Examining the post-adoptive infusion of mobile technology in a healthcare domain: determinants and outcomes

The healthcare industry is beginning to appreciate the benefits which can be obtained from using Mobile Health Systems (MHS) at the point-of-care. As a result, healthcare organisations are investing heavily in mobile health initiatives with the expectation that users will employ the system to enhance performance. Despite widespread endorsement and support for the implementation of MHS, empirical evidence surrounding the benefits of MHS remains to be fully established. For MHS to be truly valuable, it is argued that the technological tool be infused within healthcare practitioners work practices and used to its full potential in post-adoptive scenarios. Yet, there is a paucity of research focusing on the infusion of MHS by healthcare practitioners. In order to address this gap in the literature, the objective of this study is to explore the determinants and outcomes of MHS infusion by healthcare practitioners. This research study adopts a post-positivist theory building approach to MHS infusion. Existing literature is utilised to develop a conceptual model by which the research objective is explored. Employing a mixed-method approach, this conceptual model is first advanced through a case study in the UK whereby propositions established from the literature are refined into testable hypotheses. The final phase of this research study involves the collection of empirical data from a Canadian hospital which supports the refined model and its associated hypotheses. The results from both phases of data collection are employed to develop a model of MHS infusion. The study contributes to IS theory and practice by: (1) developing a model with six determinants (Availability, MHS Self-Efficacy, Time-Criticality, Habit, Technology Trust, and Task Behaviour) and individual performance-related outcomes of MHS infusion (Effectiveness, Efficiency, and Learning), (2) examining undocumented determinants and relationships, (3) identifying prerequisite conditions that both healthcare practitioners and organisations can employ to assist with MHS infusion, (4) developing a taxonomy that provides conceptual refinement of IT infusion, and (5) informing healthcare organisations and vendors as to the performance of MHS in post-adoptive scenarios.

Inclusive education policy, the general allocation model and dilemmas of practice in primary schools

Background: Inclusive education is central to contemporary discourse internationally reflecting societies’ wider commitment to social inclusion. Education has witnessed transforming approaches that have created differing distributions of power, resource allocation and accountability. Multiple actors are being forced to consider changes to how key services and supports are organised. This research constitutes a case study situated within this broader social service dilemma of how to distribute finite resources equitably to meet individual need, while advancing inclusion. It focuses on the national directive with regard to inclusive educational practice for primary schools, Department of Education and Science Special Education Circular 02/05, which introduced the General Allocation Model (GAM) within the legislative context of the Education of Persons with Special Educational Needs (EPSEN) Act (Government of Ireland, 2004). This research could help to inform policy with ‘facts about what is happening on the ground’ (Quinn, 2013). Research Aims: The research set out to unearth the assumptions and definitions embedded within the policy document, to analyse how those who are at the coalface of policy, and who interface with multiple interests in primary schools, understand the GAM and respond to it, and to investigate its effects on students and their education. It examines student outcomes in the primary schools where the GAM was investigated. Methods and Sample The post-structural study acknowledges the importance of policy analysis which explicitly links the ‘bigger worlds’ of global and national policy contexts to the ‘smaller worlds’ of policies and practices within schools and classrooms. This study insists upon taking the detail seriously (Ozga, 1990). A mixed methods approach to data collection and analysis is applied. In order to secure the perspectives of key stakeholders, semi-structured interviews were conducted with primary school principals, class teachers and learning support/resource teachers (n=14) in three distinct mainstream, non-DEIS schools. Data from the schools and their environs provided a profile of students. The researcher then used the Pobal Maps Facility (available at www.pobal.ie) to identify the Small Area (SA) in which each student resides, and to assign values to each address based on the Pobal HP Deprivation Index (Haase and Pratschke, 2012). Analysis of the datasets, guided by the conceptual framework of the policy cycle (Ball, 1994), revealed a number of significant themes. Results: Data illustrate that the main model to support student need is withdrawal from the classroom under policy that espouses inclusion. Quantitative data, in particular, highlighted an association between segregated practice and lower socioeconomic status (LSES) backgrounds of students. Up to 83% of the students in special education programmes are from lower socio-economic status (LSES) backgrounds. In some schools 94% of students from LSES backgrounds are withdrawn from classrooms daily for special education. While the internal processes of schooling are not solely to blame for class inequalities, this study reveals the power of professionals to order children in school, which has implications for segregated special education practice. Such agency on the part of key actors in the context of practice relates to ‘local constructions of dis/ability’, which is influenced by teacher habitus (Bourdieu, 1984). The researcher contends that inclusive education has not resulted in positive outcomes for students from LSES backgrounds because it is built on faulty assumptions that focus on a psycho-medical perspective of dis/ability, that is, placement decisions do not consider the intersectionality of dis/ability with class or culture. This study argues that the student need for support is better understood as ‘home/school discontinuity’ not ‘disability’. Moreover, the study unearths the power of some parents to use social and cultural capital to ensure eligibility to enhanced resources. Therefore, a hierarchical system has developed in mainstream schools as a result of funding models to support need in inclusive settings. Furthermore, all schools in the study are ‘ordinary’ schools yet participants acknowledged that some schools are more ‘advantaged’, which may suggest that ‘ordinary’ schools serve to ‘bury class’ (Reay, 2010) as a key marker in allocating resources. The research suggests that general allocation models of funding to meet the needs of students demands a systematic approach grounded in reallocating funds from where they have less benefit to where they have more. The calculation of the composite Haase Value in respect of the student cohort in receipt of special education support adopted for this study could be usefully applied at a national level to ensure that the greatest level of support is targeted at greatest need. Conclusion: In summary, the study reveals that existing structures constrain and enable agents, whose interactions produce intended and unintended consequences. The study suggests that policy should be viewed as a continuous and evolving cycle (Ball, 1994) where actors in each of the social contexts have a shared responsibility in the evolution of education that is equitable, excellent and inclusive.

