Immersive Worlds: an exploration of how performers facilitate the Three Worlds in Immersive Performance

This research will consider the notion that the immersive performance event consists of Three Worlds-The Fictional, Now and Imaginary and how an understanding of the qualities of these three worlds, in particular the Now and the Imaginary, are instrumental to a performer’s training in creating immersive theatre. To do this, the research draws upon facilitation techniques from applied drama, mapping some of the fundamental skills required from a performer making immersive theatre, that has yet to be articulated by the field. It argues that the use of core facilitation skills such as rapport, listening, reading micro gestures and effective questioning, can be used by the performer to effectively manage the demands of the Now and Imaginary worlds. To illustrate this, the paper examines a creative training day with recent graduate drama students from Liverpool John Moores University (LJMU) and students from the Community Drama degree at Liverpool Institute of Performing Arts (LIPA), as well as drawing upon the authors’ collective experience of creating and performing in immersive theatre. A key insight from the training day was for student/performers to gain an understanding into the audience member's experiences in immersive performance and how this consideration impacts on the performer's practice. The findings are significant for companies, directors, and performers interested in utilizing immersive theatre to inform the creation of immersive work

Microangiopathy in the cerebellum of patients with mitochondrial DNA disease

Neuropathological findings in mitochondrial DNA disease vary and are often dependent on the type of mitochondrial DNA defect. Many reports document neuronal cell loss, demyelination, gliosis and necrotic lesions in post-mortem material. However, previous studies highlight vascular abnormalities in patients harbouring mitochondrial DNA defects, particularly in those with the m.3243A>G mutation in whom stroke-like events are part of the mitochondrial encephalopathy lactic acidosis and stroke-like episodes syndrome. We investigated microangiopathic changes in the cerebellum of 16 genetically and clinically well-defined patients. Respiratory chain deficiency, high levels of mutated mitochondrial DNA and increased mitochondrial mass were present within the smooth muscle cells and endothelial cells comprising the vessel wall in patients. These changes were not limited to those harbouring the m.3243A>G mutation frequently associated with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, but were documented in patients harbouring m.8344A>G and autosomal recessive polymerase (DNA directed), gamma (POLG) mutations. In 8 of the 16 patients, multiple ischaemic-like lesions occurred in the cerebellar cortex suggestive of vascular smooth muscle cell dysfunction. Indeed, changes in vascular smooth muscle and endothelium distribution and cell size are indicative of vascular cell loss. We found evidence of blood–brain barrier breakdown characterized by plasma protein extravasation following fibrinogen and IgG immunohistochemistry. Reduced immunofluorescence was also observed using markers for endothelial tight junctions providing further evidence in support of blood–brain barrier breakdown. Understanding the structural and functional changes occurring in central nervous system microvessels in patients harbouring mitochondrial DNA defects will provide an important insight into mechanisms of neurodegeneration in mitochondrial DNA disease. Since therapeutic strategies targeting the central nervous system are limited, modulating vascular function presents an exciting opportunity to lessen the burden of disease in these patients

HIRDLS instrument radiometric calibration black body targets

The pre-launch calibration of the HIRDLS instrument took place in a dedicated facility at the University of Oxford. One aspect of this calibration was the determination of the response of the instrument to black body radiation. This was achieved with the use of purpose built full aperture black body targets which were mounted in the vacuum chamber together with all of the calibration equipment. Especial attention was placed on the absolute knowledge of the emission from these targets. This was done through a combination of thermometric sensor calibration traceable to the International Temperature Standard (ITS-90), surface emission measurements, cavity design and modelling and controlling the stray light sources in the vacuum chamber. This paper describes the design requirements, implementation and performance achieved

Quantitative quadruple-label immunofluorescence of mitochondrial and cytoplasmic proteins in single neurons from human midbrain tissue.

BACKGROUND: Respiratory chain (RC) deficiencies are found in primary mtDNA diseases. Focal RC defects are also associated with ageing and neurodegenerative disorders, e.g. in substantia nigra (SN) neurons from Parkinson's disease patients. In mitochondrial disease and ageing, mtDNA mutational loads vary considerably between neurons necessitating single cell-based assessment of RC deficiencies. Evaluating the full extent of RC deficiency within SN neurons is challenging because their size precludes investigations in serial sections. We developed an assay to measure RC abnormalities in individual SN neurons using quadruple immunofluorescence. NEW METHOD: Using antibodies against subunits of complex I (CI) and IV, porin and tyrosine hydroxylase together with IgG subtype-specific fluorescent labelled secondary antibodies, we quantified the expression of CI and CIV compared to mitochondrial mass in dopaminergic neurons. CI:porin and CIV:porin ratios were determined relative to a standard control. RESULTS: Quantification of expression of complex subunits in midbrain sections from patients with mtDNA disease and known RC deficiencies consistently showed reduced CI:porin and/or CIV:porin ratios. COMPARISON WITH EXISTING METHOD(S): The standard histochemical method to investigate mitochondrial dysfunction, the cytochrome c oxidase/succinate dehydrogenase assay, measures CIV and CII activities. To also study CI in a patient, immunohistology in additional sections, i.e. in different neurons, is required. Our method allows correlation of the expression of CI, CIV and mitochondrial mass at a single cell level. CONCLUSION: Quantitative quadruple-label immunofluorescence is a reliable tool to measure RC deficiencies in individual neurons that will enable new insights in the molecular mechanisms underlying inherited and acquired mitochondrial dysfunction

Mirror emissivity measurements for the NASA AURA HIRDLS instrument

The High Resolution Dynamics Limb Sounder (HIRDLS) instrument is scheduled for launch on the NASA AURA satellite in January 2004; it is a joint project between the UK and USA. HIRDLS is a mid-infrared limb emission sounder which will measure the concentrations of trace species and aerosol, and temperature and pressure variations in the Earth's atmosphere between about 8 and 100 km altitude on a finer spatial scale than been achieved before. HIRDLS has particularly stringent radiometric calibration accuracy requirements. A warm (280-300K) 'In-Flight Calibrator' (IFC) black cavity within the instrument plus a view to cold space are used to perform radiometric calibration. The cavity has an entrance aperture which is much smaller than the full beam size, and it is viewed through a focusing mirror. The cavity and focusing mirror are ideally maintained at the same temperature but differences of up to 1 C may exist, in which case a correction utilising the mirror emissivity can usefully be made. That emissivity has been measured at instrument level during pre-launch calibration by viewing an external target at the same temperature as the IFC while varying the calibration mirror temperature