The ins and outs of participation in a weather information system

In this paper our aim is to show even though access to technology, information or data holds the potential for improved participation, participation is wired into a larger network of actors, artefacts and information practices. We draw on a case study of a weather information system developed and implemented by a non-profit organisation to both describe the configuration of participation, but also critically assess inclusion and exclusion. We present a set of four questions - a basic, practical toolkit - by which we together with the organisation made sense of and evaluated participation in the system

(G)hosting television: Ghostwatch and its medium

This article’s subject is Ghostwatch (BBC, 1992), a drama broadcast on Halloween night of 1992 which adopted the rhetoric of live non-fiction programming, and attracted controversy and ultimately censure from the Broadcasting Standards Council. In what follows, we argue that Ghostwatch must be understood as a televisually-specific artwork and artefact. We discuss the programme’s ludic relationship with some key features of television during what Ellis (2000) has termed its era of ‘availability’, principally liveness, mass simultaneous viewing, and the flow of the television super-text. We trace the programme’s television-specific historicity whilst acknowledging its allusions and debts to other media (most notably film and radio). We explore the sophisticated ways in which Ghostwatch’s visual grammar and vocabulary and deployment of ‘broadcast talk’ (Scannell 1991) variously ape, comment upon and subvert the rhetoric of factual programming, and the ends to which these strategies are put. We hope that these arguments collectively demonstrate the aesthetic and historical significance of Ghostwatch and identify its relationship to its medium and that medium’s history. We offer the programme as an historically-reflexive artefact, and as an exemplary instance of the work of art in television’s age of broadcasting, liveness and co-presence

A177: Program Evaluation of the ACR/CARRA Inter‐Institutional Mentoring Program (AMIGO) in Pediatric Rheumatology

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106776/1/art38603.pd

Microstructural damage of the posterior corpus callosum contributes to the clinical severity of neglect

One theory to account for neglect symptoms in patients with right focal damage invokes a release of inhibition of the right parietal cortex over the left parieto-frontal circuits, by disconnection mechanism. This theory is supported by transcranial magnetic stimulation studies showing the existence of asymmetric inhibitory interactions between the left and right posterior parietal cortex, with a right hemispheric advantage. These inhibitory mechanisms are mediated by direct transcallosal projections located in the posterior portions of the corpus callosum. The current study, using diffusion imaging and tract-based spatial statistics (TBSS), aims at assessing, in a data-driven fashion, the contribution of structural disconnection between hemispheres in determining the presence and severity of neglect. Eleven patients with right acute stroke and 11 healthy matched controls underwent MRI at 3T, including diffusion imaging, and T1-weighted volumes. TBSS was modified to account for the presence of the lesion and used to assess the presence and extension of changes in diffusion indices of microscopic white matter integrity in the left hemisphere of patients compared to controls, and to investigate, by correlation analysis, whether this damage might account for the presence and severity of patients' neglect, as assessed by the Behavioural Inattention Test (BIT). None of the patients had any macroscopic abnormality in the left hemisphere; however, 3 cases were discarded due to image artefacts in the MRI data. Conversely, TBSS analysis revealed widespread changes in diffusion indices in most of their left hemisphere tracts, with a predominant involvement of the corpus callosum and its projections on the parietal white matter. A region of association between patients' scores at BIT and brain FA values was found in the posterior part of the corpus callosum. This study strongly supports the hypothesis of a major role of structural disconnection between the right and left parietal cortex in determining 'neglect'

Datatrust: Or, the political quest for numerical evidence and the epistemologies of Big Data

Recently, there has been renewed interest in so-called evidence-based policy making. Enticed by the grand promises of Big Data, public officials seem increasingly inclined to experiment with more data-driven forms of governance. But while the rise of Big Data and related consequences has been a major issue of concern across different disciplines, attempts to develop a better understanding of the phenomenon's historical foundations have been rare. This short commentary addresses this gap by situating the current push for numerical evidence within a broader socio-political context, demonstrating how the epistemological claims of Big Data science intersect with specific forms of trust, truth, and objectivity. We conclude by arguing that regulators' faith in numbers can be attributed to a distinct political culture, a representative democracy undermined by pervasive public distrust and uncertainty

What Difference Does Quantity Make? On the Epistemology of Big Data Biology

publication-status: Acceptedtypes: ArticleIs Big Data science a whole new way of doing research? And what difference does data quantity make to knowledge production strategies and their outputs? I argue that the novelty of Big Data science does not lie in the sheer quantity of data involved, but rather in (1) the prominence and status acquired by data as commodity and recognised output, both within and outside of the scientific community and (2) the methods, infrastructures, technologies, skills and knowledge developed to handle data. These developments generate the impression that data-intensive research is a new mode of doing science, with its own epistemology and norms. To assess this claim, one needs to consider the ways in which data are actually disseminated and used to generate knowledge. Accordingly, this article reviews the development of sophisticated ways to disseminate, integrate and re-use data acquired on model organisms over the last three decades of work in experimental biology. I focus on online databases as prominent infrastructures set up to organise and interpret such data and examine the wealth and diversity of expertise, resources and conceptual scaffolding that such databases draw upon. This illuminates some of the conditions under which Big Data needs to be curated to support processes of discovery across biological subfields, which in turn highlights the difficulties caused by the lack of adequate curation for the vast majority of data in the life sciences. In closing, I reflect on the difference that data quantity is making to contemporary biology, the methodological and epistemic challenges of identifying and analysing data given these developments, and the opportunities and worries associated with Big Data discourse and methods.Economic and Social Research CouncilES/F028180/1Leverhulme TrustRPG-2013-153European Union’s Seventh Framework Programme (FP7/2007-2013ERC grant agreement number 335925

