198,389 research outputs found
Redfern, M J, 5716567
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/412558Surname: REDFERN. Given Name(s) or Initials: M J. Military Service Number or Last Known Location: 5716567. Missing, Wounded and Prisoner of War Enquiry Card Index Number: SEA-4792.229268
Item: [2016.0049.44820] "Redfern, M J, 5716567
Triphora abacoensis Rolan & Redfern 2008
Triphora abacoensis Rolán & Redfern, 2008 Triphora abacoensis Rolán & Redfern, 2008 — Rolán & Fernández-Garces 2008: 158, fig. 31A-G. Type locality. Bahamas, Abaco, East of Chub Rocks, 26°44’00”N, 77°09’00”W, 52 m deep. Type material. BMSM 15499, holotype. ANSP 369222 BMSM 55373, BMSM 55375, paratypes. Distribution. Bahamas (Rolán & Fernández-Garcés 2008; Redfern 2013).Published as part of Bakker, Piet A. J. & Albano, Paolo G., 2022, Nomenclator, geographic and stratigraphic distribution of the family Triphoridae (Mollusca: Gastropoda), pp. 1-216 in Zootaxa 5088 (1) on page 14, DOI: 10.11646/zootaxa.5088.1.1, http://zenodo.org/record/583653
Triphora abacoensis Rolan & Redfern 2008
Triphora abacoensis Rolán & Redfern, 2008 Triphora abacoensis Rolán & Redfern, 2008 — Rolán & Fernández-Garces 2008: 158, fig. 31A-G. Type locality. Bahamas, Abaco, East of Chub Rocks, 26°44’00”N, 77°09’00”W, 52 m deep. Type material. BMSM 15499, holotype. ANSP 369222 BMSM 55373, BMSM 55375, paratypes. Distribution. Bahamas (Rolán & Fernández-Garcés 2008; Redfern 2013).Published as part of Bakker, Piet A. J. & Albano, Paolo G., 2022, Nomenclator, geographic and stratigraphic distribution of the family Triphoridae (Mollusca: Gastropoda), pp. 1-216 in Zootaxa 5088 (1) on page 14, DOI: 10.11646/zootaxa.5088.1.1, http://zenodo.org/record/583653
Performance Anxiety: An exploration of spectacle, spectatorship and moral panic in the twenty-first century
In the last decade there has been an explosion of new technologies that enable discourse, power and truth formations to be produced, contested and dispersed. As communication and information technologies continue to evolve, so too do the ways in which individuals construct identities and form communities. The notion of a moral panic is utilised to describe those critical moments in time and space when social norms are perceived to be under threat. I suggest that the complex interplay of spectacle, spectatorship and moral panic involved in such instances can be both conceptualised and interrogated as performance. This dissertation draws upon two distinct performance paradigms – one theoretical and the other practical – to inform a critical reading of three significant ‘social events’ of the last decade: the drug-trafficking trial of Australian woman Schapelle Corby in Indonesia in 2005, the end-of-life legal case focused on American woman Terri Schiavo, which culminated in 2005, and the race relations associated with the ‘Redfern riots’ which occurred in Sydney in 2004. Informed by a range of theoretical positions from Michel Foucault, Zygmunt Bauman, Giorgio Agamben, Judith Butler, Baz Kershaw, and Michael Hardt and Antonio Negri, this dissertation fleshes out contemporary understandings of mediatised spectacle and spectatorship, with the aim of revealing the ways in which they contribute to creating and sustaining moral panic. A critical finding of the dissertation is that through both subjectification and objectification processes the central players and the spectators become indivisible from the spectacle itself, thus maintaining the interweaving cycle of spectator, spectacle and moral panic. By exploring the ways in which people interpret and respond to social phenomena, the possibilities for performance and social theory can be extended
Molecular mechanisms of fenretinide-induced apoptosis of neuroblastoma
Synthetic retinoids such as fenretinide [N-(4-hydroxyphenyl)retinamide] induce apoptosis of neuroblastoma cells, act synergistically with chemotherapeutic drugs, and may provide opportunities for novel approaches to neuroblastoma therapy. Fenretinide-induced cell death of neuroblastoma cells is caspase dependent and results in the release of cytochrome c from mitochondria independently of changes in permeability transition. This is mediated by a signaling pathway characterized by the generation of reactive oxygen species (ROS) via 12-lipoxygenase (12-LOX), and an oxidative-stress-dependent induction of the transcription factor, GADD153 and the BCL2-related protein BAK. Upstream events of fenretinide-induced signaling involve increased levels of ceramide as a result of increased sphingomyelinase activity, and the subsequent metabolism of ceramide to gangliosides via glucosylceramide synthase and GD3 synthase. These gangliosides may be involved in the regulation of 12-LOX leading to oxidative stress and apoptosis via the induction of GADD153 and BAK. The targeting of sphingomyelinases or downstream effectors such as 12-LOX or GADD153 may present novel approaches for the development of more effective and selective drugs for neuroblastoma therapy
