Team-teaching for inclusive learning: Purposes, practices and perceptions of a team-teaching initiative in Irish post-primary schools

Background. Schools unequivocally privilege solo-teaching. This research seeks to enhance our understanding of team-teaching by examining how two teachers, working in the same classroom at the same time, might or might not contribute to the promotion of inclusive learning. There are well-established policy statements that encourage change and moves towards the use of team-teaching to promote greater inclusion of students with special educational needs in mainstream schools and mainstream classrooms. What is not so well established is the practice of team-teaching in post-primary settings, with little research conducted to date on how it can be initiated and sustained, and a dearth of knowledge on how it impacts upon the students and teachers involved. Research questions and aims. In light of the paucity and inconclusive nature of the research on team-teaching to date (Hattie, 2009), the orientating question in this study asks ‘To what extent, can the introduction of a formal team-teaching initiative enhance the quality of inclusive student learning and teachers’ learning at post-primary level?’ The framing of this question emerges from ongoing political, legal and educational efforts to promote inclusive education. The study has three main aims. The first aim of this study is to gather and represent the voices and experiences of those most closely involved in the introduction of team-teaching; students, teachers, principals and administrators. The second aim is to generate a theory-informed understanding of such collaborative practices and how they may best be implemented in the future. The third aim is to advance our understandings regarding the day-to-day, and moment-to-moment interactions, between teachers and students which enable or inhibit inclusive learning. Sample. In total, 20 team-teaching dyads were formed across seven project schools. The study participants were from two of the seven project schools, Ash and Oak. It involved eight teachers and 53 students, whose age ranged from 12-16 years old, with 4 teachers forming two dyads per school. In Oak there was a class of first years (n=11) with one dyad and a class of transition year students (n=24) with the other dyad. In Ash one class group (n=18) had two dyads. The subjects in which the dyads engaged were English and Mathematics. Method. This research adopted an interpretive paradigm. The duration of the fieldwork was from April 2007 to June 2008. Research methodologies included semi-structured interviews (n=44), classroom observation (n=20), attendance at monthly teacher meetings (n=6), questionnaires and other data gathering practices which included school documentation, assessment findings and joint examination of student work samples (n=4). Results. Team-teaching involves changing normative practices, and involves placing both demands and opportunities before those who occupy classrooms (teachers and students) and before those who determine who should occupy these classrooms (principals and district administrators). This research shows how team-teaching has the potential to promote inclusive learning, and when implemented appropriately, can impact positively upon the learning experiences of both teachers and students. The results are outlined in two chapters. In chapter four, Social Capital Theory is used in framing the data, the change process of bonding, bridging and linking, and in capturing what the collaborative action of team-teaching means, asks and offers teachers; within classes, between classes, between schools and within the wider educational community. In chapter five, Positioning Theory deductively assists in revealing the moment-to-moment, dynamic and inclusive learning opportunities, that are made available to students through team-teaching. In this chapter a number of vignettes are chosen to illustrate such learning opportunities. These two theories help to reveal the counter-narrative that team-teaching offers, regarding how both teachers and students teach and learn. This counter-narrative can extend beyond the field of special education and include alternatives to the manner in which professional development is understood, implemented, and sustained in schools and classrooms. Team-teaching repositions teachers and students to engage with one another in an atmosphere that capitalises upon and builds relational trust and shared cognition. However, as this research study has found, it is wise that the purposes, processes and perceptions of team-teaching are clear to all so that team-teaching can be undertaken by those who are increasingly consciously competent and not merely accidentally adequate. Conclusions. The findings are discussed in the context of the promotion of effective inclusive practices in mainstream settings. I believe that such promotion requires more nuanced understandings of what is being asked of, and offered to, teachers and students. Team-teaching has, and I argue will increasingly have, its place in the repertoire of responses that support effective inclusive learning. To capture and extend such practice requires theoretical frameworks that facilitate iterative journeys between research, policy and practice. Research to date on team-teaching has been too focused on outcomes over short timeframes and not focused enough on the process that is team-teaching. As a consequence team-teaching has been under-used, under-valued, under-theorised and generally not very well understood. Moving from classroom to staff room and district board room, theoretical frameworks used in this research help to travel with, and understand, the initiation, engagement and early consequences of team-teaching within and across the educational landscape. Therefore, conclusions from this study have implications for the triad of research, practice and policy development where efforts to change normative practices can be matched by understandings associated with what it means to try something new/anew, and what it means to say it made a positive difference.

