Solvable Critical Dense Polymers on the Cylinder

A lattice model of critical dense polymers is solved exactly on a cylinder with finite circumference. The model is the first member LM(1,2) of the Yang-Baxter integrable series of logarithmic minimal models. The cylinder topology allows for non-contractible loops with fugacity alpha that wind around the cylinder or for an arbitrary number ell of defects that propagate along the full length of the cylinder. Using an enlarged periodic Temperley-Lieb algebra, we set up commuting transfer matrices acting on states whose links are considered distinct with respect to connectivity around the front or back of the cylinder. These transfer matrices satisfy a functional equation in the form of an inversion identity. For even N, this involves a non-diagonalizable braid operator J and an involution R=-(J^3-12J)/16=(-1)^{F} with eigenvalues R=(-1)^{ell/2}. The number of defects ell separates the theory into sectors. For the case of loop fugacity alpha=2, the inversion identity is solved exactly for the eigenvalues in finite geometry. The eigenvalues are classified by the physical combinatorics of the patterns of zeros in the complex spectral-parameter plane yielding selection rules. The finite-size corrections are obtained from Euler-Maclaurin formulas. In the scaling limit, we obtain the conformal partition functions and confirm the central charge c=-2 and conformal weights Delta_t=(t^2-1)/8. Here t=ell/2 and t=2r-s in the ell even sectors with Kac labels r=1,2,3,...; s=1,2 while t is half-integer in the ell odd sectors. Strikingly, the ell/2 odd sectors exhibit a W-extended symmetry but the ell/2 even sectors do not. Moreover, the naive trace summing over all ell even sectors does not yield a modular invariant.Comment: 44 pages, v3: minor correction

A conceptual view at microtubule plus end dynamics in neuronal axons

AbstractAxons are the cable-like protrusions of neurons which wire up the nervous system. Polar bundles of microtubules (MTs) constitute their structural backbones and are highways for life-sustaining transport between proximal cell bodies and distal synapses. Any morphogenetic changes of axons during development, plastic rearrangement, regeneration or degeneration depend on dynamic changes of these MT bundles. A key mechanism for implementing such changes is the coordinated polymerisation and depolymerisation at the plus ends of MTs within these bundles. To gain an understanding of how such regulation can be achieved at the cellular level, we provide here an integrated overview of the extensive knowledge we have about the molecular mechanisms regulating MT de/polymerisation. We first summarise insights gained from work in vitro, then describe the machinery which supplies the essential tubulin building blocks, the protein complexes associating with MT plus ends, and MT shaft-based mechanisms that influence plus end dynamics. We briefly summarise the contribution of MT plus end dynamics to important cellular functions in axons, and conclude by discussing the challenges and potential strategies of integrating the existing molecular knowledge into conceptual understanding at the level of axons

Differential effects of apolipoprotein E isoforms on phosphorylation at specific sites on tau by glycogen synthase kinase-3β identified by nano-electrospray mass spectrometry

AbstractPreviously published data have shown an allele-specific variation in the in vitro binding of apolipoprotein E (apoE) to tau, which prompted the hypothesis that apoE binding may protect tau from phosphorylation, apoE3 being more efficient than apoE4. We have, therefore, investigated the effects of apoE on tau phosphorylation in vitro by the proline-directed kinase, glycogen synthase kinase (GSK)-3β. The phosphopeptide maps of tau alone, of tau with apoE3 and of tau with apoE4 were very similar. When apoE2 was present a further four spots were evident. Additionally, of the 15 peptides phosphorylated in the presence or absence of apoE, subtle differences, some isoform-specific, in the relative amounts of phosphorylation were observed

The BRAIN-Q, a tool for assessing self-reported sport-related concussions for epidemiological studies

Objectives: The BRAIN-Q is a tool aimed at maximising the accuracy, and minimising measurement error, for retrospectively assessing concussions. This paper reports agreement of the BRAIN-Q tool when compared to extant questionnaire questions, and reproducibility when compared with its telephonic version (tBRAIN-Q). Method: The BRAIN-Q entails a 3-stage process: defining concussion, creating a visual timeline with life events, and establishing detailed characteristics for each reported concussion. It was designed to be administered in-person by trained personnel, and was used in the BRAIN Study. Its performance was compared with the MSK Study which previously collected a few questions in a broader self-administered questionnaire; and with the tBRAIN-Q Recall, its telephonic version. Results: 101 participants were included; of these, nine were re-assessed with the tBRAIN-Q. Compared to the BRAIN-Q, the agreement with the MSK-Q for rugby-related concussion was 86.7% (kappa 0.6). Rugby-related concussion with loss of consciousness showed lower agreement (82.0% (kappa 0.6)). The comparison between the BRAIN-Q and the tBRAIN-Q showed a good reproducibility. Conclusions: The BRAIN-Q is a relatively easy tool to administer in face-to-face assessments, it showed an optimal reproducibility, it includes a well-established definition of concussion, and is used to collect detailed information on each concussion allowing for a number of subgroup analyses (e.g. by severity, by age, by context). The BRAIN-Q is easily adaptable to other sporting setting

The association between green space and cause-specific mortality in urban New Zealand: an ecological analysis of green space utility

<b>Background:</b> There is mounting international evidence that exposure to green environments is associated with health benefits, including lower mortality rates. Consequently, it has been suggested that the uneven distribution of such environments may contribute to health inequalities. Possible causative mechanisms behind the green space and health relationship include the provision of physical activity opportunities, facilitation of social contact and the restorative effects of nature. In the New Zealand context we investigated whether there was a socioeconomic gradient in green space exposure and whether green space exposure was associated with cause-specific mortality (cardiovascular disease and lung cancer). We subsequently asked what is the mechanism(s) by which green space availability may influence mortality outcomes, by contrasting health associations for different types of green space. <b>Methods:</b> This was an observational study on a population of 1,546,405 living in 1009 small urban areas in New Zealand. A neighbourhood-level classification was developed to distinguish between usable (i.e., visitable) and non-usable green space (i.e., visible but not visitable) in the urban areas. Negative binomial regression models were fitted to examine the association between quartiles of area-level green space availability and risk of mortality from cardiovascular disease (n = 9,484; 1996 - 2005) and from lung cancer (n = 2,603; 1996 - 2005), after control for age, sex, socio-economic deprivation, smoking, air pollution and population density. <b>Results:</b> Deprived neighbourhoods were relatively disadvantaged in total green space availability (11% less total green space for a one standard deviation increase in NZDep2001 deprivation score, p < 0.001), but had marginally more usable green space (2% more for a one standard deviation increase in deprivation score, p = 0.002). No significant associations between usable or total green space and mortality were observed after adjustment for confounders. <b>Conclusion</b> Contrary to expectations we found no evidence that green space influenced cardiovascular disease mortality in New Zealand, suggesting that green space and health relationships may vary according to national, societal or environmental context. Hence we were unable to infer the mechanism in the relationship. Our inability to adjust for individual-level factors with a significant influence on cardiovascular disease and lung cancer mortality risk (e.g., diet and alcohol consumption) will have limited the ability of the analyses to detect green space effects, if present. Additionally, green space variation may have lesser relevance for health in New Zealand because green space is generally more abundant and there is less social and spatial variation in its availability than found in other contexts