585 research outputs found

    Integrating practice based and neuroscientific perspectives on the impact of digital technology on contemporary narrative dramaturgy, investigated through live simulation exercises

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    University of Technology, Sydney. Faculty of Arts and Social Sciences.The collision of the dramatic and narrative arts with digital technology has seen the emergence of distinct narrative experiences incorporating new attributes such as interactivity and participant’s agency within the unfolding of the work. The disruption caused by these innovations and attributes has been hotly debated in many creative industry forums and further reinforced in theoretical discussions focussing on narrative and interactivity, a case in point being the ‘story versus game’ debates waged between the narratologists and the ludologists. As a director and deviser of live performance, my own use of digital technology in productions throughout the 1990s generated concomitant dramaturgical dilemmas regarding the changing structure of narrative and the shifting role of the audience. From the outset of my investigations into these challenges it was clear there was a critical problem to be addressed. Temporality, and the ordering of experience and events in time, provides the foundation of storytelling and narrative dramaturgy. While conventional story structure is predicated on a reflective, re-telling of experience, games and many emerging forms appear to be contingent on a form of lived experience and enactment. This doctorate examines particular aspects of narrative understanding as it is affected by the emergence of these new modes of dramaturgy and performance. Given that the new developments seemed to be challenging western dramatic conventions, in particular the key Aristotelian tenet of representation, I guided my research with this question: ‘How is this technological disruption renegotiating our traditional Aristotelian sense of time and presence?’ This thesis investigates the question from a neuroscientific perspective, integrating practice-based understandings and creative experimentation with neurobiological insights from Antonio Damasio, Francisco Varela and Benjamin Libet. It does so under the supposition that the shifts in narrative composition might in fact be reflective of how we process information. Further, it puts forward the proposal that we might enhance our understanding of contemporary narrative experiences by considering a model of dramaturgy that is informed by this understanding of the brain’s processing mechanisms. In order to test this proposal I firstly set up a live simulation as an example of a technologized and interactive performed narrative, and then I distil four creative micro narratives from that simulation. I then analyse and discuss the micro narratives as forms of neurobiological sense making, potentially indicative of a compositional structure based on an alternate, neurobiological temporal dynamic. The creative experiment and research findings (delivered in the exegesis) suggest the emergence of a new dramaturgical aesthetic and poetic of time; one that is predicated on a neurobiological dramaturgy distinguished by subjectivity, embodiment, enactment and above all, ‘presentness’

    A Multimodal Sensory Apparatus for Robotic Prosthetic Feet Combining Optoelectronic Pressure Transducers and IMU

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    Timely and reliable identification of control phases is functional to the control of a powered robotic lower-limb prosthesis. This study presents a commercial energy-store-and-release foot prosthesis instrumented with a multimodal sensory system comprising optoelectronic pressure sensors (PS) and IMU. The performance was verified with eight healthy participants, comparing signals processed by two different algorithms, based on PS and IMU, respectively, for real-time detection of heel strike (HS) and toe-off (TO) events and an estimate of relevant biomechanical variables such as vertical ground reaction force (vGRF) and center of pressure along the sagittal axis (CoPy). The performance of both algorithms was benchmarked against a force platform and a marker-based stereophotogrammetric motion capture system. HS and TO were estimated with a time error lower than 0.100 s for both the algorithms, sufficient for the control of a lower-limb robotic prosthesis. Finally, the CoPy computed from the PS showed a Pearson correlation coefficient of 0.97 (0.02) with the same variable computed through the force platform

    Calcified Plaques in Patients With Acute Coronary Syndromes

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    OBJECTIVES: This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). BACKGROUND: Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied. METHODS: From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. RESULTS: Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). CONCLUSIONS: Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).status: publishe

    3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

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    ObjectiveGrowing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas.MethodsEZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879 was cultured in the presence of DZNep, and its growth and survival were evaluated by counting adherent cells periodically. Apoptosis was assayed by cell cycle analysis, Apo2.7 expression using flow cytometry, and by PARP cleavage using western-blot. Cell migration was assessed by wound healing assay.ResultsChondrosarcomas (at least with high grade) highly express EZH2, at contrary to enchondromas or chondrocytes. In vitro, DZNep inhibits EZH2 protein expression, and subsequently reduces the trimethylation of lysine 27 on histone H3 (H3K27me3). Interestingly, DZNep induces cell death of chondrosarcoma cell lines by apoptosis, while it slightly reduces growth of normal chondrocytes. In addition, DZNep reduces cell migration.ConclusionThese results indicate that an epigenetic therapy that pharmacologically targets EZH2 via DZNep may constitute a novel approach to treat chondrosarcomas

