66 research outputs found

    Learning in social movements: Emotion, identity and Egyptian diaspora becoming ‘logically and emotionally invested’ in the continuing struggle

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    This article explores the implications of learning in social movements on diaspora activists’ engagement with struggle. Focussing on emotions within social movement learning and the connection to activists’ multiple identities, the paper examines the complex terrain of learning as embodied and rooted in emotionally situated beliefs and values. The theoretical framework that informs this enquiry brings diaspora and identity into conversation with emotions in social movement learning and Boler’s ‘Pedagogy of discomfort’. Developing these connections contributes a new approach to understanding the emotional dynamics of activism and the implications of learning in this context on social movement participation. Based on qualitative research with diasporic accounts of participating in activism related to the continuing Egyptian revolution, the analysis contributes a deeper understanding of how learning in struggle shapes multiple forms of connectedness and the implications learning in this context can have for activists’ engagement with struggle. The findings add to existing knowledge of learning in social movements through a framework where cognition and emotion are ‘inextricably linked’ (Boler, 1999, p. xix) and to diaspora studies by highlighting that engagement is underpinned by situated and embodied identities that shape possibilities for learning

    Agonistic possibilities for global unlearning: constraints to learning within global citizenship education and social movements

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    The continued rise of populisms and divisions alongside increasing inequalities nationally and globally make the question of how educators and activists can respond increasingly urgent. This paper examines the possibilities that emerge from the connections between global citizenship education and learning in social movements, both spaces where people seek to engage others in ideas of how the world is, could and should be. Drawing on Mouffe’s (2005) theory of agonistic pluralism to engage conflict and emotion with possibilities for learning and unlearning, the case study reveals the significance of recognising constraints created by histories and narrations of the other. The paper calls for more work on the intersections of unlearning and agonism in order to create agonistic pedagogies for activism and global citizenship education

    Freedoms ebb and flow: Boaters’ experiences of water and sanitation insecurity on the inland waterways of England and Wales

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    This article explores how boat dwellers on the inland waterways of England and Wales – 'Boaters' – experience water and sanitation services. Boating populations are not counted as customers of private water utilities, so they exist within the 'dwelling paradox' and are positioned at greater risk of water and sanitation insecurity. Interviews and auto-ethnography document a myriad of ways in which participants use these resources on different vessels and waterways. The Capability Approach emerges as an apt framework for representing nuanced journeys from water and sanitation access to perceived quality of life. Findings suggest that equitable services can be defined as those which enable Boaters to live in ways they value. This entails reckoning with diverse – and potentially divergent – definitions of a 'good life', supported by the personal freedoms to achieve it. We argue this research makes a strong case for centring lived experiences in service design, particularly in instances of disagreement on the constitution of adequate service levels. Co-creating knowledge with people living in the dwelling paradox reveals complex relationships with authority and exclusion. We extend this theory, and the principles of equitable service delivery, to emphasise the situated desires, choices, and freedoms of the populations in question

    ASUSat1: Low-Cost, Student-Designed Nanosatellite

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    On January 27, 2000 (UTC) ASUSat1 was launched into space onboard Orbital Sciences’ Minotaur rocket. The launch was the culmination of six years of effort by over 400 students. ASUSat1 is an innovative nanosatellite bringing new concepts for low-power, low-mass, highly constrained designs. Its primary mission was earth imaging, with several secondary missions including orbit determination, amateur-radio communications, passive stabilization techniques, attitude detection, and composite-material research. Following the successful launch and deployment of ASUSat1, the satellite operated for 14 hours. In spite of this, the team collected useful data from the satellite, and verified many of the design concepts incorporated into the satellite. Following the on-orbit failure of ASUSat1, the team conducted an investigation to try and single out the problem. Even though no specific problem was identified, the team has noted several design and system-level issues to be taken as lessons learned from this project to future ASUSat satellite projects

    Three Corner Sat Constellation: C&DH, Stereoscopic Imaging, and End-To-End Data System

