ORCID Profile
0000-0003-2387-6526
Current Organisation
University of South Australia
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Publisher: Informa UK Limited
Date: 12-12-2014
Publisher: Routledge
Date: 03-02-2017
Publisher: University of South Australia
Date: 2020
DOI: 10.25954/6Q7C-RM58
Publisher: Cambridge University Press
Date: 06-10-2011
Publisher: Routledge
Date: 21-06-2021
Publisher: Unpublished
Date: 2008
Publisher: Informa UK Limited
Date: 15-12-2017
Publisher: Informa UK Limited
Date: 26-11-7015
DOI: 10.1080/14786419.2014.980252
Abstract: Potential protective effects of the flavonoids quercetin and luteolin have been examined against the oxidative stress of MC3T3-E1 osteoblast-like cells. Although hydrogen peroxide and menadione reduced cell viability, the toxicity was prevented by desferrioxamine or catalase but not superoxide dismutase, suggesting the involvement of hydrogen peroxide in both cases. Quercetin and luteolin reduced the oxidative damage, especially that caused by hydrogen peroxide. When cultures were pre-incubated with quercetin or luteolin, protection was reduced or lost. Protection was also reduced when a 24 h pre-incubation with the flavonoids was followed by exposure to menadione alone. Pretreating cultures with luteolin impaired protection by quercetin, whereas quercetin pretreatment did not affect protection by luteolin. It is concluded that quercetin and luteolin suppress oxidative damage to MC3T3-E1 cells, especially caused by peroxide. The reduction in protection by pretreatment implies a down-regulation of part of the toxic transduction pathway.
Publisher: Routledge
Date: 04-09-2024
Publisher: Multilingual Matters
Date: 31-12-2022
Publisher: Routledge
Date: 04-09-2024
Publisher: Informa UK Limited
Date: 17-06-2014
Publisher: Springer Netherlands
Date: 23-09-2013
Publisher: Wiley
Date: 18-11-2022
Publisher: Wiley
Date: 03-04-2023
DOI: 10.1111/LANG.12573
Publisher: Informa UK Limited
Date: 21-07-2022
Publisher: Routledge
Date: 03-02-2017
Publisher: John Benjamins Publishing Company
Date: 27-09-2022
Abstract: Key findings, analysis and recommendations that have emerged from a research project, ‘Using Human Language Technology to enhance academic integrity, inclusivity, knowledge exchange, student ersity and retention’ at the University of South Australia conducted in 2019 are discussed in this article. The primary purpose of the project was to address some of the challenges and opportunities afforded by increasing student and teacher ersity at a predominantly English-medium Australian university through newly enhanced human language translation technology (HLT) also known as machine translation (MT). This technology is frequently used for the translation of human language, and it falls under the umbrella of Artificial Intelligence (AI) technologies. From the institution’s perspective, key aims of the project were to contribute to the university’s Digital Learning Strategy priorities and core values embedded in a structural transformation of the university. These include integrity, accountability, ersity, social justice, engagement and collaboration. The researchers’ objectives focussed on multilingual pedagogies using HLT to support knowledge exchange (transknowledging), and translanguaging for all students. These disrupt inequitable hierarchies, and position bi-/multilingual students as valuable resources for monolingual staff and students.
Publisher: Informa UK Limited
Date: 11-2010
Publisher: MGIMO University
Date: 02-10-2022
DOI: 10.24833/2410-2423-2022-3-32-122-127
Abstract: .
