Digital literacies: Understanding the literate practices of refugee kids in an Afterschool Media Club

Since the 2000s, teachers in an increasing number of Australian schools have been learning how to support students with refugee backgrounds. For some of these students, entry into the Australian school system is not easy. English literacy is integral to some of the challenges confronting the students. In response, educators have been developing and researching ways of engaging with the students’ language and literacy learning. Much of the focus has been on traditional print-based school literacies. In contrast, I look here at student engagement in digital literacies in an after-school media club. Several concepts from the theory of French sociologist, Pierre Bourdieu are useful for understanding the position of students of refugee background in the Australian school system. Like other conflict theories, Bourdieusian theory has sometimes been criticised as ‘pessimistic’, that is, for suggesting that schools necessarily reproduce social disadvantage. However, others have used Bourdieusian theory to analyse and critique the reproductive work of schooling for groups of students who experience educational disadvantage. I align myself with this latter tradition. Specifically, I use Bourdieu’s triad of concepts to explain aspects of the literacy education experiences of some young people of refugee background: field, capital and habitus. In particular, I look at questions of the legitimation of students’ competences as capital in literate fields within and beyond the school context. Data are drawn from an Australian Research Council-funded project, Digital Learning and Print Literacy: A design experiment for the reform of low socio-economic, culturally diverse schools (2009-14). The data analysed in this chapter include interviews and observations relating to the participation of two Congolese girls in an after school media club. Implications are drawn for teachers of literacy in culturally and linguistically diverse contexts. Consideration is made of early childhood, primary and secondary settings.

Wide-band spectral power fluctuations characterize the response of simulated cortical networks to increasing stimulus intensity

The hippocampus is an anatomically distinct region of the medial temporal lobe that plays a critical role in the formation of declarative memories. Here we show that a computer simulation of simple compartmental cells organized with basic hippocampal connectivity is capable of producing stimulus intensity sensitive wide-band fluctuations of spectral power similar to that seen in real EEG. While previous computational models have been designed to assess the viability of the putative mechanisms of memory storage and retrieval, they have generally been too abstract to allow comparison with empirical data. Furthermore, while the anatomical connectivity and organization of the hippocampus is well defined, many questions regarding the mechanisms that mediate large-scale synaptic integration remain unanswered. For this reason we focus less on the specifics of changing synaptic weights and more on the population dynamics. Spectral power in four distinct frequency bands were derived from simulated field potentials of the computational model and found to depend on the intensity of a random input. The majority of power occurred in the lowest frequency band (3-6 Hz) and was greatest to the lowest intensity stimulus condition (1% maximal stimulus). In contrast, higher frequency bands ranging from 7-45 Hz show an increase in power directly related with an increase in stimulus intensity. This trend continues up to a stimulus level of 15% to 20% of the maximal input, above which power falls dramatically. These results suggest that the relative power of intrinsic network oscillations are dependent upon the level of activation and that above threshold levels all frequencies are damped, perhaps due to over activation of inhibitory interneurons.

Large Scale Simulations of Hippocampal-Neocortical Interactions in a Parallel Version of Genesis

A hippocampal-CA3 memory model was constructed with PGENESIS, a recently developed version of GENESIS that allows for distributed processing of a neural network simulation. A number of neural models of the human memory system have identified the CA3 region of the hippocampus as storing the declarative memory trace. However, computational models designed to assess the viability of the putative mechanisms of storage and retrieval have generally been too abstract to allow comparison with empirical data. Recent experimental evidence has shown that selective knock-out of NMDA receptors in the CA1 of mice leads to reduced stability of firing specificity in place cells. Here a similar reduction of stability of input specificity is demonstrated in a biologically plausible neural network model of the CA3 region, under conditions of Hebbian synaptic plasticity versus an absence of plasticity. The CA3 region is also commonly associated with seizure activity. Further simulations of the same model tested the response to continuously repeating versus randomized nonrepeating input patterns. Each paradigm delivered input of equal intensity and duration. Non-repeating input patterns elicited a greater pyramidal cell spike count. This suggests that repetitive versus non-repeating neocortical inpus has a quantitatively different effect on the hippocampus. This may be relevant to the production of independent epileptogenic zones and the process of encoding new memories.

