Gas permeation through a polymer network

We study the diffusion of gas molecules through a two-dimensional network of polymers with the help of Monte Carlo simulations. The polymers are modeled as non-interacting random walks on the bonds of a two-dimensional square lattice, while the gas particles occupy the lattice cells. When a particle attempts to jump to a nearest-neighbor empty cell, it has to overcome an energy barrier which is determined by the number of polymer segments on the bond separating the two cells. We investigate the gas current $J$ as a function of the mean segment density $\rho$, the polymer length $\ell$ and the probability $q^{m}$ for hopping across $m$ segments. Whereas $J$ decreases monotonically with $\rho$ for fixed $\ell$, its behavior for fixed $\rho$ and increasing $\ell$ depends strongly on $q$. For small, non-zero $q$, $J$ appears to increase slowly with $\ell$. In contrast, for $q=0$, it is dominated by the underlying percolation problem and can be non-monotonic. We provide heuristic arguments to put these interesting phenomena into context.Comment: Dedicated to Lothar Schaefer on the occasion of his 60th birthday. 11 pages, 3 figure

Numerical studies of planar closed random walks

Lattice numerical simulations for planar closed random walks and their winding sectors are presented. The frontiers of the random walks and of their winding sectors have a Hausdorff dimension $d_H=4/3$. However, when properly defined by taking into account the inner 0-winding sectors, the frontiers of the random walks have a Hausdorff dimension $d_H\approx 1.77$.Comment: 15 pages, 15 figure

Adultery and the Rumor Mill: les bourgeois de Molinchart and El gran galeoto

This article seeks to challenge interpretations of the adultery plot as a subversive current in nineteenth-century literature by examining two texts that are often dismissed by contemporary critics: Les bourgeois de Molinchart (1854), a novel by the French writer Champfleury (the pseudonym of Jules Husson), and El gran Galeoto (1881), a play by the Spanish playwright Jos, Echegaray. In each of these works, the rumor of the adultery precedes and to a large extent precipitates the infidelity at the end of the work. In committing adultery, therefore, the protagonists are not rising up against social norms so much as capitulating to the expectations of society, enacting a plot that has been projected upon them. The essay compares and contrasts the treatment of the rumor mill in the two works and examines the literary strategies that the writers use to undercut a transgressive reading of the infidelity plot

T1 and FLAIR signal intensities are related to tau pathology in dominantly inherited Alzheimer disease

Carriers of mutations responsible for dominantly inherited Alzheimer disease provide a unique opportunity to study potential imaging biomarkers. Biomarkers based on routinely acquired clinical MR images, could supplement the extant invasive or logistically challenging) biomarker studies. We used 1104 longitudinal MR, 324 amyloid beta, and 87 tau positron emission tomography imaging sessions from 525 participants enrolled in the Dominantly Inherited Alzheimer Network Observational Study to extract novel imaging metrics representing the mean (μ) and standard deviation (σ) of standardized image intensities of T1-weighted and Fluid attenuated inversion recovery (FLAIR) MR scans. There was an exponential decrease in FLAIR-μ in mutation carriers and an increase in FLAIR and T1 signal heterogeneity (T1-σ and FLAIR-σ) as participants approached the symptom onset in both supramarginal, the right postcentral and right superior temporal gyri as well as both caudate nuclei, putamina, thalami, and amygdalae. After controlling for the effect of regional atrophy, FLAIR-μ decreased and T1-σ and FLAIR-σ increased with increasing amyloid beta and tau deposition in numerous cortical regions. In symptomatic mutation carriers and independent of the effect of regional atrophy, tau pathology demonstrated a stronger relationship with image intensity metrics, compared with amyloid pathology. We propose novel MR imaging intensity-based metrics using standard clinical T1 and FLAIR images which strongly associates with the progression of pathology in dominantly inherited Alzheimer disease. We suggest that tau pathology may be a key driver of the observed changes in this cohort of patients

Beyond crime statistics: the construction and application of a criminogenity monitor in Amsterdam

