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Search Results: 1 - 10 of 231694 matches for " Anthony R. White "
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A Review of the Impact of Requirements on Software Project Development Using a Control Theoretic Model  [PDF]
Anthony White
Journal of Software Engineering and Applications (JSEA) , 2010, DOI: 10.4236/jsea.2010.39099
Abstract: Software projects have a low success rate in terms of reliability, meeting due dates and working within assigned budgets with only 16% of projects being considered fully successful while Capers Jones has estimated that such projects only have a success rate of 65%. Many of these failures can be attributed to changes in requirements as the project progresses. This paper reviews several System Dynamics models from the literature and analyses the model of Andersson and Karlsson, showing that this model is uncontrollable and unobservable. This leads to a number of is-sues that need to be addressed in requirements acquisition.
Qualitative System Dynamics as a Tool in Accessible Design  [PDF]
Anthony S. White
Journal of Software Engineering and Applications (JSEA) , 2011, DOI: 10.4236/jsea.2011.41008
Abstract: A description of the Systems Dynamics paradigm is given and the reduced Qualitative System Dynamics (QSD) form explained. A simple example is given to illustrate the diagram construction. The principles of states (levels), rates and feedback loops are outlined. The QSD method is used to address the problem of accessibility by using human control of automation as an example, and applying the QSD method to evaluate the effects of the researcher and user in the de- sign of an accessible artefact. This simple automation model illustrates what can be found out from such a picture, in this indicating how the feedback from users has an influence on the time to deliver such designs.
Camera Trapping: A Contemporary Approach to Monitoring Invasive Rodents in High Conservation Priority Ecosystems
Anthony R. Rendall, Duncan R. Sutherland, Raylene Cooke, John White
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086592
Abstract: Invasive rodent species have established on 80% of the world's islands causing significant damage to island environments. Insular ecosystems support proportionally more biodiversity than comparative mainland areas, highlighting them as critical for global biodiversity conservation. Few techniques currently exist to adequately detect, with high confidence, species that are trap-adverse such as the black rat, Rattus rattus, in high conservation priority areas where multiple non-target species persist. This study investigates the effectiveness of camera trapping for monitoring invasive rodents in high conservation areas, and the influence of habitat features and density of colonial-nesting seabirds on rodent relative activity levels to provide insights into their potential impacts. A total of 276 camera sites were established and left in situ for 8 days. Identified species were recorded in discrete 15 min intervals, referred to as ‘events’. In total, 19 804 events were recorded. From these, 31 species were identified comprising 25 native species and six introduced. Two introduced rodent species were detected: the black rat (90% of sites), and house mouse Mus musculus (56% of sites). Rodent activity of both black rats and house mice were positively associated with the structural density of habitats. Density of seabird burrows was not strongly associated with relative activity levels of rodents, yet rodents were still present in these areas. Camera trapping enabled a large number of rodents to be detected with confidence in site-specific absences and high resolution to quantify relative activity levels. This method enables detection of multiple species simultaneously with low impact (for both target and non-target individuals); an ideal strategy for monitoring trap-adverse invasive rodents in high conservation areas.