Memory and Epileptogenesis in Complex Biological and Simulated Systems

Oscillations of neural activity may bind widespread cortical areas into a neural representation that encodes disparate aspects of an event. In order to test this theory we have turned to data collected from complex partial epilepsy (CPE) patients with chronically implanted depth electrodes. Data from regions critical to word and face information processing was analyzed using spectral coherence measurements. Similar analyses of intracranial EEG (iEEG) during seizure episodes display HippoCampal Formation (HCF)—NeoCortical (NC) spectral coherence patterns that are characteristic of specific seizure stages (Klopp et al. 1996). We are now building a computational memory model to examine whether spatio-temporal patterns of human iEEG spectral coherence emerge in a computer simulation of HCF cellular distribution, membrane physiology and synaptic connectivity. Once the model is reasonably scaled it will be used as a tool to explore neural parameters that are critical to memory formation and epileptogenesis.

Stress at the synapse : signal transduction mechanisms of adrenal steroids at neuronal membranes

As the key neuron-to-neuron interface, the synapse is involved in learning and memory, including traumatic memories during times of stress. However, the signal transduction mechanisms by which stress mediates its lasting effects on synapse transmission and on memory are not fully understood. A key component of the stress response is the increased secretion of adrenal steroids. Adrenal steroids (e.g., cortisol) bind to genomic mineralocorticoid and glucocorticoid receptors (gMRs and gGRs) in the cytosol. In addition, they may act through membrane receptors (mMRs and mGRs), and signal transduction through these receptors may allow for rapid modulation of synaptic transmission as well as modulation of membrane ion currents. mMRs increase synaptic and neuronal excitability; mechanisms include the facilitation of glutamate release through extracellular signal-regulated kinase signal transduction. In contrast, mGRs decrease synaptic and neuronal excitability by reducing calcium currents through N-methyl-D-aspartate receptors and voltage-gated calcium channels by way of protein kinase A- and G protein-dependent mechanisms. This body of functional data complements anatomical evidence localizing GRs to the postsynaptic membrane. Finally, accumulating data also suggest the possibility that mMRs and mGRs may show an inverted U-shaped dose response, whereby glutamatergic synaptic transmission is increased by low doses of corticosterone acting at mMRs and decreased by higher doses acting at mGRs. Thus, synaptic transmission is regulated by mMRs and mGRs, and part of the stress signaling response is a direct and bidirectional modulation of the synapse itself by adrenal steroids.

Polysynaptic potentials within the lateral amygdala networks as indicators of reverberatory activity

Synaptic plasticity in the lateral amygdala (LA) may underlie auditory fear conditioning. Hebb postulated that sustained activity in reverberating cellular ensembles can facilitate temporal coincidence detection. Our anatomical data show that LA neurons have extensive local axon collaterals that are topographically organized and that could provide the anatomical basis for reverberatory activity...

Quantification of the total neuronal structure of the fear conditioning circuit of the lateral amygdala of the rat

During Pavlovian auditory fear conditioning a previously neutral auditory stimulus (CS) gains emotional significance through pairing with a noxious unconditioned stimulus (US). These associations are believed to be formed by way of plasticity at auditory input synapses on principal neurons in the lateral nucleus of the amygdala (LA). In order to begin to understand how fear memories are stored and processed by synaptic changes in the LA, we have quantified both the entire neural number and the sub-cellular structure of LA principal neurons.We first used stereological cell counting methods on Gimsa or GABA immunostained rat brain. We identified 60,322+/-1408 neurons in the LA unilaterally (n=7). Of these 16,917+/-471 were GABA positive. The intercalated nuclei were excluded from the counts and thus GABA cells are believed to represent GABAergic interneurons. The sub-nuclei of the LA were also independently counted. We then quantified the morphometric properties of in vitro electrophysiologically identified principal neurons of the LA, corrected for shrinkage in xyz planes. The total dendritic length was 9.97+/-2.57mm, with 21+/-4 nodes (n=6). Dendritic spine density was 0.19+/-0.03 spines/um (n=6). Intra-LA axon collaterals had a bouton density of 0.1+/-0.02 boutons/um (n=5). These data begin to reveal the finite cellular and sub-cellular processing capacity of the lateral amygdala, and should facilitate efforts to understand mechanisms of plasticity in LA.