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.

An exploration of leadership in Irish post-primary education

The purpose of this study is to explore the nature and how of leadership in Irish post-primary schools. It considers school leadership within the context of contemporary Distributed Leadership theory. Associated concepts such as Distributed Cognition and Activity Theory are used to frame the study. From a distributed perspective, it is now widely accepted that other agents (e.g. teachers) have a leadership role, as part of collaborative, participative and supportive learning communities. Thus, this study considers how principals interact and build leadership capacity throughout the school. The study draws on two main sources of evidence. In analysing the implications of accountability agendas for school leadership, there is an exploration and focus on the conceptualisations of school leadership that are fore-grounded in 21 WSE reports. Elements of Critical Discourse Analysis are employed as an investigative tool to decipher how the construction of leadership practice is produced. The second prong of the study explores leadership in 3 case-study post-primary schools. Leadership is a complex phenomenon and not easy to describe. The findings clarify, however, that school leadership is a construct beyond the scope of the principal alone. While there is widespread support for a distributed model of leadership, the concept does not explicitly form part of the discourse in the case-study schools. It is also evident that any attempt to understand leadership practice must connect local interpretations with broader discourses. The understanding and practice of leadership is best understood in its sociohistorical context. The study reveals that, in the Irish post-primary school, the historical dimension is very influential, while the situational setting, involving a particular set of agents and agendas, strongly shapes thinking and practices. This study is novel as it synthesises two key sources of evidence. It is of great value in that it teases out the various historical and situational aspects to enhance understandings of school leadership in contemporary Ireland. It raises important questions for policy, practice and further research.

The synthetic progestin norgestrel modulates Nrf2 signaling and acts as an antioxidant in a model of retinal degeneration

Retinitis pigmentosa (RP) is one of the most common retinal degenerative conditions affecting people worldwide, and is currently incurable. It is characterized by the progressive loss of photoreceptors, in which the death of rod cells leads to the secondary death of cone cells; the cause of eventual blindness. As rod cells die, retinal-oxygen metabolism becomes perturbed, leading to increased levels of reactive oxygen species (ROS) and thus oxidative stress; a key factor in the secondary death of cones. In this study, norgestrel, an FDA-approved synthetic analog of progesterone, was found to be a powerful neuroprotective antioxidant, preventing light-induced ROS in photoreceptor cells, and subsequent cell death. Norgestrel also prevented light-induced photoreceptor morphological changes that were associated with ROS production, and that are characteristic of RP. Further investigation showed that norgestrel acts via post-translational modulation of the major antioxidant transcription factor Nrf2; bringing about its phosphorylation, subsequent nuclear translocation, and increased levels of its effector protein superoxide dismutase 2 (SOD2). In summary, these results demonstrate significant protection of photoreceptor cells from oxidative stress, and underscore the potential of norgestrel as a therapeutic option for RP.