Targeting Glycogen Synthase Kinase-3β for Therapeutic Benefit against Oxidative Stress in Alzheimer's Disease: Involvement of the Nrf2-ARE Pathway
Katja Kanninen,Anthony R. White,Jari Koistinaho,Tarja Malm
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/985085
Abstract: Specific regions of the Alzheimer's disease (AD) brain are burdened with extracellular protein deposits, the accumulation of which is concomitant with a complex cascade of overlapping events. Many of these pathological processes produce oxidative stress. Under normal conditions, oxidative stress leads to the activation of defensive gene expression that promotes cell survival. At the forefront of defence is the nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that regulates a broad spectrum of protective genes. Glycogen synthase kinase-3β (GSK-3β) regulates Nrf2, thus making this kinase a potential target for therapeutic intervention aiming to boost the protective activation of Nrf2. This paper aims to review the neuroprotective role of Nrf2 in AD, with special emphasis on the role of GSK-3β in the regulation of the Nrf2 pathway. We also examine the potential of inducing GSK-3β by small-molecule activators, dithiocarbamates, which potentially exert their beneficial therapeutic effects via the activation of the Nrf2 pathway. 1. Alzheimer’s Disease and Oxidative Stress Alzheimer's disease is a common age-associated dementia characterized by pathological, progressive loss of neurons and synapses, accumulation of intra- and extracellular protein deposits, and gliosis. The amyloid hypothesis of AD postulates that amyloid-beta (Aβ) deposition and neurotoxicity play a causative role in AD [1]. Although the mechanisms through which Aβ exerts its toxicity are numerous [2], it appears that oxidative injury is central in the pathogenesis of AD [3–5]. Oxidative stress results from an imbalance between the production and removal of physiologically important molecules collectively called reactive oxygen species (ROS) [6–8]. Oxidative stress damages all cellular macromolecules and when uncontrolled, leads to irreparable oxidative injury and cell death. The imbalance between the production and removal of ROS occurs when endogenous defence systems are overwhelmed or exhausted, usually due to disease or as part of normal aging. It is thus not surprising that oxidative stress is involved in the pathogenesis of several neurodegenerative disorders, including AD. Oxidative stress is a central feature of AD, and, in fact, it may even be one of the first pathogenic events during disease progression [5]. Markers of oxidative damage such as protein carbonyls [9, 10] and elevated lipid peroxidation [11, 12] precede pathological changes and are found in the brains of AD patients. Importantly, antioxidant defence is impaired in mouse models of AD; the
Metals and Alzheimer's Disease
Anthony R. White,Peter Faller,Craig S. Atwood,Paolo Zatta
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/659424
Mohsen Kazemi,Judith Waalen,Christopher Morgan,Anthony R. White
Journal of Sports Science and Medicine , 2006,
Abstract: The purpose of this study was to identify the profile of the Olympic champions and the other competitors who were involved in the Games. The information on each of the athletes was obtained from the "Official Site of the Sydney 2000 Olympic Games, www.olympics.com/eng/sports/TK" and included weight category, weight, height, age, points obtained, warnings, deduction point, defensive/offensive kicks and punches. One hundred and two athletes competed (54 males and 48 females) in the Games. The mean average age and BMI (Body Mass Index) of 16 male winners was 24.4 ± 3.3 years and 21.9 ± 2.4 respectively compared to 25.2 ± 4.3 years and 22.8 ± 3.3 for the 38 male non-winners. The mean average age and BMI of the 16 female winners was 23.1 ± 3.9 years and 20.8 ± 2.3 respectively compared to 24.9 ± 4.7 years and 21.3 ± 2.7 for the 32 female non-winners. For all four types of athletes, offensive kicks accounted for at least 52% of the techniques to score a point. Ninety-eight percent of all techniques used to score were kicks. Although not statistically significant, winners overall tended to be younger in age and taller with slightly lower BMI than their weight category average. Taking into account the literature cited in this article, future studies should be designed to examine the relationship between performance and functional variables such as muscle power, muscle endurance, reaction time and aerobic capacity.