GABAergic inhibition in the fear conditioning circuit of the lateral amygdala is potentiated by dopamine D1 agonists

Auditory fear conditioning is dependent on auditory signaling from the medial geniculate (MGm) and the auditory cortex (TE3) to principal neurons of the lateral amygdala (LA). Local circuit GABAergic interneurons are known to inhibit LA principal neurons via fast and slow IPSP's. Stimulation of MGm and TE3 produces excitatory post-synaptic potentials in both LA principal and interneurons, followed by inhibitory post-synaptic potentials. Manipulations of D1 receptors in the lateral and basal amygdala modulate the retrieval of learned association between an auditory CS and foot shock. Here we examined the effects of D1 agonists on GABAergic IPSP's evoked by stimulation of MGm and TE3 afferents in vitro. Whole cell patch recordings were made from principal neurons of the LA, at room temperature, in coronal brain slices using standard methods. Stimulating electrodes were placed on the fiber tracts medial to the LA and at the external capsule/layer VI border dorsal to the LA to activate (0.1-0.2mA) MGm and TE3 afferents respectively. Neurons were held at -55.0 mV by positive current injection to measure the amplitude of the fast IPSP. Changes in input resistance and membrane potential were measured in the absence of current injection. Stimulation of MGm or TE3 afferents produced EPSP's in the majority of principal neurons and in some an EPSP/IPSP sequence. Stimulation of MGm afferents produced IPSP's with amplitudes of -2.30 ± 0.53 mV and stimulation of TE3 afferents produced IPSP's with amplitudes of -1.98 ± 1.26 mV. Bath application of 20μM SKF38393 increased IPSP amplitudes to -5.94 ± 1.62 mV (MGm, n=3) and-5.46 ± 0.31 mV (TE3, n=3). Maximal effect occurred <10mins. A small increase in resting membrane potential and decrease in input resistance were observed. These data suggest that DA modulates both the auditory thalamic and auditory cortical inputs to the LA fear conditioning circuit via local GABAergic circuits. Supported by NIMH Grants 00956, 46516, and 58911.

Participatory action research for civic engagement

The future of civic engagement is characterised by both technological innovation as well as new technological user practices that are fuelled by trends towards mobile, personal devices; broadband connectivity; open data; urban interfaces; and, cloud computing. These technology trends are progressing at a rapid pace, and have led global technology vendors to package and sell the ‘Smart City’ as a centralized service delivery platform predicted to optimize and enhance cities’ key performance indicators – and generate a profitable market. The top-down deployment of these large and proprietary technology platforms have helped sectors such as energy, transport, and healthcare to increase efficiencies. However, an increasing number of scholars and commentators warn of another ‘IT bubble’ emerging. Along with some city leaders, they argue that the top-down approach does not fit the governance dynamics and values of a liberal democracy when applied across sectors. A thorough understanding is required, of the socio-cultural nuances of how people work, live, play across different environments, and how they employ social media and mobile devices to interact with, engage in, and constitute public realms. Although the term ‘slacktivism’ is sometimes used to denote a watered down version of civic engagement and activism that is reduced to clicking a ‘Like’ button and signing online petitions, we believe that we are far from witnessing another Biedermeier period that saw people focus on the domestic and the non-political. There is plenty of evidence to the contrary, such as post-election violence in Kenya in 2008, the Occupy movements in New York, Hong Kong and elsewhere, the Arab Spring, Stuttgart 21, Fukushima, the Taksim Gezi Park in Istanbul, and the Vinegar Movement in Brazil in 2013. These examples of civic action shape the dynamics of governments, and in turn, call for new processes to be incorporated into governance structures. Participatory research into these new processes across the triad of people, place and technology is a significant and timely investment to foster productive, sustainable, and livable human habitats. With this chapter, we want to reframe the current debates in academia and priorities in industry and government to allow citizens and civic actors to take their rightful centerpiece place in civic movements. This calls for new participatory approaches for co-inquiry and co-design. It is an evolving process with an explicit agenda to facilitate change, and we propose participatory action research (PAR) as an indispensable component in the journey to develop new governance infrastructures and practices for civic engagement. This chapter proposes participatory action research as a useful and fitting research paradigm to guide methodological considerations surrounding the study, design, development, and evaluation of civic technologies. We do not limit our definition of civic technologies to tools specifically designed to simply enhance government and governance, such as renewing your car registration online or casting your vote electronically on election day. Rather, we are interested in civic media and technologies that foster citizen engagement in the widest sense, and particularly the participatory design of such civic technologies that strive to involve citizens in political debate and action as well as question conventional approaches to political issues (DiSalvo, 2012; Dourish, 2010; Foth et al., 2013). Following an outline of some underlying principles and assumptions behind participatory action research, especially as it applies to cities, we will critically review case studies to illustrate the application of this approach with a view to engender robust, inclusive, and dynamic societies built on the principles of engaged liberal democracy. The rationale for this approach is an alternative to smart cities in a ‘perpetual tomorrow,’ (cf. e.g. Dourish & Bell, 2011), based on many weak and strong signals of civic actions revolving around technology seen today. It seeks to emphasize and direct attention to active citizenry over passive consumerism, human actors over human factors, culture over infrastructure, and prosperity over efficiency. First, we will have a look at some fundamental issues arising from applying simplistic smart city visions to the kind of a problem a city is (cf. Jacobs, 1961). We focus on the touch points between “the city” and its civic body, the citizens. In order to provide for meaningful civic engagement, the city must provide appropriate interfaces.