Attention-dependent modulation of cortical taste circuits revealed by granger causality with signal-dependent noise

We show, for the first time, that in cortical areas, for example the insular, orbitofrontal, and lateral prefrontal cortex, there is signal-dependent noise in the fMRI blood-oxygen level dependent (BOLD) time series, with the variance of the noise increasing approximately linearly with the square of the signal. Classical Granger causal models are based on autoregressive models with time invariant covariance structure, and thus do not take this signal-dependent noise into account. To address this limitation, here we describe a Granger causal model with signal-dependent noise, and a novel, likelihood ratio test for causal inferences. We apply this approach to the data from an fMRI study to investigate the source of the top-down attentional control of taste intensity and taste pleasantness processing. The Granger causality with signal-dependent noise analysis reveals effects not identified by classical Granger causal analysis. In particular, there is a top-down effect from the posterior lateral prefrontal cortex to the insular taste cortex during attention to intensity but not to pleasantness, and there is a top-down effect from the anterior and posterior lateral prefrontal cortex to the orbitofrontal cortex during attention to pleasantness but not to intensity. In addition, there is stronger forward effective connectivity from the insular taste cortex to the orbitofrontal cortex during attention to pleasantness than during attention to intensity. These findings indicate the importance of explicitly modeling signal-dependent noise in functional neuroimaging, and reveal some of the processes involved in a biased activation theory of selective attention

An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes.

BackgroundType 1 diabetes is a chronic autoimmune disease that leads to destruction of insulin-producing beta cells and dependence on exogenous insulin for survival. Some interventions have delayed the loss of insulin production in patients with type 1 diabetes, but interventions that might affect clinical progression before diagnosis are needed.MethodsWe conducted a phase 2, randomized, placebo-controlled, double-blind trial of teplizumab (an Fc receptor-nonbinding anti-CD3 monoclonal antibody) involving relatives of patients with type 1 diabetes who did not have diabetes but were at high risk for development of clinical disease. Patients were randomly assigned to a single 14-day course of teplizumab or placebo, and follow-up for progression to clinical type 1 diabetes was performed with the use of oral glucose-tolerance tests at 6-month intervals.ResultsA total of 76 participants (55 [72%] of whom were ≤18 years of age) underwent randomization - 44 to the teplizumab group and 32 to the placebo group. The median time to the diagnosis of type 1 diabetes was 48.4 months in the teplizumab group and 24.4 months in the placebo group; the disease was diagnosed in 19 (43%) of the participants who received teplizumab and in 23 (72%) of those who received placebo. The hazard ratio for the diagnosis of type 1 diabetes (teplizumab vs. placebo) was 0.41 (95% confidence interval, 0.22 to 0.78; P = 0.006 by adjusted Cox proportional-hazards model). The annualized rates of diagnosis of diabetes were 14.9% per year in the teplizumab group and 35.9% per year in the placebo group. There were expected adverse events of rash and transient lymphopenia. KLRG1+TIGIT+CD8+ T cells were more common in the teplizumab group than in the placebo group. Among the participants who were HLA-DR3-negative, HLA-DR4-positive, or anti-zinc transporter 8 antibody-negative, fewer participants in the teplizumab group than in the placebo group had diabetes diagnosed.ConclusionsTeplizumab delayed progression to clinical type 1 diabetes in high-risk participants. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT01030861.)

Mimicry and well known genetic friends: molecular diagnosis in an Iranian cohort of suspected Bartter syndrome and proposition of an algorithm for clinical differential diagnosis.

BACKGROUND: Bartter Syndrome is a rare, genetically heterogeneous, mainly autosomal recessively inherited condition characterized by hypochloremic hypokalemic metabolic alkalosis. Mutations in several genes encoding for ion channels localizing to the renal tubules including SLC12A1, KCNJ1, BSND, CLCNKA, CLCNKB, MAGED2 and CASR have been identified as underlying molecular cause. No genetically defined cases have been described in the Iranian population to date. Like for other rare genetic disorders, implementation of Next Generation Sequencing (NGS) technologies has greatly facilitated genetic diagnostics and counseling over the last years. In this study, we describe the clinical, biochemical and genetic characteristics of patients from 15 Iranian families with a clinical diagnosis of Bartter Syndrome. RESULTS: Age range of patients included in this study was 3 months to 6 years and all patients showed hypokalemic metabolic alkalosis. 3 patients additionally displayed hypercalciuria, with evidence of nephrocalcinosis in one case. Screening by Whole Exome Sequencing (WES) and long range PCR revealed that 12/17 patients (70%) had a deletion of the entire CLCNKB gene that was previously identified as the most common cause of Bartter Syndrome in other populations. 4/17 individuals (approximately 25% of cases) were found to suffer in fact from pseudo-Bartter syndrome resulting from congenital chloride diarrhea due to a novel homozygous mutation in the SLC26A3 gene, Pendred syndrome due to a known homozygous mutation in SLC26A4, Cystic Fibrosis (CF) due to a novel mutation in CFTR and apparent mineralocorticoid excess syndrome due to a novel homozygous loss of function mutation in HSD11B2 gene. 1 case (5%) remained unsolved. CONCLUSIONS: Our findings demonstrate deletion of CLCNKB is the most common cause of Bartter syndrome in Iranian patients and we show that age of onset of clinical symptoms as well as clinical features amongst those patients are variable. Further, using WES we were able to prove that nearly 1/4 patients in fact suffered from Pseudo-Bartter Syndrome, reversing the initial clinical diagnosis with important impact on the subsequent treatment and clinical follow up pathway. Finally, we propose an algorithm for clinical differential diagnosis of Bartter Syndrome