461 research outputs found
Correlations around an interface
We compute one-loop correlation functions for the fluctuations of an
interface using a field theory model. We obtain them from Feynman diagrams
drawn with a propagator which is the inverse of the Hamiltonian of a
Poschl-Teller problem. We derive an expression for the propagator in terms of
elementary functions, show that it corresponds to the usual spectral sum, and
use it to calculate quantities such as the surface tension and interface
profile in two and three spatial dimensions. The three-dimensional quantities
are rederived in a simple, unified manner, whereas those in two dimensions
extend the existing literature, and are applicable to thin films. In addition,
we compute the one-loop self-energy, which may be extracted from experiment, or
from Monte Carlo simulations. Our results may be applied in various scenarios,
which include fluctuations around topological defects in cosmology,
supersymmetric domain walls, Z(N) bubbles in QCD, domain walls in magnetic
systems, interfaces separating Bose-Einstein condensates, and interfaces in
binary liquid mixtures.Comment: RevTeX, 13 pages, 6 figure
Using Topological Statistics to Detect Determinism in Time Series
Statistical differentiability of the measure along the reconstructed
trajectory is a good candidate to quantify determinism in time series. The
procedure is based upon a formula that explicitly shows the sensitivity of the
measure to stochasticity. Numerical results for partially surrogated time
series and series derived from several stochastic models, illustrate the
usefulness of the method proposed here. The method is shown to work also for
high--dimensional systems and experimental time seriesComment: 23 RevTeX pages, 14 eps figures. To appear in Physical Review
Theory of the first-order isostructural valence phase transitions in mixed valence compounds YbIn_{x}Ag_{1-x}Cu_{4}
For describing the first-order isostructural valence phase transition in
mixed valence compounds we develop a new approach based on the lattice Anderson
model. We take into account the Coulomb interaction between localized f and
conduction band electrons and two mechanisms of electron-lattice coupling. One
is related to the volume dependence of the hybridization. The other is related
to local deformations produced by f- shell size fluctuations accompanying
valence fluctuations. The large f -state degeneracy allows us to use the 1/N
expansion method. Within the model we develop a mean-field theory for the
first-order valence phase transition in YbInCu_{4}. It is shown that the
Coulomb interaction enhances the exchange interaction between f and conduction
band electron spins and is the driving force of the phase transition. A
comparison between the theoretical calculations and experimental measurements
of the valence change, susceptibility, specific heat, entropy, elastic
constants and volume change in YbInCu_{4} and YbAgCu_{4} are presented, and a
good quantitative agreement is found. On the basis of the model we describe the
evolution from the first-order valence phase transition to the continuous
transition into the heavy-fermion ground state in the series of compounds
YbIn_{1-x}Ag_{x}Cu_{4}. The effect of pressure on physical properties of
YbInCu_{4} is studied and the H-T phase diagram is found.Comment: 17 pages RevTeX, 9 Postscript figures, to be submitted to Phys.Rev.
An Examination of Chimpanzee Use in Human Cancer Research
Advocates of chimpanzee research claim the genetic similarity of humans and chimpanzees make them an indispensable research tool to combat human diseases. Given that cancer is a leading cause of human death worldwide, one might expect that if chimpanzees were needed for, or were productive in, cancer research, then they would have been widely used. This comprehensive literature analysis reveals that chimpanzees have scarcely been used in any form of cancer research, and that chimpanzee tumours are extremely rare and biologically different from human cancers. Often, chimpanzee citations described peripheral use of chimpanzee cells and genetic material in predominantly human genomic studies. Papers describing potential new cancer therapies noted significant concerns regarding the chimpanzee model. Other studies described interventions that have not been pursued clinically. Finally, available evidence indicates that chimpanzees are not essential in the development of therapeutic monoclonal antibodies. It would therefore be unscientific to claim that chimpanzees are vital to cancer research. On the contrary, it is reasonable to conclude that cancer research would not suffer, if the use of chimpanzees for this purpose were prohibited in the US. Genetic differences between humans and chimpanzees, make them an unsuitable model for cancer, as well as other human diseases
Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction
