Knowledge is at the Edge! How to Search in Distributed Machine Learning Models

With the advent of the Internet of Things and Industry 4.0 an enormous amount of data is produced at the edge of the network. Due to a lack of computing power, this data is currently send to the cloud where centralized machine learning models are trained to derive higher level knowledge. With the recent development of specialized machine learning hardware for mobile devices, a new era of distributed learning is about to begin that raises a new research question: How can we search in distributed machine learning models? Machine learning at the edge of the network has many benefits, such as low-latency inference and increased privacy. Such distributed machine learning models can also learn personalized for a human user, a specific context, or application scenario. As training data stays on the devices, control over possibly sensitive data is preserved as it is not shared with a third party. This new form of distributed learning leads to the partitioning of knowledge between many devices which makes access difficult. In this paper we tackle the problem of finding specific knowledge by forwarding a search request (query) to a device that can answer it best. To that end, we use a entropy based quality metric that takes the context of a query and the learning quality of a device into account. We show that our forwarding strategy can achieve over 95% accuracy in a urban mobility scenario where we use data from 30 000 people commuting in the city of Trento, Italy.Comment: Published in CoopIS 201

Aberrant \u3ci\u3eAZIN2\u3c/i\u3e and Polyamine Metabolism Precipitates Tau Neuropathology

Tauopathies display a spectrum of phenotypes from cognitive to affective behavioral impairments; however, mechanisms promoting tau pathology and how tau elicits behavioral impairment remain unclear. We report a unique interaction between polyamine metabolism, behavioral impairment, and tau fate. Polyamines are ubiquitous aliphatic molecules that support neuronal function, axonal integrity, and cognitive processing. Transient increases in polyamine metabolism hallmark the cell’s response to various insults, known as the polyamine stress response (PSR). Dysregulation of gene transcripts associated with polyamine metabolism in Alzheimer’s disease (AD) brains were observed, and we found that ornithine decarboxylase antizyme inhibitor 2 (AZIN2) increased to the greatest extent. We showed that sustained AZIN2 overexpression elicited a maladaptive PSR in mice with underlying tauopathy (MAPT P301S; PS19). AZIN2 also increased acetylpolyamines, augmented tau deposition, and promoted cognitive and affective behavioral impairments. Higher-order polyamines displaced microtubule-associated tau to facilitate polymerization but also decreased tau seeding and oligomerization. Conversely, acetylpolyamines promoted tau seeding and oligomers. These data suggest that tauopathies launch an altered enzymatic signature that endorses a feed-forward cycle of disease progression. Taken together, the tau-induced PSR affects behavior and disease continuance, but may also position the polyamine pathway as a potential entry point for plausible targets and treatments of tauopathy, including AD

TLR2 and Nod2 Mediate Resistance or Susceptibility to Fatal Intracellular Ehrlichia Infection in Murine Models of Ehrlichiosis

Our murine models of human monocytic ehrlichiosis (HME) have shown that severe and fatal ehrlichiosis is due to generation of pathogenic T cell responses causing immunopathology and multi-organ failure. However, the early events in the liver, the main site of infection, are not well understood. In this study, we examined the liver transcriptome during the course of lethal and nonlethal infections caused by Ixodes ovatus Ehrlichia and Ehrlichia muris, respectively. On day 3 post-infection (p.i.), although most host genes were down regulated in the two groups of infected mice compared to naïve counterparts, lethal infection induced significantly higher expression of caspase 1, caspase 4, nucleotide binding oligomerization domain-containing proteins (Nod1), tumor necrosis factor-alpha, interleukin 10, and CCL7 compared to nonlethal infection. On day 7 p.i., lethal infection induced highly significant upregulation of type-1 interferon, several inflammatory cytokines and chemokines, which was associated with increased expression levels of Toll-like receptor-2 (TLR2), Nod2, MyD88, nuclear factor-kappa B (NF-kB), Caspase 4, NLRP1, NLRP12, Pycard, and IL-1β, suggesting enhanced TLR signals and inflammasomes activation. We next evaluated the participation of TLR2 and Nod2 in the host response during lethal Ehrlichia infection. Although lack of TLR2 impaired bacterial elimination and increased tissue necrosis, Nod2 deficiency attenuated pathology and enhanced bacterial clearance, which correlated with increased interferon-γ and interleukin-10 levels and a decreased frequency of pathogenic CD8+ T cells in response to lethal infection. Thus, these data indicate that Nod2, but not TLR2, contributes to susceptibility to severe Ehrlichia-induced shock. Together, our studies provide, for the first time, insight into the diversity of host factors and novel molecular pathogenic mechanisms that may contribute to severe HME. © 2013 Chattoraj et al

Regeneration of whole limbs in toad tadpoles treated with retinol palmitate after the wound-healing stage

In young Bufo melanosticus tadpoles at the spatula stage of limb development, the left hindlimb was amputated through the shank and the right hindlimb was left intact. One day later, when the amputation surface was covered by wound epidermis, the tadpoles were immersed in 15 IU/ml of retinol palmitate solution for 2 days up to blastema formation and thereafter reared in plain water. Contrary to the situation in untreated controls, all the resultant regenerates of the vitamin-treated tadpoles were complete limbs containing elements from the pelvic girdle to the phalanges. Retinol palmitate treatment inhibited the development of the foot in the unamputated right limbs. These results show that retinol palmitate has a different effect on dedifferentiating cells of a regenerating limb from that on cells that are differentiating in a normally developing limb