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    The Three Corner Sat Constellation (3~Sat) consists of three nanosatellites, which will demonstrate stereo imaging, innovative command and data handling, and formation flying with RF communications and cellular phone communications. The creation of this constellation is a joint effort between Arizona State University (ASU), the University of Colorado at Boulder (CU), and New Mexico State University (NMSU). The 3~Sat will provide accurate stereo images and range data of a variety of meteorological phenomena. With three independent nanosatellites observing a particular scene, triangulation will provide accurate range information that will be used to create three-dimensional depth maps. The cooperative communications and control of the satellites in the constellation will allow them to form a virtual formation to accomplish the mission objectives. In this paper, we will describe the science instrumentation and observing approaches, and will report on the distributed operations approach and intelligent End-to-End Mission Operations System, which enable this innovative mission

    Analysis of the asymmetrically expressed Ablim1 locus reveals existence of a lateral plate Nodal-independent left sided signal and an early, left-right independent role for nodal flow

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    BACKGROUND: Vertebrates show clear asymmetry in left-right (L-R) patterning of their organs and associated vasculature. During mammalian development a cilia driven leftwards flow of liquid leads to the left-sided expression of Nodal, which in turn activates asymmetric expression of the transcription factor Pitx2. While Pitx2 asymmetry drives many aspects of asymmetric morphogenesis, it is clear from published data that additional asymmetrically expressed loci must exist. RESULTS: A L-R expression screen identified the cytoskeletally-associated gene, actin binding lim protein 1 (Ablim1), as asymmetrically expressed in both the node and left lateral plate mesoderm (LPM). LPM expression closely mirrors that of Nodal. Significantly, Ablim1 LPM asymmetry was detected in the absence of detectable Nodal. In the node, Ablim1 was initially expressed symmetrically across the entire structure, resolving to give a peri-nodal ring at the headfold stage in a flow and Pkd2-dependent manner. The peri-nodal ring of Ablim1 expression became asymmetric by the mid-headfold stage, showing stronger right than left-sided expression. Node asymmetry became more apparent as development proceeded; expression retreated in an anticlockwise direction, disappearing first from the left anterior node. Indeed, at early somite stages Ablim1 shows a unique asymmetric expression pattern, in the left lateral plate and to the right side of the node. CONCLUSION: Left LPM Ablim1 is expressed in the absence of detectable LPM Nodal, clearly revealing existence of a Pitx2 and Nodal-independent left-sided signal in mammals. At the node, a previously unrecognised action of early nodal flow and Pkd2 activity, within the pit of the node, influences gene expression in a symmetric manner. Subsequent Ablim1 expression in the peri-nodal ring reveals a very early indication of L-R asymmetry. Ablim1 expression analysis at the node acts as an indicator of nodal flow. Together these results make Ablim1 a candidate for controlling aspects of L-R identity and patterning

    Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'.

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    Innate immune cells must be able to distinguish between direct binding to microbes and detection of components shed from the surface of microbes located at a distance. Dectin-1 (also known as CLEC7A) is a pattern-recognition receptor expressed by myeloid phagocytes (macrophages, dendritic cells and neutrophils) that detects β-glucans in fungal cell walls and triggers direct cellular antimicrobial activity, including phagocytosis and production of reactive oxygen species (ROS). In contrast to inflammatory responses stimulated upon detection of soluble ligands by other pattern-recognition receptors, such as Toll-like receptors (TLRs), these responses are only useful when a cell comes into direct contact with a microbe and must not be spuriously activated by soluble stimuli. In this study we show that, despite its ability to bind both soluble and particulate β-glucan polymers, Dectin-1 signalling is only activated by particulate β-glucans, which cluster the receptor in synapse-like structures from which regulatory tyrosine phosphatases CD45 and CD148 (also known as PTPRC and PTPRJ, respectively) are excluded (Supplementary Fig. 1). The 'phagocytic synapse' now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular antimicrobial responses only when they are required

