A service-oriented user interaction analysis framework supporting adaptive applications

A comprehensive user model, built by monitoring a user's current use of applications, can be an excellent starting point for building adaptive user-centred applications. The BaranC framework monitors all user interaction with a digital device (e.g. smartphone), and also collects all available context data (such as from sensors in the digital device itself, in a smart watch, or in smart appliances) in order to build a full model of user application behaviour. The model built from the collected data, called the UDI (User Digital Imprint), is further augmented by analysis services, for example, a service to produce activity profiles from smartphone sensor data. The enhanced UDI model can then be the basis for building an appropriate adaptive application that is user-centred as it is based on an individual user model. As BaranC supports continuous user monitoring, an application can be dynamically adaptive in real-time to the current context (e.g. time, location or activity). Furthermore, since BaranC is continuously augmenting the user model with more monitored data, over time the user model changes, and the adaptive application can adapt gradually over time to changing user behaviour patterns. BaranC has been implemented as a service-oriented framework where the collection of data for the UDI and all sharing of the UDI data are kept strictly under the user's control. In addition, being service-oriented allows (with the user's permission) its monitoring and analysis services to be easily used by 3rd parties in order to provide 3rd party adaptive assistant services. An example 3rd party service demonstrator, built on top of BaranC, proactively assists a user by dynamic predication, based on the current context, what apps and contacts the user is likely to need. BaranC introduces an innovative user-controlled unified service model of monitoring and use of personal digital activity data in order to provide adaptive user-centred applications. This aims to improve on the current situation where the diversity of adaptive applications results in a proliferation of applications monitoring and using personal data, resulting in a lack of clarity, a dispersal of data, and a diminution of user control.

Diaphragm muscle adaptation to sustained hypoxia: lessons from animal models with relevance to high altitude and chronic respiratory diseases

The diaphragm is the primary inspiratory pump muscle of breathing. Notwithstanding its critical role in pulmonary ventilation, the diaphragm like other striated muscles is malleable in response to physiological and pathophysiological stressors, with potential implications for the maintenance of respiratory homeostasis. This review considers hypoxic adaptation of the diaphragm muscle, with a focus on functional, structural, and metabolic remodeling relevant to conditions such as high altitude and chronic respiratory disease. On the basis of emerging data in animal models, we posit that hypoxia is a significant driver of respiratory muscle plasticity, with evidence suggestive of both compensatory and deleterious adaptations in conditions of sustained exposure to low oxygen. Cellular strategies driving diaphragm remodeling during exposure to sustained hypoxia appear to confer hypoxic tolerance at the expense of peak force-generating capacity, a key functional parameter that correlates with patient morbidity and mortality. Changes include, but are not limited to: redox-dependent activation of hypoxia-inducible factor (HIF) and MAP kinases; time-dependent carbonylation of key metabolic and functional proteins; decreased mitochondrial respiration; activation of atrophic signaling and increased proteolysis; and altered functional performance. Diaphragm muscle weakness may be a signature effect of sustained hypoxic exposure. We discuss the putative role of reactive oxygen species as mediators of both advantageous and disadvantageous adaptations of diaphragm muscle to sustained hypoxia, and the role of antioxidants in mitigating adverse effects of chronic hypoxic stress on respiratory muscle function.

Redox remodelling in diaphragm muscle adaptation to chronic sustained hypoxia

Chronic sustained hypoxia (CH) induces functional weakness, atrophy, and mitochondrial remodelling in the diaphragm muscle. Animal models of CH present with changes similar to patients with respiratory-related disease, thus, elucidating the molecular mechanisms driving these adaptations is clinically important. We hypothesize that ROS are pivotal in diaphragm muscle adaptation to CH. C57BL6/J mice were exposed to CH (FiO2=0.1) for one, three, and six weeks. Sternohyoid (upper airway dilator), extensor digitorum longus (EDL), and soleus were studied as reference muscles as well as the diaphragm. The diaphragm was profiled using a redox proteomics approach followed by mass spectrometry. Following this, redox-modified metabolic enzyme activities and atrophy signalling were assessed using spectrophotometric assays and ELISA. Diaphragm isotonic performance was assessed after six weeks of CH ± chronic antioxidant supplementation. Protein carbonyl and free thiol content in the diaphragm were increased and decreased respectively after six weeks of CH – indicative of protein oxidation. These changes were temporally modulated and muscle specific. Extensive remodelling of metabolic proteins occurred and the stress reached the cross-bridge. Metabolic enzyme activities in the diaphragm were, for the most part, decreased by CH and differential muscle responses were observed. Redox sensitive chymotrypsin-like proteasome activity of the diaphragm was increased and atrophy signalling was observed through decreased phospho-FOXO3a and phospho-mTOR. Phospho-p38 MAPK content was increased and this was attenuated by antioxidant treatment. Hypoxia decreased power generating capacity of the diaphragm and this was restored by N-acetyl-cysteine (NAC) but not by tempol. Redox remodelling is pivotal for diaphragm adaptation to chronic sustained hypoxia. Muscle changes are dependent on duration of the hypoxia stimulus, activity profile of the muscle, and molecular composition of the muscle. The working respiratory muscles and slow oxidative fibres are particularly susceptible. NAC (antioxidant) may be useful as an adjunct therapy in respiratory-related diseases characterised by hypoxic stress.