Edith Cowan University

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 & Context (language use). The organization has 4040 authors who have published 13529 publications receiving 339582 citations. The organization is also known as: Edith Cowan & ECU.

Authenticating mobile phone users using keystroke analysis

Abstract: Mobile handsets have found an important place in modern society, with hundreds of millions currently in use. The majority of these devices use inherently weak authentication mechanisms, based upon passwords and PINs. This paper presents a feasibility study into a biometric-based technique, known as keystroke analysis – which authenticates the user based upon their typing characteristic. In particular, this paper identifies two typical handset interactions, entering telephone numbers and typing text messages, and seeks to authenticate the user during their normal handset interaction. It was found that neural network classifiers were able to perform classification with average equal error rates of 12.8%. Based upon these results, the paper concludes by proposing a flexible and robust framework to permit the continuous and transparent authentication of the user, thereby maximising security and minimising user inconvenience, to service the needs of the insecure and evermore functional mobile handset.

Muscle expression of a local Igf-1 isoform protects motor neurons in an ALS mouse model

Abstract: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by a selective degeneration of motor neurons, atrophy, and paralysis of skeletal muscle. Although a significant proportion of familial ALS results from a toxic gain of function associated with dominant SOD1 mutations, the etiology of the disease and its specific cellular origins have remained difficult to define. Here, we show that muscle-restricted expression of a localized insulin-like growth factor (Igf) -1 isoform maintained muscle integrity and enhanced satellite cell activity in SOD1G93A transgenic mice, inducing calcineurin-mediated regenerative pathways. Muscle-specific expression of local Igf-1 (mIgf-1) isoform also stabilized neuromuscular junctions, reduced inflammation in the spinal cord, and enhanced motor neuronal survival in SOD1G93A mice, delaying the onset and progression of the disease. These studies establish skeletal muscle as a primary target for the dominant action of inherited SOD1 mutation and suggest that muscle fibers provide appropriate factors, such as mIgf-1, for neuron survival.

Possible stimuli for strength and power adaptation: acute hormonal responses

Abstract: A great deal of literature has investigated the effects of various resistance training programmes on strength and power changes. Surprisingly, however, our understanding of the stimuli that affect adaptation still remains relatively unexplained. It is thought that strength and power adaptation is mediated by mechanical stimuli, that is the kinematics and kinetics associated with resistance exercise (e.g. forces, contraction duration, power and work), and their interaction with other hormonal and metabolic factors. However, the effect of different combinations of kinematic and kinetic variables and their contribution to adaptation is unclear. The mechanical response to single repetitions has been investigated by a number of researchers; however, it seems problematic to extrapolate the findings of this type of research to the responses associated with a typical resistance training session. That is, resistance training is typified by multiple repetitions, sets and exercises, rest periods of varying durations and different movement techniques (e.g. controlled and explosive). Understanding the mechanical stimuli afforded by such loading schemes would intuitively lead to a better appreciation of how various mechanical stimuli affect adaptation. It will be evident throughout this article that very little research has adopted such an approach; hence our understanding in this area remains rudimentary at best. One should therefore remain cognizant of the limitations that exist in the interpretation of research in this field. We contend that strength and power research needs to adopt a set kinematic and kinetic analysis to improve our understanding of how to optimise strength and power.

Authentic activities and online learning

Abstract: There has been a renewed interest in the role of student activities within course units as constructivist philosophy and advances in technology impact on educational design and practice. This paper proposes ten characteristics of authentic activities, based on a substantial body of educational theory and research, which can assist teachers to design more authentic activities for online learning environments. The paper includes a short review of the literature, together with the list of characteristics attributed to appropriate authors and theorists. The paper concludes with a discussion of how the affordances of Internet technologies can facilitate the operationalisation of authentic activities in online courses of study.

N-myc downstream-regulated gene 1 is mutated in hereditary motor and sensory neuropathy-Lom.

Abstract: Hereditary motor and sensory neuropathies, to which Charcot-Marie-Tooth (CMT) disease belongs, are a common cause of disability in adulthood. Growing awareness that axonal loss, rather than demyelination per se, is responsible for the neurological deficit in demyelinating CMT disease has focused research on the mechanisms of early development, cell differentiation, and cell-cell interactions in the peripheral nervous system. Autosomal recessive peripheral neuropathies are relatively rare but are clinically more severe than autosomal dominant forms of CMT, and understanding their molecular basis may provide a new perspective on these mechanisms. Here we report the identification of the gene responsible for hereditary motor and sensory neuropathy–Lom (HMSNL). HMSNL shows features of Schwann-cell dysfunction and a concomitant early axonal involvement, suggesting that impaired axon-glia interactions play a major role in its pathogenesis. The gene was previously mapped to 8q24.3, where conserved disease haplotypes suggested genetic homogeneity and a single founder mutation. We have reduced the HMSNL interval to 200 kb and have characterized it by means of large-scale genomic sequencing. Sequence analysis of two genes located in the critical region identified the founder HMSNL mutation: a premature-termination codon at position 148 of the N-myc downstream-regulated gene 1 (NDRG1). NDRG1 is ubiquitously expressed and has been proposed to play a role in growth arrest and cell differentiation, possibly as a signaling protein shuttling between the cytoplasm and the nucleus. We have studied expression in peripheral nerve and have detected particularly high levels in the Schwann cell. Taken together, these findings point to NDRG1 having a role in the peripheral nervous system, possibly in the Schwann-cell signaling necessary for axonal survival.