    Menstruation angina: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Menstruation is commonly associated with migraine and irritable bowel but is rarely correlated with angina or myocardial ischaemia. Only a small number of cases have been reported suggesting a link between menstruation and myocardial ischaemic events.</p> <p>Case presentation</p> <p>A case of menstruation angina is reported in order to raise awareness of this association. A 47-year-old South Asian woman presented with recurrent chest pains in a monthly fashion coinciding with her menstruations. Each presentation was associated with troponin elevation. Angioplasty failed to resolve her symptoms but she eventually responded to hormonal therapy.</p> <p>Conclusions</p> <p>The possibility of menstruation angina should always be taken into account in any female patients from puberty to menopause presenting with recurrent chest pains. This can allow an earlier introduction of hormonal therapy to arrest further myocardial damage.</p

    Decitabine impact on the endocytosis regulator RhoA, the folate carriers RFC1 and FOLR1, and the glucose transporter GLUT4 in human tumors.

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    BackgroundIn 31 solid tumor patients treated with the demethylating agent decitabine, we performed tumor biopsies before and after the first cycle of decitabine and used immunohistochemistry (IHC) to assess whether decitabine increased expression of various membrane transporters. Resistance to chemotherapy may arise due to promoter methylation/downregulation of expression of transporters required for drug uptake, and decitabine can reverse resistance in vitro. The endocytosis regulator RhoA, the folate carriers FOLR1 and RFC1, and the glucose transporter GLUT4 were assessed.ResultsPre-decitabine RhoA was higher in patients who had received their last therapy &gt;3&nbsp;months previously than in patients with more recent prior therapy (P = 0.02), and varied inversely with global DNA methylation as assessed by LINE1 methylation (r = -0.58, P = 0.006). Tumor RhoA scores increased with decitabine (P = 0.03), and RFC1 also increased in patients with pre-decitabine scores ≤150 (P = 0.004). Change in LINE1 methylation with decitabine did not correlate significantly with change in IHC scores for any transporter assessed. We also assessed methylation of the RFC1 gene (alias SLC19A1). SLC19A1 methylation correlated with tumor LINE1 methylation (r = 0.45, P = 0.02). There was a small (statistically insignificant) decrease in SLC19A1 methylation with decitabine, and there was a trend towards change in SLC19A1 methylation with decitabine correlating with change in LINE1 methylation (r = 0.47, P &lt;0.15). While SLC19A1 methylation did not correlate with RFC1 scores, there was a trend towards an inverse correlation between change in SLC19A1 methylation and change in RFC1 expression (r = -0.45, P = 0.19).ConclusionsIn conclusion, after decitabine administration, there was increased expression of some (but not other) transporters that may play a role in chemotherapy uptake. Larger patient numbers will be needed to define the extent to which this increased expression is associated with changes in DNA methylation

    Identification of the haemodynamic environment permissive for plaque erosion

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    Endothelial erosion of atherosclerotic plaques is the underlying cause of approximately 30% of acute coronary syndromes (ACS). As the vascular endothelium is profoundly affected by the haemodynamic environment to which it is exposed, we employed computational fluid dynamic (CFD) analysis of the luminal geometry from 17 patients with optical coherence tomography (OCT)-defined plaque erosion, to determine the flow environment permissive for plaque erosion. Our results demonstrate that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (interquartile range 28–52%), where all but one of the adherent thrombi located proximal to, or within the region of maximum stenosis. Consequently, all flow metrics related to elevated flow were significantly increased (time averaged wall shear stress, maximum wall shear stress, time averaged wall shear stress gradient) with a reduction in relative residence time, compared to a non-diseased reference segment. We also identified two cases that did not exhibit an elevation of flow, but occurred in a region exposed to elevated oscillatory flow. Our study demonstrates that the majority of OCT-defined erosions occur where the endothelium is exposed to elevated flow, a haemodynamic environment known to evoke a distinctive phenotypic response in endothelial cells
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