431 research outputs found

    Recording of time-varying back-pain data: A wireless solution

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    Chronic back pain is a debilitating experience for a considerable proportion of the adult population, with a significant impact on countries’ economies and health systems. While there has been increasing anecdotal evidence to support the fact that for certain categories of patients (such as wheelchair users), the back pain experienced is dynamically varying with time, there is a relative scarcity of data to support and document this observation, with consequential impact upon such patients’ treatment and care. Part of the reason behind this state of affairs is the relative difficulty in gathering pain measurements at precisely defined moments in time. In this paper,we describe a wireless-enabled solution that collects both questionnaire and diagrammatic, visual-based data, via a pain drawing, which overcomes such limitations, enabling seamless data collection and its upload to a hospital server using existing wireless fidelity technology. Results show that it is generally perceived to be an easy-to-use and convenient solution to the challenges of anywhere/anytime data collection

    Integrating perceptual, device and location characteristics for wireless multimedia transmission

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    In this paper,we describe an investigation exploring user experiences of accessing streamed multimedia content, when that content is tailored according to perceptual, device and location characteristics. To this end, we have created pre-defined transmission profiles and stream perceptually tailored multimedia content to three different locations, each characterised by different infotainment requirements. In the light of our results, we propose that multimedia transmission to mobile and wireless devices should be made based on pre-defined profiles, which contains a combination of static (perceptual, device type, CPU speed, and display specifications) and dynamic information (streamed content type location of the device/user, context of the device/user). The evaluation of such a system showed that the users and service providers can gain from such an approach considerably, as user perceptions of quality were not detrimentally affected by QoS degradations. Consequently, service providers can utilise this information to effectively manage local network traffic and bandwidth

    トルコ北アナトリア断層ゲレデセグメントにおける地震学的不均質構造の研究

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    International Collaborative Research (Project No.: 2020W-02

    Mechanisms for Insulin-dependent Regulation of Skeletal Muscle Mitochondria by OPA-1

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    Augmentation of mitochondrial oxidative metabolism by insulin might be mediated in part by induction of the inner mitochondrial membrane protein, Optic Atrophy-1 (OPA-1). Decreased OPA-1 in skeletal muscle has been reported in both murine and human type II diabetic models. Reduced OPA-1 in these contexts correlates with mitochondrial content, oxidative capacity, and dynamics. In addition to increasing mitochondrial fusion, OPA-1 mediates cristae remodeling toenhance mitochondrial bioenergetics through oligomer formation. Therefore, we hypothesized that insulin stimulation increases OPA-1 protein levels and mitochondrial respiration by increasing OPA-1 oligomerization and cristae remodeling in skeletal muscle cells. To investigate the role of insulin on mitochondrial dynamics and cristae organization, Cre-LoxP technology was used to ablate OPA-1 from skeletal myoblasts isolated from floxed OPA-1 mice. Confocal microscopy and MitoTracker orange was employed to obtain three-dimensional images of mitochondria networks, and transmission electron microscopy (TEM) was used to analyze ultrastructure of mitochondrial cristae. Two hours of insulin treatment increased OPA-1 protein levels, promoted mitochondrial fusion, elevated mitochondrial respiration, increased cristae number along with volume density and area, decreased the distance of ER-mitochondria contacts, and it may have even changed OPA-1 oligomerization. Depletion of OPA-1 and MFN-2 blocked the metabolic effects of insulin stimulation. OPA-1 depletion reduced cristae number, volume density, and area. Loss of OPA-1 resulted in a compensatory elevation of mitochondrial associated membrane proteins (MAMs), increasing the number of ER-mitochondria contacts, blocking OPA-1 oligomerization, and decreasing the ER-mitochondria contact distance. Together, ablation of OPA-1 alters metabolic responses to insulin in skeletal muscle cells. Furthermore, insulin stimulation promotes changes in cristae morphology and triggers mitochondrial fusion through an IR-pAKT pathway that increases OPA-1. ER-mitocontacts increase after ablation of OPA-1 due to an increase in MAMs. Lastly, Loss of OPA-1 inhibits OPA-1 oligomerization formation
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