Monte Carlo simulations of 2d hard core lattice gases

Monte Carlo simulations are used to study lattice gases of particles with extended hard cores on a two dimensional square lattice. Exclusions of one and up to five nearest neighbors (NN) are considered. These can be mapped onto hard squares of varying side length, $\lambda$ (in lattice units), tilted by some angle with respect to the original lattice. In agreement with earlier studies, the 1NN exclusion undergoes a continuous order-disorder transition in the Ising universality class. Surprisingly, we find that the lattice gas with exclusions of up to second nearest neighbors (2NN) also undergoes a continuous phase transition in the Ising universality class, while the Landau-Lifshitz theory predicts that this transition should be in the universality class of the XY model with cubic anisotropy. The lattice gas of 3NN exclusions is found to undergo a discontinuous order-disorder transition, in agreement with the earlier transfer matrix calculations and the Landau-Lifshitz theory. On the other hand, the gas of 4NN exclusions once again exhibits a continuous phase transition in the Ising universality class -- contradicting the predictions of the Landau-Lifshitz theory. Finally, the lattice gas of 5NN exclusions is found to undergo a discontinuous phase transition.Comment: 13 pages, lots of figure

Evolution of vacancy-related defects upon annealing of ion-implanted germanium

Positron annihilation spectroscopy was used to study defects created during the ion implantation and annealing of Ge. Ge and Si ions with energies from 600 keV to 2 MeV were implanted at fluences between 1×10 exp 12 cm exp−2 and 4×10 exp 14 cm exp−2. Ion channeling measurements on as-implanted samples show considerable lattice damage at a fluence of 1×10 exp 13 cm exp −2 and a fluence of 1×10 exp 14 cm exp -2 was enough to amorphize the samples. Positron experiments reveal that the average free volume in as-irradiated samples is of divacancy size. Larger vacancy clusters are formed during regrowth of the damaged layers when the samples are annealed in the temperature range 200–400 °C. Evolution of the vacancy-related defects upon annealing depends noticeably on fluence of ion implantation and for the highest fluences also on ion species.Peer reviewe

Eight decades of adaptive changes in herring reproductive investment: the joint effect of environment and exploitation

publishedVersio

Vacancy generation in liquid phase epitaxy of Si

Concerted experiments and theoretical analysis are applied to conclusively demonstrate the vacancy generation during fast melting and regrowth of Si by laser irradiation. Experiments, based on the positron annihilation spectroscopy and designed to test the theoretical predictions, evidence a vacancy supersaturation after the laser process depending on the irradiation conditions. Stochastic atomistic simulations of the molten Si recrystallization show trapping of vacancies in the recrystallized region. Finally, continuum phase-field simulations of the full process, calibrated using the Monte Carlo results, show a defect evolution in close agreement with the experiments.Peer reviewe

Phenomenological model for the remanent magnetization of dilute quasi-one-dimensional antiferromagnets

We present a phenomenological model for the remanent magnetization at low temperatures in the quasi-one-dimensional dilute antiferromagnets CH_{3}NH_{3}Mn_{1-x}Cd_{x} Cl_{3}\cdot 2H_{2}O and (CH_{3})_{2}NH_{2}Mn_{1-x}Cd_{x}Cl_{3}\cdot 2H_{2}O. The model assumes the existence of uncompensated magnetic moments induced in the odd-sized segments generated along the Mn(^{2+}) chains upon dilution. These moments are further assumed to correlate ferromagnetically after removal of a cooling field. Using a (mean-field) linear-chain approximation and reasonable set of model parameters, we are able to reproduce the approximate linear temperature dependence observed for the remanent magnetization in the real compounds.Comment: 5 pages, 2 figures; final version to appear in Physical Review

