A unified data representation theory for network visualization, ordering and coarse-graining

Representation of large data sets became a key question of many scientific disciplines in the last decade. Several approaches for network visualization, data ordering and coarse-graining accomplished this goal. However, there was no underlying theoretical framework linking these problems. Here we show an elegant, information theoretic data representation approach as a unified solution of network visualization, data ordering and coarse-graining. The optimal representation is the hardest to distinguish from the original data matrix, measured by the relative entropy. The representation of network nodes as probability distributions provides an efficient visualization method and, in one dimension, an ordering of network nodes and edges. Coarse-grained representations of the input network enable both efficient data compression and hierarchical visualization to achieve high quality representations of larger data sets. Our unified data representation theory will help the analysis of extensive data sets, by revealing the large-scale structure of complex networks in a comprehensible form.Comment: 13 pages, 5 figure

Evidence-Based PET for Neurological Diseases

Over the past two decades, one of the major breakthroughs for the approach to neurological diseases both in the clinical and research settings has been represented by the validation of diagnostic biomarkers able to demonstrate the presence of pathological mechanisms, alteration in neurotransmission as well as to predict disease progression [1, 2]. The use of PET with different tracers as well as other imaging biomarkers support the etiological diagnosis of neurological disorders in vivo. This approach is particularly relevant in the field of neurodegenerative diseases. In fact, neurodegenerative diseases are characterized by the progressive degeneration and death of neurons. They represent a heterogeneous group of conditions characterized by different etiologies, different neuropathological and neurochemical alterations leading to different clinical pictures and courses [3]. Indeed, an early accurate diagnosis allows to tackle the disease with available or experimental intervention, lifestyle changes, or logistical arrangements, before disability has developed. Early intervention is expected to have greater clinical impact, extend independent and active life, improve its quality, and decrease the burden and costs of the disease [4]. However, the validation of PET tracers in neurological disease is still ongoing, and evidence on its comparative and combined diagnostic value with respect to other biomarkers is incomplete [4, 5]. As a matter of fact, the increasing pressure for cost-effectiveness requires systematic assessment and validation of all biomarker performance in the clinical settings. Similarly only an evidence-based approach to new PET tracers can allow to select the most promising tracers for PET imaging in the research field both for pathophysiological investigations and for upcoming diagnostic approaches

Immunological memory ≠ protective immunity

So-called ‘immunological memory' is, in my view, a typical example where a field of enquiry, i.e. to understand long-term protection to survive reexposure to infection, has been overtaken by ‘l'art pour l'art' of ‘basic immunology'. The aim of this critical review is to point out some key differences between academic text book-defined immunological memory and protective immunity as viewed from a co-evolutionary point of view, both from the host and the infectious agents. A key conclusion is that ‘immunological memory' of course exists, but only in particular experimental laboratory models measuring ‘quicker and better' responses after an earlier immunization. These often do correlate with, but are not the key mechanisms of, protection. Protection depends on pre-existing neutralizing antibodies or pre-activated T cells at the time of infection—as documented by the importance of maternal antibodies around birth for survival of the offspring. Importantly, both high levels of antibodies and of activated T cells are antigen driven. This conclusion has serious implications for our thinking about vaccines and maintaining a level of protection in the population to deal with old and new infectious disease