Published online: 11 September 2023Despite the high prevalence of heart failure in the western world, there are few effective treatments. Fibulin-3 is a protein involved in extracellular matrix (ECM) structural integrity, however its role in the heart is unknown. We have demonstrated, using single cell RNA-seq, that fibulin-3 was highly expressed in quiescent murine cardiac fibroblasts, with expression highest prior to injury and late post-infarct (from ~ day-28 to week-8). In humans, fibulin-3 was upregulated in left ventricular tissue and plasma of heart failure patients. Fibulin-3 knockout (Efemp1-/-) and wildtype mice were subjected to experimental myocardial infarction. Fibulin-3 deletion resulted in significantly higher rate of cardiac rupture days 3-6 post-infarct, indicating a weak and poorly formed scar, with severe ventricular remodelling in surviving mice at day-28 post-infarct. Fibulin-3 knockout mice demonstrated less collagen deposition at day-3 post-infarct, with abnormal collagen fibre-alignment. RNA-seq on day-3 infarct tissue revealed upregulation of ECM degradation and inflammatory genes, but downregulation of ECM assembly/structure/organisation genes in fibulin-3 knockout mice. GSEA pathway analysis showed enrichment of inflammatory pathways and a depletion of ECM organisation pathways. Fibulin-3 originates from cardiac fibroblasts, is upregulated in human heart failure, and is necessary for correct ECM organisation/structural integrity of fibrotic tissue to prevent cardiac rupture post-infarct.Lucy A. Murtha, Sean A. Hardy, Nishani S. Mabotuwana, Mark J. Bigland, Taleah Bailey, Kalyan Raguram, Saifei Liu, Doan T. Ngo, Aaron L. Sverdlov, Tamara Tomin, Ruth Birner, Gruenberger, Robert D. Hume, Siiri E. Iismaa, David T. Humphreys, Ralph Patrick, James J. H. Chong, Randall J. Lee, Richard P. Harvey, Robert M. Graham, Peter P. Rainer and Andrew J. Boyl
Holographic Hydrodynamics with a Chemical Potential
We consider five-dimensional gravity coupled to a negative cosmological
constant and a single U(1) gauge field, including a general set of
four-derivative interactions. In this framework, we construct charged planar
AdS black hole solutions perturbatively and consider the thermal and
hydrodynamic properties of the plasma in the dual CFT. In particular, we
calculate the ratio of shear viscosity to entropy density and argue that the
violation of the KSS bound is enhanced in the presence of a chemical potential.
We also compute the electrical conductivity and comment on various conjectured
bounds related to this coefficient.Comment: v2: comparison to supergravity lagrangian added, references added,
typos fixe
Hybrid Genetic Bees Algorithm applied to Single Machine Scheduling with Earliness and Tardiness Penalties
This paper presents a hybrid Genetic-Bees Algorithm based optimised solution for the single machine scheduling problem. The enhancement of the Bees Algorithm (BA) is conducted using the Genetic Algorithm's (GA's) operators during the global search stage. The proposed enhancement aims to increase the global search capability of the BA gradually with new additions. Although the BA has very successful implementations on various type of optimisation problems, it has found that the algorithm suffers from weak global search ability which increases the computational complexities on NP-hard type optimisation problems e.g. combinatorial/permutational type optimisation problems. This weakness occurs due to using a simple global random search operation during the search process. To reinforce the global search process in the BA, the proposed enhancement is utilised to increase exploration capability by expanding the number of fittest solutions through the genetical variations of promising solutions. The hybridisation process is realised by including two strategies into the basic BA, named as â\u80\u9creinforced global searchâ\u80\u9d and â\u80\u9cjumping functionâ\u80\u9d strategies. The reinforced global search strategy is the first stage of the hybridisation process and contains the mutation operator of the GA. The second strategy, jumping function strategy, consists of four GA operators as single point crossover, multipoint crossover, mutation and randomisation. To demonstrate the strength of the proposed solution, several experiments were carried out on 280 well-known single machine benchmark instances, and the results are presented by comparing to other well-known heuristic algorithms. According to the experiments, the proposed enhancements provides better capability to basic BA to jump from local minima, and GBA performed better compared to BA in terms of convergence and the quality of results. The convergence time reduced about 60% with about 30% better results for highly constrained jobs
Of Research reviews and practice guides: Translating rapidly growing research on adolescent literacy into updated practice recommendations.
