42,070 research outputs found

    Random pinning limits the size of membrane adhesion domains

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    Theoretical models describing specific adhesion of membranes predict (for certain parameters) a macroscopic phase separation of bonds into adhesion domains. We show that this behavior is fundamentally altered if the membrane is pinned randomly due to, e.g., proteins that anchor the membrane to the cytoskeleton. Perturbations which locally restrict membrane height fluctuations induce quenched disorder of the random-field type. This rigorously prevents the formation of macroscopic adhesion domains following the Imry-Ma argument [Y. Imry and S. K. Ma, Phys. Rev. Lett. 35, 1399 (1975)]. Our prediction of random-field disorder follows from analytical calculations, and is strikingly confirmed in large-scale Monte Carlo simulations. These simulations are based on an efficient composite Monte Carlo move, whereby membrane height and bond degrees of freedom are updated simultaneously in a single move. The application of this move should prove rewarding for other systems also.Comment: revised and extended versio

    Collapse and revival oscillations as a probe for the tunneling amplitude in an ultra-cold Bose gas

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    We present a theoretical study of the quantum corrections to the revival time due to finite tunneling in the collapse and revival of matter wave interference after a quantum quench. We study hard-core bosons in a superlattice potential and the Bose-Hubbard model by means of exact numerical approaches and mean-field theory. We consider systems without and with a trapping potential present. We show that the quantum corrections to the revival time can be used to accurately determine the value of the hopping parameter in experiments with ultracold bosons in optical lattices.Comment: 10 pages, 12 figures, typos in section 3A correcte

    Renormalization and resummation in finite temperature field theories

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    Resummation, ie. reorganization of perturbative series, can result in an inconsistent perturbation theory, unless the counterterms are reorganized in an appropriate way. In this paper two methods are presented for resummation of counterterms: one is a direct method where the necessary counterterms are constructed order by order; the other is a general one, based on renormalization group arguments. We demonstrate at one hand that, in mass independent schemes, mass resummation can be performed by gap equations renormalized prior to the substitution of the resummed mass for its argument. On the other hand it is shown that any (momentum-independent) form of mass and coupling constant resummation is compatible with renormalization, and one can explicitly construct the corresponding counterterms.Comment: 10 pages, 4 figures, revtex

    Anomalous Pinning Fields in Helical Magnets: Screening of the Quasiparticle Interaction

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    The spin-orbit interaction strength g_so in helical magnets determines both the pitch wave number q and the critical field H_c1 where the helix aligns with an external magnetic field. Within a standard Landau-Ginzburg-Wilson (LGW) theory, a determination of g_so in MnSi and FeGe from these two observables yields values that differ by a factor of 20. This discrepancy is remedied by considering the fermionic theory underlying the LGW theory, and in particular the effects of screening on the effective electron-electron interaction that results from an exchange of helical fluctuations.Comment: 4pp, 2 fig

    Post-Impact Thermal Evolution of Porous Planetesimals

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    Impacts between planetesimals have largely been ruled out as a heat source in the early Solar System, by calculations that show them to be an inefficient heat source and unlikely to cause global heating. However, the long-term, localized thermal effects of impacts on planetesimals have never been fully quantified. Here, we simulate a range of impact scenarios between planetesimals to determine the post-impact thermal histories of the parent bodies, and hence the importance of impact heating in the thermal evolution of planetesimals. We find on a local scale that heating material to petrologic type 6 is achievable for a range of impact velocities and initial porosities, and impact melting is possible in porous material at a velocity of > 4 km/s. Burial of heated impactor material beneath the impact crater is common, insulating that material and allowing the parent body to retain the heat for extended periods (~ millions of years). Cooling rates at 773 K are typically 1 - 1000 K/Ma, matching a wide range of measurements of metallographic cooling rates from chondritic materials. While the heating presented here is localized to the impact site, multiple impacts over the lifetime of a parent body are likely to have occurred. Moreover, as most meteorite samples are on the centimeter to meter scale, the localized effects of impact heating cannot be ignored.Comment: 38 pages, 9 figures, Revised for Geochimica et Cosmochimica Acta (Sorry, they do not accept LaTeX

    Local and global persistence exponents of two quenched continuous lattice spin models

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    Local and global persistence exponents associated with zero temperature quenched dynamics of two dimensional XY model and three dimensional Heisenberg model have been estimated using numerical simulations. We have used the method of block persistence to find both global and local exponents simultaneously (in a single simulation). Temperature universality of both the exponents for three dimensional Heisenberg model has been confirmed by simulating the stochastic (with noise) version of the equation of motion. The noise amplitudes added were small enough to retain the dynamics below criticality. In the second part of our work we have studied scaling associated with correlated persistence sites in the three dimensional Heisenberg model in the later stages of the dynamics. The relevant length scale associated with correlated persistent sites was found to behave in a manner similar to the dynamic length scale associated with the phase ordering dynamics.Comment: 20 pages, 7 figure