Publisher: Informa UK Limited
Date: 11-2009
Publisher: Palgrave Macmillan UK
Date: 20-12-2017
Publisher: Informa UK Limited
Date: 23-08-2019
Publisher: Springer Science and Business Media LLC
Date: 14-07-2016
Publisher: Walter de Gruyter GmbH
Date: 16-01-2013
Publisher: Elsevier
Date: 2006
Publisher: Springer US
Date: 2008
Publisher: Informa UK Limited
Date: 03-07-2023
Publisher: Springer International Publishing
Date: 2017
Publisher: IMR Press
Date: 2008
DOI: 10.2741/2926
Abstract: Substantial pieces of direct and indirect evidence have mounted over the years linking the induction of oxidative stress to a plethora of disease conditions, not least those associated with the death of neurons. The causal relationship between oxidative damage and neurodegeneration is, however, not yet clear and still a subject of intense investigation. Nevertheless, the phenomenon of oxidative neuronal death has received considerable attention in a frantic search for efficacious therapies for the management of neurological and neurodegenerative conditions. The redox-active nature of reactive oxygen species (ROS), which in their excessive levels induce oxidative stress, the prevalence of ROS production in biological systems, the complexity of interrelationships among these species, and the context-dependent adequacy and resilience of the antioxidant defense systems are some of the challenges that basic research has to grapple with to advance successfully to the translational stage. Much still has to be understood for research efforts in this field to yield enduring therapies. In this review, we examine the nature (chemistry) of ROS, the relationships between them, their physiological functions, the roles of oxidative stress in neurodegeneration, the mechanisms of cell death induced by oxidant species, and the available means of protecting neurons against oxidative damage.
Publisher: JSTOR
Date: 2000
DOI: 10.2307/4066276
Publisher: John Benjamins Publishing Company
Date: 2011
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.BRAINRES.2008.06.109
Abstract: Nitric oxide (NO) induces cell proliferation or cell death, depending on the cell type involved, the isoform of nitric oxide synthase activated, and its cellular localisation. In neurons, the damaging effect of NO is usually attributed to the highly toxic peroxynitrite, formed by its reaction with superoxide. Peroxynitrite induces DNA damage and consequently the activation of poly (ADP-ribose) polymerase (PARP). This study set out to examine the contribution of peroxynitrite to the damage induced in cerebellar granule neurons (CGNs) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for short (6 h) or prolonged (24 h) exposures. The Alamar blue assay was used to quantify CGN viability, which was also assessed by morphological examination. SNAP (10 microM-1 mM) induced a concentration- and time-dependent reduction of CGN viability, with associated damage to cell bodies and neurite processes evident following 100 microM SNAP treatments. Damage from 6 h exposures was prevented by the presence of haemoglobin (a NO scavenger), uric acid (a peroxynitrite scavenger), melatonin (a non-specific antioxidant), and by cyclosporin A (a permeability transition pore blocker). It was reduced by the PARP-1 inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone (DPQ), whilst superoxide dismutase (SOD) potentiated the effects. Following 24 h exposure to SNAP, damage was only partially blocked by haemoglobin, melatonin, cyclosporin A and DPQ, but was not affected by uric acid or SOD. The data suggest that short exposure to NO induces neuronal damage through peroxynitrite produced by its interaction with superoxide, whereas a longer exposure to NO can induce damage partly by a mechanism which is independent of peroxynitrite formation.
Publisher: Stellenbosch University
Date: 20-02-2013
DOI: 10.5785/9-1-263
Publisher: Elsevier BV
Date: 06-2008
DOI: 10.1016/J.BRAINRES.2008.04.013
Abstract: During cerebral hypoxia or ischaemia, mitochondrial dysfunction is induced which can lead to free radical production and cell death. This phenomenon is mimicked by the acute administration of mitochondrial poisons such as 3-nitropropionic acid (3-NPA) and potassium cyanide (KCN), with the production of reactive molecular species secondary to the activation of glutamate receptors. Also during ischaemia, the kynurenine pathway of tryptophan metabolism is activated, leading to the production of quinolinic acid and kynurenic acid which can modulate N-methyl-D-aspartate (NMDA) receptors as agonist and antagonist respectively. Since kynurenic acid is known to be neuroprotective, we have now examined its ability to prevent the neurotoxic effects of mitochondrial dysfunction in primary cultures of postnatal rat cerebellar granule neurons. Viability was quantified using the Alamar Blue (AB) assay and by direct morphological examination. Both 3-NPA and KCN (10 microM-1 mM) reduced neuronal viability in a concentration-dependent manner. The NMDA receptor antagonists 2-amino-5-phosphonopentanoic acid (D-AP5) at a concentration of 50 microM, and a 10 microM dose of (+)-5-Methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine hydrogen maleate (MK-801) prevented cell death, although the non-NMDA receptor blocker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration of 10 microM did not. The antioxidant enzymes catalase and superoxide dismutase, and the nitric oxide synthase inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME) afforded partial protection. Kynurenic acid, a glutamate antagonist with preference for the glycine site of the NMDA receptors, had no protective effect at all against 3-NPA or KCN toxicity at concentrations up to 1 mM. Although these data confirm a major role for NMDA receptors and oxidative stress in the neurotoxic effects of mitochondrial inhibitors, they reveal a resistance to kynurenic acid which suggests a non-classical activation of NMDA receptors by mitochondrial inhibitors that is independent of the glycine site or which occurs distal to the site of action of kynurenic acid.