The demand for evidence-based instructional practices has driven a large
supply of research on adolescent literacy. Documenting this supply, Baye,
Inns, Lake, and Slavin’s 2019 article in Reading Research Quarterly synthesized
far more studies, with far more rigorous methodology, than had ever
been collected before. What does this mean for practice? Inspired by this article,
I investigated how this synthesis compared with the 2008 U.S. Institute of
Education Sciences practice guide for adolescent literacy. I also include two
contemporary documents for context: Herrera, Truckenmiller, and Foorman’s
(2016) review and the U.K. Education Endowment Foundation’s 2019 practice
guide for secondary schools. I first examine how these documents define
adolescent, reading, and evidence, and propose more inclusive definitions. I
then compare their respective evidence bases, finding that the quality and
quantity of evidence have dramatically changed. Only one of the 34 studies in
the 2008 U.S. practice guide met Baye et al.’s inclusion criteria in 2019, and
the average sample size in Baye et al.’s studies was 22 times as large as those
in the 2008 U.S. practice guide. I also examine the potential implications for
a new practice guide’s instructional recommendations and comment on the
expansion of research in technology, disciplinary literacy, and writing—topics
scarcely covered in the 2008 U.S. practice guide but which have been extensively
researched since then. Finally, I call for revision of the U.S. practice
guide and the establishment of standing committees on adolescent literacy to
help educators translate the latest research findings into updated practices
Genetic loci regulate Sarbecovirus pathogenesis: A comparison across mice and humans
Coronavirus (CoV) cause considerable morbidity and mortality in humans and other mammals, as evidenced by the emergence of Severe Acute Respiratory CoV (SARS-CoV) in 2003, Middle East Respiratory CoV (MERS-CoV) in 2012, and SARS-CoV-2 in 2019. Although poorly characterized, natural genetic variation in human and other mammals modulate virus pathogenesis, as reflected by the spectrum of clinical outcomes ranging from asymptomatic infections to lethal disease. Using multiple human epidemic and zoonotic Sarbecoviruses, coupled with murine Collaborative Cross genetic reference populations, we identify several dozen quantitative trait loci that regulate SARS-like group-2B CoV pathogenesis and replication. Under a Chr4 QTL, we deleted a candidate interferon stimulated gene, Trim14 which resulted in enhanced SARS-CoV titers and clinical disease, suggesting an antiviral role during infection. Importantly, about 60 % of the murine QTL encode susceptibility genes identified as priority candidates from human genome-wide association studies (GWAS) studies after SARS-CoV-2 infection, suggesting that similar selective forces have targeted analogous genes and pathways to regulate Sarbecovirus disease across diverse mammalian hosts. These studies provide an experimental platform in rodents to investigate the molecular-genetic mechanisms by which potential cross mammalian susceptibility loci and genes regulate type-specific and cross-SARS-like group 2B CoV replication, immunity, and pathogenesis in rodent models. Our study also provides a paradigm for identifying susceptibility loci for other highly heterogeneous and virulent viruses that sporadically emerge from zoonotic reservoirs to plague human and animal populations
A Multitrait Locus Regulates Sarbecovirus Pathogenesis
Infectious diseases have shaped the human population genetic structure, and genetic variation influences the susceptibility to many viral diseases. However, a variety of challenges have made the implementation of traditional human Genomewide Association Studies (GWAS) approaches to study these infectious outcomes challenging. In contrast, mouse models of infectious diseases provide an experimental control and precision, which facilitates analyses and mechanistic studies of the role of genetic variation on infection. Here we use a genetic mapping cross between two distinct Collaborative Cross mouse strains with respect to severe acute respiratory syndrome coronavirus (SARS-CoV) disease outcomes. We find several loci control differential disease outcome for a variety of traits in the context of SARS-CoV infection. Importantly, we identify a locus on mouse chromosome 9 that shows conserved synteny with a human GWAS locus for SARS-CoV-2 severe disease. We follow-up and confirm a role for this locus, and identify two candidate genes, CCR9 and CXCR6, that both play a key role in regulating the severity of SARS-CoV, SARS-CoV-2, and a distantly related bat sarbecovirus disease outcomes. As such we provide a template for using experimental mouse crosses to identify and characterize multitrait loci that regulate pathogenic infectious outcomes across species. IMPORTANCE Host genetic variation is an important determinant that predicts disease outcomes following infection. In the setting of highly pathogenic coronavirus infections genetic determinants underlying host susceptibility and mortality remain unclear. To elucidate the role of host genetic variation on sarbecovirus pathogenesis and disease outcomes, we utilized the Collaborative Cross (CC) mouse genetic reference population as a model to identify susceptibility alleles to SARS-CoV and SARS-CoV-2 infections. Our findings reveal that a multitrait loci found in chromosome 9 is an important regulator of sarbecovirus pathogenesis in mice. Within this locus, we identified and validated CCR9 and CXCR6 as important regulators of host disease outcomes. Specifically, both CCR9 and CXCR6 are protective against severe SARS-CoV, SARS-CoV-2, and SARS-related HKU3 virus disease in mice. This chromosome 9 multitrait locus may be important to help identify genes that regulate coronavirus disease outcomes in humans
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