Critical behavior of a three-dimensional dimer model

The phase transition behavior of a dimer model on a three-dimensional lattice is studied. This model is of biological interest because of its relevance to the lipid bilayer main phase transition. The model has the same kind of inactive low-temperature behavior as the exactly solvable Kasteleyn dimer model on a two-dimensional honeycomb lattice. Because of low-temperature inactivity, determination of the lowest-lying excited states allows one to locate the critical temperature. In this paper the second-lowest-lying excited states are studied and exact asymptotic results are obtained in the limit of large lattices. These results together with a finite-size scaling ansatz suggest a logarithmic divergence of the specific heat aboveT c for the three-dimensional model. Use of the same ansatz recovers the exact divergence (α=½) for the two-dimensional model

Energy Loss of a Heavy Fermion in an Anisotropic QED Plasma

We compute the leading-order collisional energy loss of a heavy fermion propagating in a QED plasma with an electron distribution function which is anisotropic in momentum space. We show that in the presence of such anisotropies there can be a significant directional dependence of the heavy fermion energy loss with the effect being quite large for highly-relativistic velocities. We also repeat the analysis of the isotropic case more carefully and show that the final result depends on the intermediate scale used to separate hard and soft contributions to the energy loss. We then show that the canonical isotropic result is obtained in the weak-coupling limit. For intermediate-coupling we use the residual scale dependence as a measure of our theoretical uncertainty. We also discuss complications which could arise due to the presence of unstable soft photonic modes and demonstrate that the calculation of the energy loss is safe.Comment: 19 pages, 18 figures. v2 - Correction to normalization of numerical results; some figures modified as a result; discussion of role of unstable modes added along with two new figure

Air sensitivity of MoS2, MoSe2, MoTe2, HfS2 and HfSe2

A surface sensitivity study was performed on different transition-metal dichalcogenides (TMDs) under ambient conditions in order to understand which material is the most suitable for future device applications. Initially, Atomic Force Microscopy and Scanning Electron Microscopy studies were carried out over a period of 27 days on mechanically exfoliated flakes of 5 different TMDs, namely, MoS2, MoSe2, MoTe2, HfS2, and HfSe2. The most reactive were MoTe2 and HfSe2. HfSe2, in particular, showed surface protrusions after ambient exposure, reaching a height and width of approximately 60 nm after a single day. This study was later supplemented by Transmission Electron Microscopy (TEM) cross-sectional analysis, which showed hemispherical-shaped surface blisters that are amorphous in nature, approximately 180–240 nm tall and 420–540 nm wide, after 5 months of air exposure, as well as surface deformation in regions between these structures, related to surface oxidation. An X-ray photoelectron spectroscopy study of atmosphere exposed HfSe2 was conducted over various time scales, which indicated that the Hf undergoes a preferential reaction with oxygen as compared to the Se. Energy-Dispersive X-Ray Spectroscopy showed that the blisters are Se-rich; thus, it is theorised that HfO2 forms when the HfSe2 reacts in ambient, which in turn causes the Se atoms to be aggregated at the surface in the form of blisters. Overall, it is evident that air contact drastically affects the structural properties of TMD materials. This issue poses one of the biggest challenges for future TMD-based devices and technologies

The Eurace@Unibi Model: An Agent-Based Macroeconomic Model for Economic Policy Analysis

Dawid H, Gemkow S, Harting P, van der Hoog S, Neugart M. The Eurace@Unibi Model: An Agent-Based Macroeconomic Model for Economic Policy Analysis. Working Papers in Economics and Management. Vol 05-2012. Bielefeld: Bielefeld University, Department of Business Administration and Economics; 2012.This document provides a description of the modeling assumptions and economic features of the Eurace@Unibi model. Furthermore, the document shows typical patterns of the output generated by this model and compares it to empirically observable stylized facts. The Eurace@Unibi model provides a representation of a closed macroeconomic model with spatial structure. The main objective is to provide a micro-founded macroeconomic model that can be used as a unified framework for policy analysis in different economic policy areas and for the examination of generic macroeconomic research questions. In spite of this general agenda the model has been constructed with certain specific research questions in mind and therefore certain parts of the model, e.g. the mechanisms driving technological change, have been worked out in more detail than others. The purpose of this document is to give an overview over the model itself and its features rather than discussing how insights into particular economic issues can be obtained using the Eurace@Unibi model. The model has been designed as a framework for economic analysis in various domains of economics. A number of economic issues have been examined using (prior versions of) the model (see Dawid et al. (2008), Dawid et al. (2009), Dawid et al. (2011a), Dawid and Harting (2011), van der Hoog and Deissenberg (2011), Cincotti et al. (2010)) and recent extensions of the model have substantially extended its applicability in various economic policy domains, however results of such policy analyses will be reported elsewhere. Whereas the overall modeling approach, the different modeling choices and the economic rationale behind these choices is discussed in some detail in this document, no detailed description of the implementation is given. Such a detailed documentation is provided in the accompanying document Dawid et al. (2011b)

Polymorphisms near EXOC4 and LRGUK on chromosome 7q32 are associated with Type 2 Diabetes and fasting glucose; The NHLBI Family Heart Study

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

A Genome-Wide Association Study of Pulmonary Function Measures in the Framingham Heart Study

The ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC) is a measure used to diagnose airflow obstruction and is highly heritable. We performed a genome-wide association study in 7,691 Framingham Heart Study participants to identify single-nucleotide polymorphisms (SNPs) associated with the FEV1/FVC ratio, analyzed as a percent of the predicted value. Identified SNPs were examined in an independent set of 835 Family Heart Study participants enriched for airflow obstruction. Four SNPs in tight linkage disequilibrium on chromosome 4q31 were associated with the percent predicted FEV1/FVC ratio with p-values of genome-wide significance in the Framingham sample (best p-value = 3.6e-09). One of the four chromosome 4q31 SNPs (rs13147758; p-value 2.3e-08 in Framingham) was genotyped in the Family Heart Study and produced evidence of association with the same phenotype, percent predicted FEV1/FVC (p-value = 2.0e-04). The effect estimates for association in the Framingham and Family Heart studies were in the same direction, with the minor allele (G) associated with higher FEV1/FVC ratio levels. Results from the Family Heart Study demonstrated that the association extended to FEV1 and dichotomous airflow obstruction phenotypes, particularly among smokers. The SNP rs13147758 was associated with the percent predicted FEV1/FVC ratio in independent samples from the Framingham and Family Heart Studies producing a combined p-value of 8.3e-11, and this region of chromosome 4 around 145.68 megabases was associated with COPD in three additional populations reported in the accompanying manuscript. The associated SNPs do not lie within a gene transcript but are near the hedgehog-interacting protein (HHIP) gene and several expressed sequence tags cloned from fetal lung. Though it is unclear what gene or regulatory effect explains the association, the region warrants further investigation

Proteasome inhibition for treatment of leishmaniasis, Chagas disease and sleeping sickness

Chagas disease, leishmaniasis and sleeping sickness affect 20 million people worldwide and lead to more than 50,000 deaths annually. The diseases are caused by infection with the kinetoplastid parasites Trypanosoma cruzi, Leishmania spp. and Trypanosoma brucei spp., respectively. These parasites have similar biology and genomic sequence, suggesting that all three diseases could be cured with drugs that modulate the activity of a conserved parasite target. However, no such molecular targets or broad spectrum drugs have been identified to date. Here we describe a selective inhibitor of the kinetoplastid proteasome (GNF6702) with unprecedented in vivo efficacy, which cleared parasites from mice in all three models of infection. GNF6702 inhibits the kinetoplastid proteasome through a non-competitive mechanism, does not inhibit the mammalian proteasome or growth of mammalian cells, and is well-tolerated in mice. Our data provide genetic and chemical validation of the parasite proteasome as a promising therapeutic target for treatment of kinetoplastid infections, and underscore the possibility of developing a single class of drugs for these neglected diseases

The Gly2019Ser mutation in LRRK2 is not fully penetrant in familial Parkinson's disease: the GenePD study

<p>Abstract</p> <p>Background</p> <p>We report age-dependent penetrance estimates for leucine-rich repeat kinase 2 (<it>LRRK2</it>)-related Parkinson's disease (PD) in a large sample of familial PD. The most frequently seen <it>LRRK2 </it>mutation, Gly2019Ser (G2019S), is associated with approximately 5 to 6% of familial PD cases and 1 to 2% of idiopathic cases, making it the most common known genetic cause of PD. Studies of the penetrance of <it>LRRK2 </it>mutations have produced a wide range of estimates, possibly due to differences in study design and recruitment, including in particular differences between samples of familial PD versus sporadic PD.</p> <p>Methods</p> <p>A sample, including 903 affected and 58 unaffected members from 509 families ascertained for having two or more PD-affected members, 126 randomly ascertained PD patients and 197 controls, was screened for five different <it>LRRK2 </it>mutations. Penetrance was estimated in families of <it>LRRK2 </it>carriers with consideration of the inherent bias towards increased penetrance in a familial sample.</p> <p>Results</p> <p>Thirty-one out of 509 families with multiple cases of PD (6.1%) were found to have 58 <it>LRRK2 </it>mutation carriers (6.4%). Twenty-nine of the 31 families had G2019S mutations while two had R1441C mutations. No mutations were identified among controls or unaffected relatives of PD cases. Nine PD-affected relatives of G2019S carriers did not carry the <it>LRRK2 </it>mutation themselves. At the maximum observed age range of 90 to 94 years, the unbiased estimated penetrance was 67% for G2019S families, compared with a baseline PD risk of 17% seen in the non-<it>LRRK2</it>-related PD families.</p> <p>Conclusion</p> <p>Lifetime penetrance of <it>LRRK2 </it>estimated in the unascertained relatives of multiplex PD families is greater than that reported in studies of sporadically ascertained <it>LRRK2 </it>cases, suggesting that inherited susceptibility factors may modify the penetrance of <it>LRRK2 </it>mutations. In addition, the presence of nine PD phenocopies in the <it>LRRK2 </it>families suggests that these susceptibility factors may also increase the risk of non-<it>LRRK2</it>-related PD. No differences in penetrance were found between men and women, suggesting that the factors that influence penetrance for <it>LRRK2 </it>carriers are independent of the factors which increase PD prevalence in men.</p