Publisher: Cambridge University Press
Date: 17-10-2002
Publisher: Elsevier BV
Date: 06-2008
DOI: 10.1016/J.EJPHAR.2008.03.024
Abstract: MC3T3-E1 osteoblast-like cells represent a suitable model for studying osteogenic development in vitro. The current investigation extends our previous work on the response of these cells to hydrogen peroxide by considering the effects of reactive oxygen species from other sources, and by determining whether differentiation alters sensitivity to oxidative damage. Aspects of hydrogen peroxide-mediated apoptotic and necrotic death were also examined. Cell viability was determined using the Alamar Blue assay and accompanying morphological changes monitored by phase-contrast microscopy. Sensitivity to hydrogen peroxide increased significantly in cultures which had been induced to differentiate. Hydrogen peroxide and copper (II) ions, when combined, produced greater damage than hydrogen peroxide alone, whilst the hydroxyl radical scavengers mannitol or dimethylsulphoxide had no effect. Cyclosporin A and nicotinamide afforded partial protection. The tryptophan metabolite, 3-hydroxykynurenine significantly reduced viability, although 3-hydroxyanthranilic acid did not. The xanthine/xanthine oxidase system also reduced cell viability, an effect prevented by catalase but potentiated by superoxide dismutase. S-nitroso-N-acetylpenicillamine did not impair viability at the concentrations tested. Cultures were resistant to mitochondrial poisoning by potassium cyanide, but succumbed to 24-h exposures to 3-nitropropionic acid (1 mM). The results reveal a differential sensitivity of MC3T3-E1 cells to hydrogen peroxide-induced oxidative stress, an enhancement of sensitivity by cellular differentiation, and a potential preference for the glycolytic pathway by MC3T3-E1 cells. This study gives new insight into how bone cells may succumb to the toxic effects of oxidative stress generated by different stimuli and has relevance to conditions such as osteoporosis.
Publisher: Palgrave Macmillan UK
Date: 2014
Publisher: SAGE Publications
Date: 07-2013
Publisher: Informa UK Limited
Date: 02-2011
Publisher: Informa UK Limited
Date: 13-03-2021
Publisher: Routledge
Date: 13-08-2014
Publisher: Stellenbosch University
Date: 20-02-2013
DOI: 10.5785/12-2-206
Publisher: DE GRUYTER
Date: 14-03-2013
Publisher: Informa UK Limited
Date: 24-08-2019
Publisher: Informa UK Limited
Date: 19-06-2014
Publisher: Cambridge University Press (CUP)
Date: 03-2013
DOI: 10.1017/S0267190513000135
Abstract: Multilingual education policy has been a controversial affair in South Africa, especially over the last 60 years. Recent research conducted by government-led and independent agencies shows declining student achievement within an education system that employs 11 home languages for education in the first three grades of primary school, followed by a transition to English medium for the majority (approximately 80%) of speakers of African languages. Research that focuses on the linguistic practices of students in urban settings suggests that there is a disjuncture between the construction of multilingualism within contemporary education policy and the multilingual reality of students (e.g., Heugh, 2003 Makoni, 2003 Makoni & Pennycook, 2012 Plüddemann, 2013 Probyn, 2009 Stroud & Heugh, 2011). There is also a disjunction between constitutional and other government policies that advance, on paper, a multilingual policy, yet are implemented through an assimilatory drive towards English (Alexander & Heugh, 1999). As predicted nearly two decades ago, the ideological framing of multilingualism during the negotiations in the early 1990s was to have consequences for the way in which language policy would unfold in the education sector over the next 20 to 30 years (Heugh, 1995, 1999). While poor student achievement in school may be ascribed to a range of socioeconomic indicators, this article draws attention to contributory factors that relate to language(s) in education. These include different constructions of multilingualism in education in relation to sociolinguistic and educational linguistic considerations, contradictory interpretations of multilingual education in a series of education policy documents, pedagogical weaknesses, and recent attempts to strengthen the provision of African languages education alongside English in the first 10 years of school (Grades R and 0–9 e.g., Department of Basic Education (DBE), 2013a, 2013b).
