Institution
Edith Cowan University
Education•Perth, Western Australia, Australia•
About: Edith Cowan University is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Tourism. The organization has 4040 authors who have published 13529 publications receiving 339582 citations. The organization is also known as: Edith Cowan & ECU.
Topics: Population, Tourism, Isometric exercise, Higher education, Health care
Papers published on a yearly basis
Papers
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01 Dec 2007TL;DR: This paper considers game design for successful exergames and draws on established principles from sports science for the prescription of exercise programs to identify success factors to guide designers of exergaming systems.
Abstract: Exergaming is the use of video games in an exercise activity. In this paper we consider game design for successful exergames. To do this, we review the history of exergaming and the current state of research in this field. We find that there exists some research aimed at evaluating the physical and health characteristics of exergames, but research on how to design exercise games is still in the early stages. From an analysis of this information, and drawing on established principles from sports science for the prescription of exercise programs, we then attempt to identify success factors to guide designers of exergaming systems.
355 citations
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Washington University in St. Louis1, Indiana University – Purdue University Indianapolis2, Edith Cowan University3, University of Melbourne4, Columbia University5, University of California, Los Angeles6, University College London7, Brown University8, Neuroscience Research Australia9, University of New South Wales10, Brigham and Women's Hospital11
TL;DR: Analysis of cerebrospinal fluid (CSF) collected longitudinally in research participants in the Dominantly Inherited Alzheimer Network (DIAN), a multicenter, international biomarker study of ADAD, revealed reductions in amyloid-β1–42 (indicating the presence ofAmyloid plaques) and increases in markers of neuronal injury (tau, ptau181, and VILIP-1) in mutation carriers during the early presymptomatic stage.
Abstract: Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. Biomarkers are required to identify affected individuals during this asymptomatic ("preclinical") stage to permit intervention with potential disease-modifying therapies designed to preserve normal brain function. Studies of families with autosomal-dominant AD (ADAD) mutations provide a unique and powerful means to investigate AD biomarker changes during the asymptomatic period. In this biomarker study, we collected cerebrospinal fluid (CSF), plasma, and in vivo amyloid imaging cross-sectional data at baseline in individuals from ADAD families enrolled in the Dominantly Inherited Alzheimer Network. Our study revealed reduced concentrations of CSF amyloid-β1-42 (Aβ1-42) associated with the presence of Aβ plaques, and elevated concentrations of CSF tau, ptau181 (phosphorylated tau181), and VILIP-1 (visinin-like protein-1), markers of neurofibrillary tangles and neuronal injury/death, in asymptomatic mutation carriers 10 to 20 years before their estimated age at symptom onset (EAO) and before the detection of cognitive deficits. When compared longitudinally, however, the concentrations of CSF biomarkers of neuronal injury/death within individuals decreased after their EAO, suggesting a slowing of acute neurodegenerative processes with symptomatic disease progression. These results emphasize the importance of longitudinal, within-person assessment when modeling biomarker trajectories across the course of the disease. If corroborated, this pattern may influence the definition of a positive neurodegenerative biomarker outcome in clinical trials.
352 citations
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TL;DR: After improvements in basic public health measures, life expectancy in most developed nations increased over the course of the 20th century, and this trend included people with learning disability, and by the end of that century, the survival estimates for people with mild learning disability living in developed countries was 70 years, and nearly 60 years of age for those with severe learning disability.
Abstract: Between 1 and 4% of the populations of developed nations are diagnosed with learning disability. In Australia, an estimated 1.9% of the population exhibit learning disability either as a primary disability or as a secondary condition, and approximately half of these people require continuing support in daily living, including mobility, self-care, and socialization. After improvements in basic public health measures, life expectancy in most developed nations increased over the course of the 20th century, and this trend included people with learning disability. Thus, by the end of that century, the survival estimates for people with mild learning disability living in developed countries was 70 years, and nearly 60 years of age for those with severe learning disability.
349 citations
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TL;DR: The results suggest that Cu interactions with Abeta could be responsible for causing the covalent cross-linking of Abeta in these structures.