    Bacillus anthracis TIR Domain-Containing Protein Localises to Cellular Microtubule Structures and Induces Autophagy

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    Toll-like receptors (TLRs) recognise invading pathogens and mediate downstream immune signalling via Toll/IL-1 receptor (TIR) domains. TIR domain proteins (Tdps) have been identified in multiple pathogenic bacteria and have recently been implicated as negative regulators of host innate immune activation. A Tdp has been identified in Bacillus anthracis, the causative agent of anthrax. Here we present the first study of this protein, designated BaTdp. Recombinantly expressed and purified BaTdp TIR domain interacted with several human TIR domains, including that of the key TLR adaptor MyD88, although BaTdp expression in cultured HEK293 cells had no effect on TLR4- or TLR2- mediated immune activation. During expression in mammalian cells, BaTdp localised to microtubular networks and caused an increase in lipidated cytosolic microtubule-associated protein 1A/1B-light chain 3 (LC3), indicative of autophagosome formation. In vivo intra-nasal infection experiments in mice showed that a BaTdp knockout strain colonised host tissue faster with higher bacterial load within 4 days post-infection compared to the wild type B. anthracis. Taken together, these findings indicate that BaTdp does not play an immune suppressive role, but rather, its absence increases virulence. BaTdp present in wild type B. anthracis plausibly interact with the infected host cell, which undergoes autophagy in self-defence

    Upregulation of PKD1L2 provokes a complex neuromuscular disease in the mouse

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    Following a screen for neuromuscular mouse mutants, we identified ostes, a novel N-ethyl N-nitrosourea-induced mouse mutant with muscle atrophy. Genetic and biochemical evidence shows that upregulation of the novel, uncharacterized transient receptor potential polycystic (TRPP) channel PKD1L2 (polycystic kidney disease gene 1-like 2) underlies this disease. Ostes mice suffer from chronic neuromuscular impairments including neuromuscular junction degeneration, polyneuronal innervation and myopathy. Ectopic expression of PKD1L2 in transgenic mice reproduced the ostes myopathic changes and, indeed, caused severe muscle atrophy in Tg(Pkd1l2)/Tg(Pkd1l2) mice. Moreover, double-heterozygous mice (ostes/+, Tg(Pkd1l2)/0) suffer from myopathic changes more profound than each heterozygote, indicating positive correlation between PKD1L2 levels and disease severity. We show that, in vivo, PKD1L2 primarily associates with endogenous fatty acid synthase in normal skeletal muscle, and these proteins co-localize to costameric regions of the muscle fibre. In diseased ostes/ostes muscle, both proteins are upregulated, and ostes/ostes mice show signs of abnormal lipid metabolism. This work shows the first role for a TRPP channel in neuromuscular integrity and disease

    Characterisation of Innate Fungal Recognition in the Lung

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    The innate recognition of fungi by leukocytes is mediated by pattern recognition receptors (PRR), such as Dectin-1, and is thought to occur at the cell surface triggering intracellular signalling cascades which lead to the induction of protective host responses. In the lung, this recognition is aided by surfactant which also serves to maintain the balance between inflammation and pulmonary function, although the underlying mechanisms are unknown. Here we have explored pulmonary innate recognition of a variety of fungal particles, including zymosan, Candida albicans and Aspergillus fumigatus, and demonstrate that opsonisation with surfactant components can limit inflammation by reducing host-cell fungal interactions. However, we found that this opsonisation does not contribute directly to innate fungal recognition and that this process is mediated through non-opsonic PRRs, including Dectin-1. Moreover, we found that pulmonary inflammatory responses to resting Aspergillus conidia were initiated by these PRRs in acidified phagolysosomes, following the uptake of fungal particles by leukocytes. Our data therefore provides crucial new insights into the mechanisms by which surfactant can maintain pulmonary function in the face of microbial challenge, and defines the phagolysosome as a novel intracellular compartment involved in the innate sensing of extracellular pathogens in the lung
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