Publisher: Multilingual Matters
Date: 28-02-2018
DOI: 10.21832/LIM9658
Publisher: National Inquiry Services Center (NISC)
Date: 06-2013
Publisher: Cambridge University Press
Date: 17-10-2002
Publisher: Routledge
Date: 18-07-2013
Publisher: Informa UK Limited
Date: 04-2003
Publisher: Routledge
Date: 07-11-2019
Publisher: Springer Science and Business Media LLC
Date: 27-11-2007
DOI: 10.1007/S00221-007-1218-3
Abstract: Agonists at A(1) receptors and antagonists at A(2A) receptors are known to be neuroprotective against excitotoxicity. We set out to clarify the mechanisms involved by studying interactions between adenosine receptor ligands and endogenous glutamate in cultures of rat cerebellar granule neurons (CGNs). Glutamate and the selective agonist N-methyl-D: -aspartate (NMDA), applied to CGNs at 9 (days in vitro), both induced cell death in a concentration-dependent manner, which was attenuated by treatment with the NMDA receptor antagonists dizocilpine, D: -2-amino-5-phosphono-pentanoic acid (D: -AP5) or kynurenic acid (KYA), but not by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Glutamate toxicity was reduced in the presence of all of the following: cyclosporin A (CsA), a blocker of the membrane permeability transition pore, the caspase-3 inhibitor, benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone (Z-DEVD-fmk), the poly (ADP-ribose) polymerase (PARP-1) inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone (DPQ), and nicotinamide. This is indicative of involvement of both apoptotic and necrotic processes. The A(1) receptor agonist, N (6)-cyclopentyladenosine (CPA), and the A(2A) receptor antagonist 4-(2-[7-amino-2-[2-furyl][1,2,4]triazolo[2,3-a][1,3,5]triazo-5-yl-amino]ethyl)phenol (ZM241385) afforded significant protection, while the A(1) receptor blocker 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and the A(2A) receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxyamidoadenosine (CGS21680) had no effect. These results confirm that glutamate-induced neurotoxicity in CGNs is mainly via the NMDA receptor, but show that a form of cell death which exhibits aspects of both apoptosis and necrosis is involved. The protective activity of A(1) receptor activation or A(2A) receptor blockade occurs against this mixed profile of cell death, and appears not to involve the selective inhibition of classical apoptotic or necrotic cascades.
Publisher: Routledge
Date: 04-09-2023
Publisher: Cambridge University Press
Date: 16-05-2019
Publisher: Elsevier BV
Date: 07-1999
Publisher: Cambridge University Press
Date: 07-11-2019
Publisher: Informa UK Limited
Date: 02-01-2015
Publisher: Wiley
Date: 05-11-2012
DOI: 10.1002/9781405198431.WBEAL0782
Abstract: Approximately 2,100 (30% of the world's) languages are spoken in Africa (Lewis, 2009), with multilingualism a defining characteristic of the continent.
No related grants have been discovered for Kathleen Heugh.