Mechanisms underlying the effect of acupuncture on cognitive improvement: A systematic review of animal studies

Acupuncture has been reported to be beneficial in treating cognitive impairment in various pathological conditions. This review describes the effort to understand the signaling pathways that underlie the acupunctural therapeutic effect on cognitive function. We searched the literature in 12 electronic databases from their inception to November 2013, with full text available and language limited to English. Twenty-three studies were identified under the selection criteria. All recruited animal studies demonstrate a significant positive effect of acupuncture on cognitive impairment. Findings suggest acupuncture may improve cognitive function through modulation of signaling pathways involved in neuronal survival and function, specifically, through promoting cholinergic neural transmission, facilitating dopaminergic synaptic transmission, enhancing neurotrophin signaling, suppressing oxidative stress, attenuating apoptosis, regulating glycometabolic enzymes and reducing microglial activation. However, the quality of reviewed studies has room for improvement. Further high-quality animal studies with randomization, blinding and estimation of sample size are needed to strengthen the recognition of group differences.

Rallying the troops or beating the horses? How project-related demands can lead to either high performance or abusive supervision

In today's high-pressure work environment, project managers are often forced to “do more with less.” We argue that this imperative can lead project managers to engage in either high-performance or abusive supervision behaviors. To understand this process, we develop a model and associated propositions linking a project manager's cognitive appraisal of project-related demands to high-performance work practices versus abusive supervision behaviors—both of which impact three project outcomes: stakeholder relationships, people-related project success factors, and employee well-being. We propose that the choice between high-performance work practices and abusive supervision behaviors is moderated by a project manager's personal resources (psychological capital, emotional intelligence, and dark triad personality).

Differential interaction between the C2B domain of synaptotagmin-I and the Drosophila stonedA and stonedB proteins

The stoned locus in Drosophila encodes two proteins StonedA (STNA) and StonedB (STNB), both of which have been suggested to act as adaptins in mediating synaptic vesicle recycling. A combination of immunological, genetic and biochemical studies have shown an interaction of STNA and STNB with the C2B domain of Synaptotagmin-I (SYT-1), an integral synaptic vesicle protein that mediates Ca2+-dependent exocytosis, as well as endocytosis. The C2B domain of SYT-1 contains an AP-2 binding site that controls the size of recycled vesicles, and a C-terminal tryptophan-containing motif that acts as an internalization signal. Investigation of SYT-1 mutations in Drosophila has shown that altering the Ca2+ binding region of the C2B domain, results in a reduction in the rate of vesicle recycling, implicating this region in SYT-I endocytosis. In this poster, we report the molecular dissection of the interactions between the STNA and STNB proteins and the C2B domain of SYT-1. Deletion of the AP-2 binding site decreased the binding of both STNA and STNB. However, C-terminal deletions of the C2B domain significantly increased STNB binding. In contrast, the same C-terminal deletions reduced the affinity of the C2B domain for STNA. The possible interactions of both STNB and STNA with the Ca2+ binding region of SYT-1 will be also investigated.

