Sound in the Aboriginal Australian Films of Rolf de Heer

Anna Hickey-Mody and Melissa Iocca invented a new name for the cinema-goer at "Bad Boy Bubby" (1993) when they wrote: "In de Heer's film, the viewer is primarily a listener, or aurator, and secondly a spectator" and I have argued the label 'aurator' can also be used for the person experiencing "Ten Canoes" (2006). This Aboriginal Australian Dreamtime fable features dialogue recorded entirely in the Ganalbingu language of the Indigenous people it stars, and is a prime example of what I would suggest can be labeled 'The Aboriginal Australian Films of Rolf de Heer'. "The Tracker" (2002) and "Dr. Plonk" (2007) have also included depictions of Aboriginal Australians and each of the trio utilizes Cat Hope's "innovative sound ideas" to present what I argue is an aural auteur's signature revealing a post-colonial Australian world-view that privileges the justice system and eco-spirituality of Aboriginal Australians.

Shared material on dying

Shared Material on Dying is a trio/solo work commissioned by Jenny Roche and the Dublin Dance Festival in 2008 from choreographer Liz Roche. Touring widely since its creation, it continues to be a rich research environment for the interrogation by Jenny Roche of the dancer’s first-person perspective in choreographic production and performance. The research perspective drawn from the live performance of this iteration was how the exploration of the same dancing moment might be expressed from multiple perspectives by three different dancers and what this might reveal about the dancer’s inner configuring of the performance environment. Erin Manning (2009) describes the unstable and emergent moment before movement materialises as the preacceleration of the movement, when the potentialities of the gesture collapse and stabilize into form. It is this threshold of potentiality that is interesting, the moment before the dance happens when the configuring process of the dancer brings it into being. Cynthia Roses Thema (2007), after neuroscientist Antonio Damasio, writes that embodied experience is mapped as it unfolds and alters from moment to moment in line with a constantly changing internal milieu. As a performer in this piece, I explored the inner terrain of the three performers (myself included) by externalizing these inner states. This research contributed to a paper presentation at the Digital Resources for the Arts and Humanities Conference, UK 2013.

Your Loss is Our Gain

2 x 2.5 metre text based wall painting with a hidden automatic air freshener timed to spray every 60 seconds. The work formed part of a group exhibition that dealt with Humour,Politics and Art. It was part of a series of ongoing works made under the pseudonym Eve Roleston. Roleston is part of a trio of pseudonyms I use, the others being Ernesto Love, and Ernest Olove, to explore the research potential of the fictocritical in a visual arts practice.This forms part of an ongoing body of practice-led research undertaken in my PhD dealing with reconfiguring the relationship between art and politics.

Human Fly

Human Fly, originally choreographed as a trio existed as one section of a larger work titled Élet [the Hungarian word for Life). Informed by the lyrics of six songs performed by French cover band Nouvelle Vague, Élet [Life] was created to be absorbed and interpreted openly by each individual. In the reworking of Human Fly I have endeavored to keep to the original intent; embracing aspects of promiscuity and seduction.

Characterization of epitopes for virus-neutralizing monoclonal antibodies to Ross River virus E2 using phage-displayed random peptide libraries

Ross River virus (RRV) is the predominant cause of epidemic polyarthritis in Australia, yet the antigenic determinants are not well defined. We aimed to characterize epitope(s) on RRV-E2 for a panel of monoclonal antibodies (MAbs) that recognize overlapping conformational epitopes on the E2 envelope protein of RRV and that neutralize virus infection of cells in vitro. Phage-displayed random peptide libraries were probed with the MAbs T1E7, NB3C4, and T10C9 using solution-phase and solid-phase biopanning methods. The peptides VSIFPPA and KTAISPT were selected 15 and 6 times, respectively, by all three of the MAbs using solution-phase biopanning. The peptide LRLPPAP was selected 8 times by NB3C4 using solid-phase biopanning; this peptide shares a trio of amino acids with the peptide VSIFPPA. Phage that expressed the peptides VSIFPPA and LRLPPAP were reactive with T1E7 and/or NB3C4, and phage that expressed the peptides VSIFPPA, LRLPPAP, and KTAISPT partially inhibited the reactivity of T1E7 with RRV. The selected peptides resemble regions of RRV-E2 adjacent to sites mutated in neutralization escape variants of RRV derived by culture in the presence of these MAbs (E2 210-219 and 238-245) and an additional region of E2 172-182. Together these sites represent a conformational epitope of E2 that is informative of cellular contact sites on RRV.