Properties, Redfern Croydon and Homebush, in the estate of the late Wm. Hudson Esq. [cartographic material] : for sale by order of the Perpetual Trustee Compy., at the rooms 11 a m. 17 April 1893 /
Sales plan for land in the suburbs of Redfern, Croydon and Homebush in Sydney, New South Wales, bounded by George Street (in Redfern), Liverpool Road and Brighton Street (in Croydon) & Creek Street and Underwood Road (in Homebush).; "Terms liberal."; "J. Haydon Cardew, surveyor licensed under Real Property Act, Victoria Chambers, Elizabeth Street."; Includes local sketches of Redfern, Croydon and Homebush.; Also available in an electronic version via the internet at: http://nla.gov.au/nla.map-lfsp2771
Gangliosides Link the Acidic Sphingomyelinase– Mediated Induction of Ceramide to 12-Lipoxygenase– Dependent Apoptosis of Neuroblastoma in Response to Fenretinide
The lipid second messenger ceramide, which is
generated by acidic and neutral sphingomyelinases or ceramide
synthases, is a common intermediate of many apoptotic
pathways. Metabolism of ceramide involves several enzymes,
including glucosylceramide synthase and GD3
synthase, and results in the formation of gangliosides (GM3,
GD3, and GT3), which in turn promote the generation of
reactive oxygen species (ROS) and apoptosis. Fenretinide, a
retinoic acid derivative, is thought to induce apoptosis via
increases in ceramide levels, but the link between ceramide
and subsequent apoptosis in neuroblastoma cells is unclear.
Methods: SH-SY5Y and HTLA230 neuroblastoma cells were
treated with fenretinide in the presence or absence of inhibitors
of enzymes important in ceramide metabolism (fumonisin
B1, inhibitor of ceramide synthase; desipramine, inhibitor
of acidic and neutral sphingomyelinases; and PDMP,
inhibitor of glucosylceramide). Small interfering RNAs were
used to specifically block acidic sphingomyelinase or GD3
synthase activities. Apoptosis, ROS, and GD3 expression
were measured by flow cytometry. Results: In neuroblastoma
cells, ROS generation and apoptosis were associated
with fenretinide-induced increased levels of ceramide, glucosylceramide
synthase activity, GD3 synthase activity, and
GD3. Fenretinide also induced increased levels of GD2, a
ganglioside derived from GD3. Inhibition of acidic sphingomyelinase
but not of neutral sphingomyelinase or ceramide
synthase, blocked fenretinide-induced increases in ceramide,
ROS, and apoptosis. Exogenous GD3 induced ROS and apoptosis
in SH-SY5Y cells but not in SH-SY5Y cells treated
with baicalein, a specific 12-lipoxygenase inhibitor. Exogenous
GD2 did not induce apoptosis. Conclusions: A novel
pathway of fenretinide-induced apoptosis is mediated by
acidic sphingomyelinase, glucosylceramide synthase, and
GD3 synthase, which may represent targets for future drug
development. GD3 may be a key signaling intermediate leading
to apoptosis via the activation of 12-lipoxygenas
The role of gangliosides in fenretinide-induced apoptosis of neuroblastoma
Fenretinide is thought to induce apoptosis via increases in ceramide levels but the mechanisms of ceramide generation and the link between ceramide and subsequent apoptosis in neuroblastoma cells is unclear. In SH-SY5Y neuroblastoma cells, evidence suggests that acid sphingomyelinase activity is essential for the induction of ceramide and apoptosis in response to fenretinide. Downstream of ceramide, apoptosis in response to fenretinide is mediated by increased glucosylceramide synthase activity resulting in increased levels of gangliosides GD3 and GD2 via GD3 synthase. GD3 is a key signalling intermediate leading to apoptosis via the activation of 12-Lipoxygenase, and the parallel induction of GD2 suggests that fenretinide might enhance the response of neuroblastoma to therapy with anti-GD2 antibodies
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