Genetic basis and timing of a major mating system shift in Capsella

YesA crucial step in the transition from outcrossing to self-fertilization is the loss of genetic self-incompatibility (SI). In the Brassicaceae, SI involves the interaction of female and male speci-ficity components, encoded by the genesSRKandSCRat the self-incompatibility locus (S-lo-cus). Theory predicts thatS-linked mutations, and especially dominant mutations inSCR, arelikely to contribute to loss of SI. However, few studies have investigated the contribution ofdominant mutations to loss of SI in wild plant species. Here, we investigate the genetic basis of loss of SI in the self-fertilizing crucifer speciesCapsella orientalis, by combining genetic mapping, long-read sequencing of completeS-hap-lotypes, gene expression analyses and controlled crosses. We show that loss of SI inC. orientalisoccurred<2.6 Mya and maps as a dominant trait totheS-locus. We identify a fixed frameshift deletion in the male specificity geneSCRand con-firm loss of male SI specificity. We further identify anS-linked small RNA that is predicted tocause dominance of self-compatibility. Our results agree with predictions on the contribution of dominantS-linked mutations toloss of SI, and thus provide new insights into the molecular basis of mating system transitions.Work at Uppsala Genome Center is funded by 550 RFI / VR and Science for Life Laboratory, Sweden. The SNP&SEQ Platform is supported by 551 the Swedish Research Council and the Knut and Alice Wallenberg Foundation. V.C. 552 acknowledges support by a grant from the European Research Council (NOVEL project, 553 grant #648321). The authors thank the French Ministère de l’Enseignement Supérieur et de la 554 Recherche, the Hauts de France Region and the European Funds for Regional Economical 555 Development for their financial support to this project. This work was supported by a grant 556 from the Swedish Research Council (grant #D0432001) and by a grant from the Science for 557 Life Laboratory, Swedish Biodiversity Program to T.S. The Swedish Biodiversity Program is 558 supported by the Knut and Alice Wallenberg Foundation

CUP-1 Is a Novel Protein Involved in Dietary Cholesterol Uptake in Caenorhabditis elegans

Sterols transport and distribution are essential processes in all multicellular organisms. Survival of the nematode Caenorhabditis elegans depends on dietary absorption of sterols present in the environment. However the general mechanisms associated to sterol uptake in nematodes are poorly understood. In the present work we provide evidence showing that a previously uncharacterized transmembrane protein, designated Cholesterol Uptake Protein-1 (CUP-1), is involved in dietary cholesterol uptake in C. elegans. Animals lacking CUP-1 showed hypersensitivity to cholesterol limitation and were unable to uptake cholesterol. A CUP-1-GFP fusion protein colocalized with cholesterol-rich vesicles, endosomes and lysosomes as well as the plasma membrane. Additionally, by FRET imaging, a direct interaction was found between the cholesterol analog DHE and the transmembrane “cholesterol recognition/interaction amino acid consensus” (CRAC) motif present in C. elegans CUP-1. In-silico analysis identified two mammalian homologues of CUP-1. Most interestingly, CRAC motifs are conserved in mammalian CUP-1 homologous. Our results suggest a role of CUP-1 in cholesterol uptake in C. elegans and open up the possibility for the existence of a new class of proteins involved in sterol absorption in mammals

Sphingomyelin Functions as a Novel Receptor for Helicobacter pylori VacA

The vacuolating cytotoxin (VacA) of the gastric pathogen Helicobacter pylori binds and enters epithelial cells, ultimately resulting in cellular vacuolation. Several host factors have been reported to be important for VacA function, but none of these have been demonstrated to be essential for toxin binding to the plasma membrane. Thus, the identity of cell surface receptors critical for both toxin binding and function has remained elusive. Here, we identify VacA as the first bacterial virulence factor that exploits the important plasma membrane sphingolipid, sphingomyelin (SM), as a cellular receptor. Depletion of plasma membrane SM with sphingomyelinase inhibited VacA-mediated vacuolation and significantly reduced the sensitivity of HeLa cells, as well as several other cell lines, to VacA. Further analysis revealed that SM is critical for VacA interactions with the plasma membrane. Restoring plasma membrane SM in cells previously depleted of SM was sufficient to rescue both toxin vacuolation activity and plasma membrane binding. VacA association with detergent-resistant membranes was inhibited in cells pretreated with SMase C, indicating the importance of SM for VacA association with lipid raft microdomains. Finally, VacA bound to SM in an in vitro ELISA assay in a manner competitively inhibited by lysenin, a known SM-binding protein. Our results suggest a model where VacA may exploit the capacity of SM to preferentially partition into lipid rafts in order to access the raft-associated cellular machinery previously shown to be required for toxin entry into host cells