal defense responses against Golovinomyces cichoracearum, a biotrophic fungal pathogen. The basal levels of expression and the induction of ATL9 by chitin, in wild type plants, depends on the activity of NADPH oxidases suggesting that chitin-mediated defense response is NADPH oxidase dependent. Although ATL9 expression is not induced by treatment with known defense hormones (SA, JA or ET), full expression in response to chitin is compromised slightly in mutants where ET- or SA-dependent signaling is suppressed. Microarray analysis of the atl9 mutant revealed candidate genes that appear to act downstream of ATL9 in chitin-mediated defenses. These results hint at the complexity of chitin-mediated signaling and the potential interplay between elicitor-mediated signaling, signaling via known defense pathways and the oxidative burst

Designing for and with children with special needs in multiple settings

Interaction design methodologies have become increasingly popular in the design and development of technologies for children with special needs. However, designing within this area remains fraught with difficulties. This workshop aims to explore the issues that occur when working with children with special needs and seeks to establish a set of guidelines for interaction design researchers who are working with such a diverse group. This will be achieved through the discussion of a number of themes that have highlighted as important when designing within this complicated area

Pegylated interferon-2 alpha invokes graft-versus-leukemia effects in patients relapsing after allogeneic stem cell transplantation

Allogeneic stem cell transplantation (SCT) is a curative therapy for patients with hematological malignancies related largely to an immunological graft-versus-leukemia (GVL) effect mediated by donor T cells and natural killer cells. Relapse of disease after SCT represents failure of GVL and is now the major cause of treatment failure. We sought to augment GVL effects in patients (n = 29) relapsing after SCT in a prospective phase I/II clinical trial of dose-escalated pegylated interferon-2 alpha (peg-IFN alpha). The administration of peg-IFN alpha after reinduction chemotherapy, with or without subsequent donor lymphocyte infusion (DLI), resulted in a 2-year overall survival (OS) of 31% (95% confidence interval, 17.3%-49.2%), which rejects the null hypothesis of 7% generated by observations in an institutional historical cohort. As expected, peg-IFN alpha was associated with graft-versus-host disease (GVHD) and hematological toxicity, which was manageable with scheduled dose modifications. Progression-free survival (PFS) was greatest in patients who experienced GVHD, although the majority of those patients still eventually progressed. Higher PFS and OS were associated with pretreatment proportions of immune cell populations with regulatory function, including mucosal invariant T cells, regulatory T cells, and plasmacytoid dendritic cells, independent of any association with GVHD. Peg-IFN alpha administration after relapse thus constitutes a logical strategy to invoke GVL effects and should be studied in a larger, multicenter cohort. This trial was registered at www.anzctr. org.au as #ACTRN12612000728831

Addition of interleukin-6 inhibition with tocilizumab to standard graft-versus-host disease prophylaxis after allogeneic stem-cell transplantation: a phase 1/2 trial

Background Interleukin 6 mediates graft-versus-host disease (GVHD) in experimental allogeneic stem-cell transplantation (allogeneic SCT) and represents an attractive therapeutic target. We aimed to assess whether the humanised anti-interleukin-6 receptor monoclonal antibody, tocilizumab, could attenuate the incidence of acute GVHD