Criminologists have devoted a great deal of attention to risk factors - also called criminogenic factors - leading to criminal offending. This paper presents a criminogenity monitor which includes 19 risk factors that underlie crime. These factors do not themselves cause criminal behaviour; rather, they must be seen as signals that crimes may be committed. After discussing how the criminogenity monitor was constructed, we apply the risk factors we examined to the situation in Amsterdam, capital city of the Netherlands. The monitor is intended to function particularly as an instrument to rationalise policy-makers' work in targeting and preventing symptoms of crime at three geographical levels: the entire city, its boroughs and its neighbourhoods. © 2012 The Author(s)

Positron emission tomography and magnetic resonance imaging methods and datasets within the Dominantly Inherited Alzheimer Network (DIAN)

The Dominantly Inherited Alzheimer Network (DIAN) is an international collaboration studying autosomal dominant Alzheimer disease (ADAD). ADAD arises from mutations occurring in three genes. Offspring from ADAD families have a 50% chance of inheriting their familial mutation, so non-carrier siblings can be recruited for comparisons in case-control studies. The age of onset in ADAD is highly predictable within families, allowing researchers to estimate an individual's point in the disease trajectory. These characteristics allow candidate AD biomarker measurements to be reliably mapped during the preclinical phase. Although ADAD represents a small proportion of AD cases, understanding neuroimaging-based changes that occur during the preclinical period may provide insight into early disease stages of 'sporadic' AD also. Additionally, this study provides rich data for research in healthy aging through inclusion of the non-carrier controls. Here we introduce the neuroimaging dataset collected and describe how this resource can be used by a range of researchers

Positron emission tomography and magnetic resonance imaging methods and datasets within the dominantly inherited Alzheimer network (DIAN)

The Dominantly Inherited Alzheimer Network (DIAN) is an international collaboration studying autosomal dominant Alzheimer disease (ADAD). ADAD arises from mutations occurring in three genes. Offspring from ADAD families have a 50% chance of inheriting their familial mutation, so non-carrier siblings can be recruited for comparisons in case–control studies. The age of onset in ADAD is highly predictable within families, allowing researchers to estimate an individual’s point in the disease trajectory. These characteristics allow candidate AD biomarker measurements to be reliably mapped during the preclinical phase. Although ADAD represents a small proportion of AD cases, understanding neuroimaging-based changes that occur during the preclinical period may provide insight into early disease stages of ‘sporadic’ AD also. Additionally, this study provides rich data for research in healthy aging through inclusion of the non-carrier controls. Here we introduce the neuroimaging dataset collected and describe how this resource can be used by a range of researchers

Scaling of Brain Metabolism with a Fixed Energy Budget per Neuron: Implications for Neuronal Activity, Plasticity and Evolution

It is usually considered that larger brains have larger neurons, which consume more energy individually, and are therefore accompanied by a larger number of glial cells per neuron. These notions, however, have never been tested. Based on glucose and oxygen metabolic rates in awake animals and their recently determined numbers of neurons, here I show that, contrary to the expected, the estimated glucose use per neuron is remarkably constant, varying only by 40% across the six species of rodents and primates (including humans). The estimated average glucose use per neuron does not correlate with neuronal density in any structure. This suggests that the energy budget of the whole brain per neuron is fixed across species and brain sizes, such that total glucose use by the brain as a whole, by the cerebral cortex and also by the cerebellum alone are linear functions of the number of neurons in the structures across the species (although the average glucose consumption per neuron is at least 10× higher in the cerebral cortex than in the cerebellum). These results indicate that the apparently remarkable use in humans of 20% of the whole body energy budget by a brain that represents only 2% of body mass is explained simply by its large number of neurons. Because synaptic activity is considered the major determinant of metabolic cost, a conserved energy budget per neuron has several profound implications for synaptic homeostasis and the regulation of firing rates, synaptic plasticity, brain imaging, pathologies, and for brain scaling in evolution