Fine mapping of the MHC Class III region demonstrates association of AIF1 and rheumatoid arthritis

Objective. The heritability of RA has been estimated to be ∼55%, of which the MHC contributes about one-third. HLA-DRB1 alleles are strongly associated with RA, but it is likely that significant non-DRB1 MHC genetic susceptibility factors are involved. Previously, we identified two three-marker haplotypes in a 106-kb region in the MHC class III region immediately centromeric to TNF, which are strongly associated with RA on HLA-DRB1*0404 haplotypes. In the present study, we aimed to refine these associations further using a combination of genotyping and gene expression studies. Methods. Thirty-nine nucleotide polymorphisms (SNPs) were genotyped in 95 DRB1*0404 carrying unrelated RA cases, 125 DRB1*0404 - carrying healthy controls and 87 parent-case trio RA families in which the affected child carried HLA-DRB1*04. Quantitative RT-PCR was used to assess the expression of the positional candidate MHC class III genes APOM, BAT2, BAT3, BAT4, BAT5, AIF1, C6orf47, CSNK2β and LY6G5C, and the housekeeper genes, hypoxanthine-guanine phosphoribosyltransferase (HPRT) and β2-microglobulin (B2M) in 31 RA cases and 21 ethnically, age- and sex-matched healthy controls. Synovial membrane specimens from RA, PsA and OA cases were stained by an indirect immunoperoxidase technique using a mouse-anti-human AIF1 monoclonal antibody. Results. Association was observed between RA and single markers or two marker haplotypes involving AIF1, BAT3 and CSNK. AIF1 was also significantly overexpressed in RA mononuclear cells (1.5- to 1.9-fold difference, P = 0.02 vs HPRT, P = 0.002 vs B2M). AIF1 protein was clearly expressed by synovial macrophages in all the inflammatory synovial samples in contrast to the non-inflammatory OA samples. Conclusions. The results of the genotyping and expression studies presented here suggest a role for AIF1 in both the aetiology and pathogenesis of RA.

Polymorphisms of the CYP2D6 gene increase susceptibility to ankylosing spondylitis

Ankylosing spondylitis (AS) is a common and highly familial rheumatic disorder. The sibling recurrence risk ratio for the disease is 63 and heritability assessed in twins > 90%. Although MHC genes, including HLA-B27, contribute only 20-50% of the genetic risk for the disease, no non-MHC gene has yet been convincingly demonstrated to influence either susceptibility to the disease or its phenotypic expression. Previous linkage and association studies have suggested the presence of a susceptibility gene for AS close to, or within, the cytochrome P450 2D6 gene (CYP2D6, debrisoquine hydroxylase) located at chromosome 22q13.1. We performed a linkage study of chromosome 22 in 200 families with AS affected sibling-pairs. Association of alleles of the CYP2D6 gene was examined by both case-control and within-family means. For case-control studies, 617 unrelated individuals with AS (361 probands from sibling-pair and parent-case trio families and 256 unrelated non-familial sporadic cases) and 402 healthy ethnically matched controls were employed. For within-family association studies, 361 families including 161 parent-case trios and 200 affected sibling-pair families were employed. Homozygosity for poor metabolizer alleles was found to be associated with AS. Heterozygosity for the most frequent poor metabolizer allele (CYP2D6*4) was not associated with increased susceptibility to AS. Significant within-family association of CYP2D6*4 alleles and AS was demonstrated. Weak linkage was also demonstrated between CYP2D6 and AS. We postulate that altered metabolism of a natural toxin or antigen by the CYP2D6 gene may increase susceptibility to AS.