Towards enhanced divine-human-earth relations: a Christian-Buddhist contribution

The central claim of the dissertation is that lesser known and somewhat neglected, yet influential thinkers, within classical religious traditions have something worthwhile to contribute to the kind of ethos we should adopt in the face of the world’s various environmental crises. Moreover an exploration of such perspectives is best done in dialogue, particularly between Eastern and Western thought. I examine this claim primarily through a dialogue between the Christian philosopher John Scottus Eriugena and the Japanese Buddhist philosopher Kūkai (Kōbō Daishi). This dialogue, framed by the triad of divine-human-earth relations, primarily emphasises the oneness of all reality, and it finds expression in Eriugena’s concept of natura or phusis and Kūkai’s central teaching that the phenomenal world is the cosmic Buddha Dainichi. By highlighting this focus, I contribute to the existing academic field of ecology and religion on the subject of holism. However, I go beyond the materialist focus that generally marks such ecological holism within that field, offering instead a more metaphysical approach. This is indicated through my use of the concept of ‘immanental transcendence’ to describe Eriugena’s and Kūkai’s dynamic, numinous and mysterious notion of reality, as well as my exploration of Eriugena’s concept of theophany and Kūkai’s notion of kaji. I further explore how both philosophers highlight the human role in the process of reaching enlightenment—understood as attaining union with the whole. In that regard, I note significant differences in their positions: in particular, I note that Kūkai’s emphasis on bodily practices contrasts with Eriugena’s more conceptual approach. Finally to bolster my claim, I examine some ecologically oriented understandings of contemporary phenomenological approaches found particularly in the work of Jean-Luc Marion and to a lesser extent Merleau-Ponty, arguing that these reflect notions of reality and of the human role similar to those of the medieval philosophers.

Akt signal transduction dysfunction in the 3xTg-AD mouse model of Alzheimer's disease

Alzheimer’s disease (AD) is an incurable neurodegenerative disorder, accounting for over 60% of all cases of dementia. The primary risk factor for AD is age, however several genetic and environmental factors are also involved. The pathological characteristics of AD include extracellular deposition of the beta-amyloid peptide (Aβ) and intraneuronal accumulation of neurofibrillary tangles (NFTs) made of aggregated paired helical filaments (PHFs) of the hyperphosphorylated tau protein, along with synaptic loss and neuronal death. There are numerous biochemical mechanisms involved in AD pathogenesis, however the reigning hypothesis points to toxic oligomeric Aβ species as the primary causative factor in a cascade of events leading to neuronal stress and dyshomeostasis that initiate abnormal regulation of tau. The insulin and IGF-1 receptors (IR, IGF-1R) are the primary activators of PI3- K/Akt through which they regulate cell growth, development, glucose metabolism, and learning and memory. Work in our lab and others shows increased Akt activity and phosphorylation of its downstream targets in AD brain, along with insulin and insulin-like growth factor-1 signalling (IIS) dysfunction. This is supported by studies of AD models in vivo and in vitro. Our group and others hypothesise that Aβ activates Akt through IIS to initiate a negative feedback mechanism that desensitises neurons to insulin/IGF-1, and sustains activation of Akt. In this study the functions of endogenous Akt, IR, and the insulin receptor substrate (IRS-1) were examined in relationship to Aβ and tau pathology in the 3xTg-AD mouse model, which contains three mutant human transgenes associated with familial AD or dementia. The 3xTg-AD mouse develops Aβ and tau pathology in a spatiotemporal manner that best recapitulates the progression of AD in human brain. Western blotting and immunofluorescent microscopy techniques were utilised in vivo and in vitro, to examine the relationship between IIS, Akt, and AD pathology. I first characterised in detail AD pathology in 3xTg-AD mice, where an age-related accumulation of intraneuronal Aβ and tau was observed in the hippocampal formation, amygdala, and entorhinal cortex, and at late stages (18 months), extracellular amyloid plaques and NFTs, primarily in the subiculum and the CA1 layer of the hippocampal formation. Increased activity of Akt, detected with antibody to phosphoSer473-Akt, was increased in 3xTg-AD mice compared to age-matched non-transgenic mice (non-Tg), and in direct correlation to the accumulation of Aβ and tau in neuronal somatodendritic compartments. Akt phosphorylates tau at residue Ser214 within a highly specific consensus sequence for Akt phosphorylation, and phosphoSer214-tau strongly decreases microtubule (MT) stabilisation by preventing tau-MT binding. PhosphoSer214-tau increased concomitantly with this in the same age-related and region-specific fashion. Polarisation of tau phosphorylation was observed, where PHF-1 (tauSer396/404) and phosphoSer214-tau both appeared early in 3xTg-AD mice in distinct neuronal compartments: PHF-1 in axons, and phosphoSer214-tau in neuronal soma and dendrites. At 18 months, phosphoSer214-tau strongly colocalised with NFTs positive for the PHF- 1 and AT8 (tauSer202/Thr205) phosphoepitopes. IR was decreased with age in 3xTg-AD brain and in comparison to age-matched non-Tg, and this was specific for brain regions containing Aβ, tau, and hyperactive Akt. IRS-1 was similarly decreased, and both proteins showed altered subcellular distribution. Phosphorylation of IRS-1Ser312 is a strong indicator of IIS dysfunction and insulin resistance, and was increased in 3xTg-AD mice with age and in relation to pathology. Of particular note was our observation that abberant IIS and Akt signalling in 3xTg-AD brain related to Aβ and tau pathology on a gross anatomical level, and specifically localised to the brain regions and circuitry of the perforant path. Finally, I conducted a preliminary study of the effects of synthetic Aβ oligomers on embryonic rat hippocampus neuronal cultures to support these results and those in the literature. Taken together, these novel findings provide evidence for IIS and Akt signal transduction dysfunction as the missing link between Aβ and tau pathogenesis, and contribute to the overall understanding of the biochemical mechanisms of AD.