    Nutrient supply affects the mRNA expression profile of the porcine skeletal muscle

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    Background: The genetic basis of muscle fat deposition in pigs is not well known. So far, we have only identified a limited number of genes involved in the absorption, transport, storage and catabolism of lipids. Such information is crucial to interpret, from a biological perspective, the results of genome-wide association analyses for intramuscular fat content and composition traits. Herewith, we have investigated how the ingestion of food changes gene expression in the gluteus medius muscle of Duroc pigs. Results: By comparing the muscle mRNA expression of fasted pigs (T0) with that of pigs sampled 5 h (T1) and 7 h (T2) after food intake, we have detected differential expression (DE) for 148 (T0-T1), 520 (T0-T2) and 135 (T1-T2) genes (q-value of 1.5). Many of these DE genes were transcription factors, suggesting that we have detected the coordinated response of the skeletal muscle to nutrient supply. We also found DE genes with a dual role in oxidative stress and angiogenesis (THBS1, THBS2 and TXNIP), two biological processes that are probably activated in the post-prandial state. Finally, we have identified several loci playing a key role in the modulation of circadian rhythms (ARNTL, PER1, PER2, BHLHE40, NR1D1, SIK1, CIART and CRY2), a result that indicates that the porcine muscle circadian clock is modulated by nutrition. Conclusion: We have shown that hundreds of genes change their expression in the porcine skeletal muscle in response to nutrient intake. Many of these loci do not have a known metabolic role, a result that suggests that our knowledge about the genetic basis of muscle energy homeostasis is still incomplete

    Identification of novel Y chromosome encoded transcripts by testis transcriptome analysis of mice with deletions of the Y chromosome long arm.

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    BACKGROUND: The male-specific region of the mouse Y chromosome long arm (MSYq) is comprised largely of repeated DNA, including multiple copies of the spermatid-expressed Ssty gene family. Large deletions of MSYq are associated with sperm head defects for which Ssty deficiency has been presumed to be responsible. RESULTS: In a search for further candidate genes associated with these defects we analyzed changes in the testis transcriptome resulting from MSYq deletions, using testis cDNA microarrays. This approach, aided by accumulating mouse MSYq sequence information, identified transcripts derived from two further spermatid-expressed multicopy MSYq gene families; like Ssty, each of these new MSYq gene families has multicopy relatives on the X chromosome. The Sly family encodes a protein with homology to the chromatin-associated proteins XLR and XMR that are encoded by the X chromosomal relatives. The second MSYq gene family was identified because the transcripts hybridized to a microarrayed X chromosome-encoded testis cDNA. The X loci ('Astx') encoding this cDNA had 92-94% sequence identity to over 100 putative Y loci ('Asty') across exons and introns; only low level Asty transcription was detected. More strongly transcribed recombinant loci were identified that included Asty exons 2-4 preceded by Ssty1 exons 1, 2 and part of exon 3. Transcription from the Ssty1 promotor generated spermatid-specific transcripts that, in addition to the variable inclusion of Ssty1 and Asty exons, included additional exons because of the serendipitous presence of splice sites further downstream. CONCLUSION: We identified further MSYq-encoded transcripts expressed in spermatids and deriving from multicopy Y genes, deficiency of which may underlie the defects in sperm development associated with MSYq deletions.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    Mining the LIPG Allelic Spectrum Reveals the Contribution of Rare and Common Regulatory Variants to HDL Cholesterol

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    Genome-wide association studies (GWAS) have successfully identified loci associated with quantitative traits, such as blood lipids. Deep resequencing studies are being utilized to catalogue the allelic spectrum at GWAS loci. The goal of these studies is to identify causative variants and missing heritability, including heritability due to low frequency and rare alleles with large phenotypic impact. Whereas rare variant efforts have primarily focused on nonsynonymous coding variants, we hypothesized that noncoding variants in these loci are also functionally important. Using the HDL-C gene LIPG as an example, we explored the effect of regulatory variants identified through resequencing of subjects at HDL-C extremes on gene expression, protein levels, and phenotype. Resequencing a portion of the LIPG promoter and 5′ UTR in human subjects with extreme HDL-C, we identified several rare variants in individuals from both extremes. Luciferase reporter assays were used to measure the effect of these rare variants on LIPG expression. Variants conferring opposing effects on gene expression were enriched in opposite extremes of the phenotypic distribution. Minor alleles of a common regulatory haplotype and noncoding GWAS SNPs were associated with reduced plasma levels of the LIPG gene product endothelial lipase (EL), consistent with its role in HDL-C catabolism. Additionally, we found that a common nonfunctional coding variant associated with HDL-C (rs2000813) is in linkage disequilibrium with a 5′ UTR variant (rs34474737) that decreases LIPG promoter activity. We attribute the gene regulatory role of rs34474737 to the observed association of the coding variant with plasma EL levels and HDL-C. Taken together, the findings show that both rare and common noncoding regulatory variants are important contributors to the allelic spectrum in complex trait loci
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