Abstract: We have previously reported that amyloid Abeta, the major component of senile plaques in Alzheimer's disease (AD), binds Cu with high affinity via histidine and tyrosine residues [Atwood, C. S., et al. (1998) J. Biol. Chem. 273, 12817-12826; Atwood, C. S., et al. (2000) J. Neurochem. 75, 1219-1233] and produces H(2)O(2) by catalyzing the reduction of Cu(II) or Fe(III) [Huang, X., et al. (1999) Biochemistry 38, 7609-7616; Huang, X., et al. (1999) J. Biol. Chem. 274, 37111-37116]. Incubation with Cu induces the SDS-resistant oligomerization of Abeta [Atwood, C. S., et al. (2000) J. Neurochem. 75, 1219-1233], a feature characteristic of neurotoxic soluble Abeta extracted from the AD brain. Since residues coordinating Cu are most vulnerable to oxidation, we investigated whether modifications of these residues were responsible for Abeta cross-linking. SDS-resistant oligomerization of Abeta caused by incubation with Cu was found to induce a fluorescence signal characteristic of tyrosine cross-linking. Using ESI-MS and a dityrosine specific antibody, we confirmed that Cu(II) (at concentrations lower than that associated with amyloid plaques) induces the generation of dityrosine-cross-linked, SDS-resistant oligomers of human, but not rat, Abeta peptides. The addition of H2O2 strongly promoted Cu-induced dityrosine cross-linking of Abeta1-28, Abeta1-40, and Abeta1-42, suggesting that the oxidative coupling is initiated by interaction of H2O2 with a Cu(II) tyrosinate. The dityrosine modification is significant since it is highly resistant to proteolysis and is known to play a role in increasing structural strength. Given the elevated concentration of Cu in senile plaques, our results suggest that Cu interactions with Abeta could be responsible for causing the covalent cross-linking of Abeta in these structures.
347 citations
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TL;DR: There is an urgent need for more information on the variability in seagrass carbon stock and accumulation rates, and the factors driving this variability, in order to improve global estimates of seagRass Blue Carbon storage.
Abstract: The recent focus on carbon trading has intensified interest in ‘Blue Carbon’–carbon sequestered by coastal vegetated ecosystems, particularly seagrasses. Most information on seagrass carbon storage is derived from studies of a single species, Posidonia oceanica, from the Mediterranean Sea. We surveyed 17 Australian seagrass habitats to assess the variability in their sedimentary organic carbon (Corg) stocks. The habitats encompassed 10 species, in mono-specific or mixed meadows, depositional to exposed habitats and temperate to tropical habitats. There was an 18-fold difference in the Corg stock (1.09–20.14 mg Corg cm−3 for a temperate Posidonia sinuosa and a temperate, estuarine P. australis meadow, respectively). Integrated over the top 25 cm of sediment, this equated to an areal stock of 262–4833 g Corg m−2. For some species, there was an effect of water depth on the Corg stocks, with greater stocks in deeper sites; no differences were found among sub-tidal and inter-tidal habitats. The estimated carbon storage in Australian seagrass ecosystems, taking into account inter-habitat variability, was 155 Mt. At a 2014–15 fixed carbon price of A$25.40 t−1 and an estimated market price of $35 t−1 in 2020, the Corg stock in the top 25 cm of seagrass habitats has a potential value of $AUD 3.9–5.4 bill. The estimates of annual Corg accumulation by Australian seagrasses ranged from 0.093 to 6.15 Mt, with a most probable estimate of 0.93 Mt y−1 (10.1 t. km−2 y−1). These estimates, while large, were one-third of those that would be calculated if inter-habitat variability in carbon stocks were not taken into account. We conclude that there is an urgent need for more information on the variability in seagrass carbon stock and accumulation rates, and the factors driving this variability, in order to improve global estimates of seagrass Blue Carbon storage.
341 citations
Authors
Showing all 4128 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul Jackson | 141 | 1372 | 93464 |
William J. Kraemer | 123 | 755 | 54774 |
D. Allan Butterfield | 115 | 504 | 43528 |
Kerry S. Courneya | 112 | 608 | 49504 |
Robert U. Newton | 109 | 753 | 42527 |
Roger A. Barker | 101 | 620 | 39728 |
Ralph N. Martins | 95 | 630 | 35394 |
Wei Wang | 95 | 3544 | 59660 |
David W. Dunstan | 91 | 403 | 37901 |
Peter E.D. Love | 90 | 546 | 24815 |
Andrew Jones | 83 | 695 | 28290 |
Hongqi Sun | 81 | 265 | 20354 |
Leon Flicker | 79 | 465 | 22669 |
Mark A. Jenkins | 79 | 472 | 21100 |
Josep M. Gasol | 77 | 313 | 22638 |