Investigations into the cellular and molecular changes in the amygdala in models of temporal lobe epilepsy and maternal immune activation

The amygdala is a limbic structure that is involved in many of our emotions and processing of these emotions such as fear, anger and pleasure. Conditions such as anxiety, autism, and also epilepsy, have been linked to abnormal functioning of the amygdala, owing to improper neurodevelopment or damage. This thesis investigated the cellular and molecular changes in the amygdala in models of temporal lobe epilepsy (TLE) and maternal immune activation (MIA). The kainic acid (KA) model of temporal lobe epilepsy (TLE) was used to induce Ammon’s-horn sclerosis (AHS) and to investigate behavioural and cytoarchitectural changes that occur in the amygdala related to Neuropeptide Y1 receptor expression. Results showed that KA-injected animals showed increased anxiety-like behaviours and displayed histopathological hallmarks of AHS including CA1 ablation, granule cell dispersion, volume reduction and astrogliosis. Amygdalar volume and neuronal loss was observed in the ipsilateral nuclei which was accompanied by astrogliosis. In addition, a decrease in Y1 receptor expressing cells in the ipsilateral CA1 and CA3 sectors of the hippocampus, ipsi- and contralateral granule cell layer of the dentate gyrus and ipsilateral central nucleus of the amygdala was found, consistent with a reduction in Y1 receptor protein levels. The results suggest that plastic changes in hippocampal and/or amygdalar Y1 receptor expression may negatively impact anxiety levels. Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain and tight regulation and appropriate control of GABA is vital for neurochemical homeostasis. GABA transporter-1 (GAT-1) is abundantly expressed by neurones and astrocytes and plays a key role in GABA reuptake and regulation. Imbalance in GABA homeostasis has been implicated in epilepsy with GAT-1 being an attractive pharmacological target. Electron microscopy was used to examine the distribution, expression and morphology of GAT-1 expressing structures in the amygdala of the TLE model. Results suggest that GAT-1 was preferentially expressed on putative axon terminals over astrocytic processes in this TLE model. Myelin integrity was examined and results suggested that in the TLE model myelinated fibres were damaged in comparison to controls. Synaptic morphology was studied and results suggested that asymmetric (excitatory) synapses occurred more frequently than symmetric (inhibitory) synapses in the TLE model in comparison to controls. This study illustrated that the amygdala undergoes ultrastructural alterations in this TLE model. Maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders such as autism, schizophrenia and also epilepsy. MIA was induced at a critical window of amygdalar development at E12 using bacterial mimetic lipopolysaccharide (LPS). Results showed that MIA activates cytokine, toll-like receptor and chemokine expression in the fetal brain that is prolonged in the postnatal amygdala. Inflammation elicited by MIA may prime the fetal brain for alterations seen in the glial environment and this in turn have deleterious effects on neuronal populations as seen in the amygdala at P14. These findings may suggest that MIA induced during amygdalar development may predispose offspring to amygdalar related disorders such as heightened anxiety, fear impairment and also neurodevelopmental disorders.