Metals and Alzheimer's Disease
Anthony R. White,Peter Faller,Craig S. Atwood,Paolo Zatta
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/659424
Neuroinflammation and Copper in Alzheimer’s Disease
Xin Yi Choo,Lobna Alukaidey,Anthony R. White,Alexandra Grubman
International Journal of Alzheimer's Disease , 2013, DOI: 10.1155/2013/145345
Abstract: Inflammation is the innate immune response to infection or tissue damage. Initiation of proinflammatory cascades in the central nervous system (CNS) occurs through recognition of danger associated molecular patterns by cognate immune receptors expressed on inflammatory cells and leads to rapid responses to remove the danger stimulus. The presence of activated microglia and astrocytes in the vicinity of amyloid plaques in the brains of Alzheimer’s disease (AD) patients and mouse models implicates inflammation as a contributor to AD pathogenesis. Activated microglia play a critical role in amyloid clearance, but chronic deregulation of CNS inflammatory pathways results in secretion of neurotoxic mediators that ultimately contribute to neurodegeneration in AD. Copper (Cu) homeostasis is profoundly affected in AD, and accumulated extracellular Cu drives Aβ aggregation, while intracellular Cu deficiency limits bioavailable Cu required for CNS functions. This review presents an overview of inflammatory events that occur in AD in response to Aβ and highlights recent advances on the role of Cu in modulation of beneficial and detrimental inflammatory responses in AD. 1. Inflammation Inflammation is a protective response rapidly triggered by innate immune cells in the event of tissue injury, as well as endogenous or exogenous insults (reviewed in [1]). The process is highly complicated, involving the complex interplay of cells and mediators. In brief, acute inflammatory responses involve vasodilation to increase blood flow combined with alterations in microvascular structure to allow exit of circulating leukocytes and plasma proteins, followed by accumulation and activation of leukocytes at the site of injury, where leukocyte extravasation is largely facilitated by cytokines including tumour necrosis factor (TNF) and interleukin-1 (IL-1) [1]. In addition, activated innate immune cells at site of injury remove cellular debris and/or pathogens via phagocytosis with concomitant cytokine production to facilitate the initiation of adaptive responses [1]. Due to the variability in the nature, severity, and site of injuries, resolution of inflammatory processes, where all injury and insults become resolved with little tissue damage, is not always possible. For severe tissue damage where regeneration is insufficient, healing with fibrosis may occur instead. The third possible outcome is progression from acute to chronic inflammation. This occurs when danger signals persist and inflammation cannot be resolved. Notably, a wide range of diseases, including asthma [2],
Art Beyond the Globe: Lucio Fontana’s Spatial Identity
Anthony White
EMAJ : Electronic Melbourne Art Journal , 2008,
Abstract: In several works produced in the 1950s and 60s, the Argentine-Italian artist Lucio Fontana (1899 – 1968) proposed that the advent of space travel would lead to a profound decentring of human identity. In this article selected works by Fontana are discussed with reference to statements made by the artist and his contemporary critics as well as to more recent, theoretical writings on space and the body. It is argued that Fontana put forward in his work the idea that travel through outer space would render the image of the modern subject unrecognisable.
Biometals in rare neurodegenerative disorders of childhood
Sarah J. Parker,Jari Koistinaho,Anthony R. White,Katja M. Kanninen
Frontiers in Aging Neuroscience , 2013, DOI: 10.3389/fnagi.2013.00014
Abstract: Copper, iron, and zinc are just three of the main biometals critical for correct functioning of the central nervous system (CNS). They have diverse roles in many functional processes including but not limited to enzyme catalysis, protein stabilization, and energy production. The range of metal concentrations within the body is tightly regulated and when the balance is perturbed, debilitating effects ensue. Homeostasis of brain biometals is mainly controlled by various metal transporters and metal sequestering proteins. The biological roles of biometals are vastly reviewed in the literature with a large focus on the connection to neurological conditions associated with ageing. Biometals are also implicated in a variety of debilitating inherited childhood disorders, some of which arise soon following birth or as the child progresses into early adulthood. This review acts to highlight what we know about biometals in childhood neurological disorders such as Wilson's disease (WD), Menkes disease (MD), neuronal ceroid lipofuscinoses (NCLs), and neurodegeneration with brain iron accumulation (NBIA). Also discussed are some of the animal models available to determine the pathological mechanisms in these childhood disorders, which we hope will aid in our understanding of the role of biometals in disease and in attaining possible therapeutics in the future.
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