Using Bourdieu in education research: Theory and methods

This workshop will snapshot Bourdieu's sociology. In recognition of Bourdieu's work as a powerful theoretical instrument to speculate the reproduction of social orders and cultural values, the workshop will firstly discuss the core concepts of habitus, capital, and field – the foundational triad of Bourdieu's sociology. Although Bourdieu's original work was built on some quantitative studies, his sociology has been largely qualitatively used in education research. Different from the bulk of extant research, the workshop will secondly showcase some quantitative and mixed methods research that uses a Bourdieusian framework. Mindful of such a framework helping understand social practice at a macro level, the workshop will then make an attempt to think through the macro and the micro by weaving together Bourdieu's sociology with Garfinkel's ethnomethodology. The workshop will conclude with some reflections and communications in terms of how to better realise the full value of Bourdieu in education research.

Targeting glucocorticoid receptors that promote resilience in the treatment of addiction

There is strong evidence to suggest that the combination of alcohol and chronic repetitive stress leads to long-lasting effects on brain function, specifically areas associated with stress, motivation and decision-making such as the amygdala, nucleus accumbens and prefrontal cortex. Alcohol and stress together facilitate the imprinting of long-lasting memories. The molecular mechanisms and circuits involved are being studied but are not fully understood. Current evidence suggests that corticosterone (animals) or cortisol (humans), in addition to direct transcriptional effects on the genome, can directly regulate pre- and postsynaptic synaptic transmission through membrane bound glucocorticoid receptors (GR). Indeed, corticosterone-sensitive synaptic receptors may be critical sites for stress regulation of synaptic responses. Direct modulation of synaptic transmission by corticosterone may contribute to the regulation of synaptic plasticity and memory during stress (Johnson et al., 2005; Prager et al., 2010). Specifically, previous data has shown that long term alcohol (1) increases the expression of NR2Bcontaining NMDA receptors at glutamate synapses, (2) changes receptor density, and (3) changes morphology of dendritic spines (Prendergast and Mulholland; 2012). During alcohol withdrawal these changes are associated with increased glucocorticoid signalling and increased neuronal excitability. It has therefore been proposed that these synapse changes lead to the anxiety and alcohol craving associated with withdrawal (Prendergast and Mulholland; 2012). My lab is targeting this receptor system and the amygdala in order to understand the effect of combining alcohol and stress on these pathways. Lastly, we are testing GR specific compounds as potential new medications to promote the development of resilience to developing addiction.

The multiple sclerosis whole blood mRNA transcriptome and genetic associations indicate dysregulation of specific T cell pathways in pathogenesis

Multiple sclerosis (MS) is an autoimmune disease with a genetic component, caused at least in part by aberrant lymphocyte activity. The whole blood mRNA transcriptome was measured for 99 untreated MS patients: 43 primary progressive MS, 20 secondary progressive MS, 36 relapsing remitting MS and 45 age-matched healthy controls. The ANZgene Multiple Sclerosis Genetics Consortium genotyped more than 300 000 SNPs for 115 of these samples. Transcription from genes on translational regulation, oxidative phosphorylation, immune synapse and antigen presentation pathways was markedly increased in all forms of MS. Expression of genes tagging T cells was also upregulated (P < 10-12) in MS. A T cell gene signature predicts disease state with a concordance index of 0.79 with age and gender as co-variables, but the signature is not associated with clinical course or disability. The ANZgene genome wide association screen identified two novel regions with genome wide significance: one encoding the T cell co-stimulatory molecule, CD40; the other a region on chromosome 12q13-14. The CD40 haplotype associated with increased MS susceptibility has decreased gene expression in MS (P < 0.0007). The second MS susceptibility region includes 17 genes on 12q13-14 in tight linkage disequilibrium. Of these, only 13 are expressed in leukocytes, and of these the expression of one, FAM119B, is much lower in the susceptibility haplotype (P tdthomlt; 10-14). Overall, these data indicate dysregulation of T cells can be detected in the whole blood of untreated MS patients, and supports targeting of activated T cells in therapy for all forms of MS.