On the renormalisation group for the boundary Truncated Conformal Space Approach

In this paper we continue the study of the truncated conformal space approach to perturbed boundary conformal field theories. This approach to perturbation theory suffers from a renormalisation of the coupling constant and a multiplicative renormalisation of the Hamiltonian. We show how these two effects can be predicted by both physical and mathematical arguments and prove that they are correct to leading order for all states in the TCSA system. We check these results using the TCSA applied to the tri-critical Ising model and the Yang-Lee model. We also study the TCSA of an irrelevant (non-renormalisable) perturbation and find that, while the convergence of the coupling constant and energy scales are problematic, the renormalised and rescaled spectrum remain a very good fit to the exact result, and we find a numerical relationship between the IR and UV couplings describing a particular flow. Finally we study the large coupling behaviour of TCSA and show that it accurately encompasses several different fixed points.Comment: 27 pages, 19 figure

Defect flows in minimal models

In this paper we study a simple example of a two-parameter space of renormalisation group flows of defects in Virasoro minimal models. We use a combination of exact results, perturbation theory and the truncated conformal space approach to search for fixed points and investigate their nature. For the Ising model, we confirm the recent results of Fendley et al. In the case of central charge close to one, we find six fixed points, five of which we can identify in terms of known defects and one of which we conjecture is a new non-trivial conformal defect. We also include several new results on exact properties of perturbed defects and on the renormalisation group in the truncated conformal space approach.Comment: 35 pages, 21 figures. 1 reference adde

Alzheimer's disease and symbiotic microbiota: an evolutionary medicine perspective

Microorganisms resident in our bodies participate in a variety of regulatory and pathogenic processes. Here, we describe how etiological pathways implicated in Alzheimer’s disease (AD) may be regulated or disturbed by symbiotic microbial activity. Furthermore, the composition of symbiotic microbes has changed dramatically across human history alongside the rise of agriculturalism, industrialization, and globalization. We postulate that each of these lifestyle transitions engendered progressive depletion of microbial diversity and enhancement of virulence, thereby enhancing AD risk pathways. It is likely that the human life span extended into the eighth decade tens of thousands of years ago, yet little is known about premodern geriatric epidemiology. We propose that microbiota of the gut, oral cavity, nasal cavity, and brain may modulate AD pathogenesis, and that changes in the microbial composition of these body regions across history suggest escalation of AD risk. Dysbiosis may promote immunoregulatory dysfunction due to inadequate education of the immune system, chronic inflammation, and epithelial barrier permeability. Subsequently, proinflammatory agents—and occasionally microbes—may infiltrate the brain and promote AD pathogenic processes. APOE genotypes appear to moderate the effect of dysbiosis on AD risk. Elucidating the effect of symbiotic microbiota on AD pathogenesis could contribute to basic and translational research

Circulating microRNAs in sera correlate with soluble biomarkers of immune activation but do not predict mortality in ART treated individuals with HIV-1 infection: A case control study

10.1371/journal.pone.0139981PLoS ONE1010e013998