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BACKGROUND: Mobilisation alarms are a falls prevention strategy used in hospitals to alert staff when an at risk patient is attempting to mobilise. Mobilisation alarms have an estimated annual cost of $AUD58MIL in Australia. There is growing evidence from randomised controlled trials indicating mobilisation alarms are unlikely to prevent falls. AIM: The primary aim of this study was to describe the rate of mobilisation alarm false triggers and staff response time across different health services. The secondary aim was to compare pre to post mobilisation alarm utilisation following the introduction of policy to reduce or eliminate mobilisation alarms. METHOD(S): This descriptive and comparative study was conducted through Monash Partners Falls Alliance across six health services in Melbourne, Australia. This study described true and false alarm triggers and trigger response times across three health services and usual care mobilisation alarm utilisation across six health services; and then compared alarm utilisation across two health services following the introduction of policy to reduce (<2.5%) or eliminate (0.0%) mobilisation alarms in the acute and rehabilitation settings. RESULT(S): The most frequent observation was a false alarm (n = 74, 52%), followed by a true alarm (n = 67, 47%) and no alarm (n = 3, 2%). Time to respond to the true and false alarms was an average of 37 s (SD 92) and this included 61 occasions of 0 s as a member of staff was present when the alarm triggered. If the 61 occasions of staff being present when the alarm triggered were removed, the average time to respond was 65 seconds (SD114). Usual care mobilisation alarm utilisation in acute was 7% (n=171/2,338) and in rehabilitation was 11% (n=286/2,623). Introducing policy for reduced and eliminated mobilisation alarm conditions was successful with a reduced utilisation rate of 1.8% (n=11/609) and an eliminated utilisation rate of 0.0% (n=0/521). CONCLUSION(S): Half of mobilisation alarm trig

Interspeech 2020, 25 oktober 2020, Contains fulltext : 228158.pdf (publisher's version ) (Open Access)

EVA1 is describing a new class of emotion-aware autonomous systems delivering intelligent personal assistant functionalities. EVA requires a multi-disciplinary approach, combining a number of critical building blocks into a cybernetics systems/software architecture: emotion aware systems and algorithms, multimodal interaction design, cognitive modelling, decision making and recommender systems, emotion sensing as feedback for learning, and distributed (edge) computing delivering cognitive services., QC 20180831

Copyright © 2017 ISCA. Autism spectrum disorder (ASD) is a neurodevelopmental disorder usually diagnosed in or beyond toddlerhood. ASD is defined by repetitive and restricted behaviours, and deficits in social communication. The early speech-language development of individuals with ASD has been characterised as delayed. However, little is known about ASD-related characteristics of pre-linguistic vocalisations at the feature level. In this study, we examined pre-linguistic vocalisations of 10-month-old individuals later diagnosed with ASD and a matched control group of typically developing individuals (N = 20). We segmented 684 vocalisations from parent-child interaction recordings. All vocalisations were annotated and signal-analytically decomposed. We analysed ASD-related vocalisation specificities on the basis of a standardised set (eGeMAPS) of 88 acoustic features selected for clinical speech analysis applications. 54 features showed evidence for a differentiation between vocalisations of individuals later diagnosed with ASD and controls. In addition, we evaluated the feasibility of automated, vocalisation-based identification of individuals later diagnosed with ASD.We compared linear kernel support vector machines and a 1-layer bidirectional long short-term memory neural network. Both classification approaches achieved an accuracy of 75% for subject-wise identification in a subject-independent 3-fold cross-validation scheme. Our promising results may be an important contribution en-route to facilitate earlier identification of ASD.

Suicide is one of the leading causes of death globally, and is notably a significant cause of death amongst young people. A suicide outcome is a complex combination of personal, social, and health factors, and therefore suicide prevention is a challenge, requiring a systems approach incorporating public health strategies, screening at-risk individuals, targeted interventions, and follow-up for suicide survivors and those bereaved by suicide. Engineering practice has been implicated in the hindrance of the adoption of suicide prevention strategies, such as installing safety barriers at the Golden Gate Bridge, however technological developments offer new opportunities in suicide prevention, and the potential to reduce the number of deaths by suicide. We present an overview of current technological developments which are facilitating research in the field of suicide prevention, including multiple modes of screening such as network analysis of mobile-phone collected connectivity data, automatic detection of suicidality from social media content, and crisis detection from acoustic variability in speech patterns. The current field of mhealth apps for suicide prevention is assessed, and an innovative app for an Indigenous population is presented. From this overview, future challenges - technical and ethical - are discussed.

Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss of neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes in indicators of oxidative stress have not yet been demonstrated in oligodendrocytes vulnerable to secondary degeneration in vivo. We show increases in the oxidative stress indicator carboxymethyl lysine at days 1 and 3 after injury in oligodendrocytes vulnerable to secondary degeneration. Dihydroethidium staining for superoxide is reduced, indicating endogenous control of this particular reactive species after injury. Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation. Therapeutic administration of 670 nm light is thought to improve oxidative metabolism via mechanisms that may include increased activity of cytochrome c oxidase. Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes. Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site. In optic nerve vulnerable to secondary degeneration superoxide in oligodendrocytes is reduced relative to handling controls, and is associated with reduced paranode abnormalities. Long term (3 month) administration of 670 nm light preserves retinal ganglion cells vulnerable to secondary degeneration and maintains visual function, as assessed by the optokinetic nystagmus visual reflex. Light at a wavelength of 670 nm may serve as a therapeutic intervention for treatment of secondary degeneration following neurotrauma.

Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss of neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes in indicators of oxidative stress have not yet been demonstrated in oligodendrocytes vulnerable to secondary degeneration in vivo. We show increases in the oxidative stress indicator carboxymethyl lysine at days 1 and 3 after injury in oligodendrocytes vulnerable to secondary degeneration. Dihydroethidium staining for superoxide is reduced, indicating endogenous control of this particular reactive species after injury. Concurrently, node of Ranvier/paranode complexes are altered, with significant lengthening of the paranodal gap and paranode as well as paranode disorganisation. Therapeutic administration of 670 nm light is thought to improve oxidative metabolism via mechanisms that may include increased activity of cytochrome c oxidase. Here, we show that light at 670 nm, delivered for 30 minutes per day, results in in vivo increases in cytochrome c oxidase activity co-localised with oligodendrocytes. Short term (1 day) 670 nm light treatment is associated with reductions in reactive species at the injury site. In optic nerve vulnerable to secondary degeneration superoxide in oligodendrocytes is reduced relative to handling controls, and is associated with reduced paranode abnormalities. Long term (3 month) administration of 670 nm light preserves retinal ganglion cells vulnerable to secondary degeneration and maintains visual function, as assessed by the optokinetic nystagmus visual reflex. Light at a wavelength of 670 nm may serve as a therapeutic intervention for treatment of secondary degeneration following neurotrauma. © 2013 Szymanski et al.

Background: Traumatic injury to the central nervous system results in damage to tissue beyond the primary injury, termed secondary degeneration. Key events thought to be associated with secondary degeneration involve aspects of mitochondrial function which may be modulated by red/near-infrared irradiation therapy (R/NIR-IT), but precisely how mitochondria are affected in vivo has not been investigated. Secondary degeneration was modelled by transecting the dorsal aspect of the optic nerve in adult rats and mitochondrial ultrastructure in intact ventral optic nerve vulnerable to secondary degeneration investigated with transmission electron microscopy. Results: Despite reported increases in fission following central nervous system injury, we saw no change in mitochondrial densities in optic nerve vulnerable to secondary degeneration in vivo. However, in axons, frequency distributions of mitochondrial profile areas showed higher cumulative probabilities of smaller mitochondrial profiles at day 1 after injury. Glial mitochondrial profiles did not exhibit changes in area, but a more elliptical mitochondrial shape was observed at both day 1 and 7 following injury. Importantly, mitochondrial autophagic profiles were observed at days 1 and 7 in optic nerve vulnerable to secondary degeneration in vivo. Citrate synthase activity was used as an additional measure of mitochondrial mass in ventral optic nerve and was decreased at day 7, whereas mitochondrial aconitase activity increased at day 1 and day 28 after injury in optic nerve vulnerable to secondary degeneration. R/NIRIT has been used to treat the injured central nervous system, with reported improvements in oxidative metabolism suggesting mitochondrial involvement, but ultrastructural information is lacking. Here we show that R/NIR-IT of injured animals resulted in distributions of mitochondrial areas and shape not significantly different from control and significantly reduced mitochondrial autophagic profiles. R/NIR-I