An Investigation into Trust and Reputation Frameworks for Autonomous Underwater Vehicles

As Autonomous Underwater Vehicles (AUVs) become more technically capable and economically feasible, they are being increasingly used in a great many areas of defence, commercial and environmental applications. These applications are tending towards using independent, autonomous, ad-hoc, collaborative behaviour of teams or fleets of these AUV platforms. This convergence of research experiences in the Underwater Acoustic Network (UAN) and Mobile Ad-hoc Network (MANET) fields, along with the increasing Level of Automation (LOA) of such platforms, creates unique challenges to secure the operation and communication of these networks. The question of security and reliability of operation in networked systems has usually been resolved by having a centralised coordinating agent to manage shared secrets and monitor for misbehaviour. However, in the sparse, noisy and constrained communications environment of UANs, the communications overheads and single-point-of-failure risk of this model is challenged (particularly when faced with capable attackers). As such, more lightweight, distributed, experience based systems of “Trust” have been proposed to dynamically model and evaluate the “trustworthiness” of nodes within a MANET across the network to prevent or isolate the impact of malicious, selfish, or faulty misbehaviour. Previously, these models have monitored actions purely within the communications domain. Moreover, the vast majority rely on only one type of observation (metric) to evaluate trust; successful packet forwarding. In these cases, motivated actors may use this limited scope of observation to either perform unfairly without repercussions in other domains/metrics, or to make another, fair, node appear to be operating unfairly. This thesis is primarily concerned with the use of terrestrial-MANET trust frameworks to the UAN space. Considering the massive theoretical and practical difference in the communications environment, these frameworks must be reassessed for suitability to the marine realm. We find that current single-metric Trust Management Frameworks (TMFs) do not perform well in a best-case scaling of the marine network, due to sparse and noisy observation metrics, and while basic multi-metric communications-only frameworks perform better than their single-metric forms, this performance is still not at a reliable level. We propose, demonstrate (through simulation) and integrate the use of physical observational metrics for trust assessment, in tandem with metrics from the communications realm, improving the safety, security, reliability and integrity of autonomous UANs. Three main novelties are demonstrated in this work: Trust evaluation using metrics from the physical domain (movement/distribution/etc.), demonstration of the failings of Communications-based Trust evaluation in sparse, noisy, delayful and non-linear UAN environments, and the deployment of trust assessment across multiple domains, e.g. the physical and communications domains. The latter contribution includes the generation and optimisation of cross-domain metric composition or“synthetic domains” as a performance improvement method

The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse

Muscle wasting that occurs with cancer cachexia is caused by an imbalance in the rates of muscle protein synthesis and degradation. The ApcMin/+ mouse is a model of colorectal cancer that develops cachexia that is dependent on circulating IL-6. However, the IL-6 regulation of muscle protein turnover during the initiation and progression of cachexia in the ApcMin/+ mouse is not known. Cachexia progression was studied in ApcMin/+ mice that were either weight stable (WS) or had initial (≤5%), intermediate (6–19%), or extreme (≥20%) body weight loss. The initiation of cachexia reduced %MPS 19% and a further ∼50% with additional weight loss. Muscle IGF-1 mRNA expression and mTOR targets were suppressed with the progression of body weight loss, while muscle AMPK phosphorylation (Thr 172), AMPK activity, and raptor phosphorylation (Ser 792) were not increased with the initiation of weight loss, but were induced as cachexia progressed. ATP dependent protein degradation increased during the initiation and progression of cachexia. However, ATP independent protein degradation was not increased until cachexia had progressed beyond the initial phase. IL-6 receptor antibody administration prevented body weight loss and suppressed muscle protein degradation, without any effect on muscle %MPS or IGF-1 associated signaling. In summary, the %MPS reduction during the initiation of cachexia is associated with IGF-1/mTOR signaling repression, while muscle AMPK activation and activation of ATP independent protein degradation occur later in the progression of cachexia. IL-6 receptor antibody treatment blocked cachexia progression through the suppression of muscle protein degradation, while not rescuing the suppression of muscle protein synthesis. Attenuation of IL-6 signaling was effective in blocking the progression of cachexia, but not sufficient to reverse the process

The role of IGF-1 signaling in skeletal muscle atrophy

Insulin-like growth factor 1 (IGF-1) is a key anabolic growth factor stimulating phosphatidylinositol 3-kinase (PI3K)/Akt signaling which is well known for regulating muscle hypertrophy. However, the role of IGF-1 in muscle atrophy is less clear. This review provides an overview of the mechanisms via which IGF-1 signaling is implicated in several conditions of muscle atrophy and via which mechanisms protein turnover is altered. IGF-1/PI3K/Akt signaling stimulates the rate of protein synthesis via p70S6Kinase and p90 ribosomal S6 kinase and negatively regulates protein degradation, predominantly by its inhibiting effect on proteasomal and lysosomal protein degradation. Caspase-dependent protein degradation is also attenuated by IGF/PI3K/Akt signaling, whereas evidence for an effect on calpain-dependent protein degradation is inconclusive. IGF-1/PI3K/Akt signaling reduces during denervation-, unloading-, and joint immobilization-induced muscle atrophy, whereas IGF-1/PI3K/Akt signaling seems unaltered during aging-associated muscle atrophy. During denervation and aging, IGF-1 overexpression or injection counteracts denervation- and aging-associated muscle atrophy, despite enhanced anabolic resistance with regard to IGF-1 signaling with aging. It remains unclear whether pharmacological stimulation of IGF-1/PI3K/Akt signaling attenuates immobilization- or unloading-induced muscle atrophy. Exploration of the possibilities to interfere with IGF-1/PI3K/Akt signaling reveals that microRNAs targeting IGF-1 signaling components are promising targets to counterbalance muscle atrophy. Overall, the findings summarized in this review show that in disuse conditions, but not with aging, IGF-1/PI3K/Akt signaling is attenuated and that in some conditions stimulation of this pathway may alleviate skeletal muscle atrophy