123 research outputs found
Kinetics in one-dimensional lattice gas and Ising models from time-dependent density functional theory
Time-dependent density functional theory, proposed recently in the context of
atomic diffusion and non-equilibrium processes in solids, is tested against
Monte Carlo simulation. In order to assess the basic approximation of that
theory, the representation of non-equilibrium states by a local equilibrium
distribution function, we focus on one-dimensional lattice models, where all
equilibrium properties can be worked exactly from the known free energy as a
functional of the density. This functional determines the thermodynamic driving
forces away from equilibrium. In our studies of the interfacial kinetics of
atomic hopping and spin relaxation, we find excellent agreement with
simulations, suggesting that the method is useful also for treating more
complex problems.Comment: 8 pages, 5 figures, submitted to Phys. Rev.
Time-Dependent Density Functional Theory for Driven Lattice Gas Systems with Interactions
We present a new method to describe the kinetics of driven lattice gases with
particle-particle interactions beyond hard-core exclusions. The method is based
on the time-dependent density functional theory for lattice systems and allows
one to set up closed evolution equations for mean site occupation numbers in a
systematic manner. Application of the method to a totally asymmetric site
exclusion process with nearest-neighbor interactions yields predictions for the
current-density relation in the bulk, the phase diagram of non-equilibrium
steady states and the time evolution of density profiles that are in good
agreement with results from kinetic Monte Carlo simulations.Comment: 11 pages, 3 figure
Cluster density functional theory for lattice models based on the theory of Mobius functions
Rosenfeld's fundamental measure theory for lattice models is given a rigorous
formulation in terms of the theory of Mobius functions of partially ordered
sets. The free-energy density functional is expressed as an expansion in a
finite set of lattice clusters. This set is endowed a partial order, so that
the coefficients of the cluster expansion are connected to its Mobius function.
Because of this, it is rigorously proven that a unique such expansion exists
for any lattice model. The low-density analysis of the free-energy functional
motivates a redefinition of the basic clusters (zero-dimensional cavities)
which guarantees a correct zero-density limit of the pair and triplet direct
correlation functions. This new definition extends Rosenfeld's theory to
lattice model with any kind of short-range interaction (repulsive or
attractive, hard or soft, one- or multi-component...). Finally, a proof is
given that these functionals have a consistent dimensional reduction, i.e. the
functional for dimension d' can be obtained from that for dimension d (d'<d) if
the latter is evaluated at a density profile confined to a d'-dimensional
subset.Comment: 21 pages, 2 figures, uses iopart.cls, as well as diagrams.sty
(included
Fundamental measure theory for lattice fluids with hard core interactions
We present the extension of Rosenfeld's fundamental measure theory to lattice
models by constructing a density functional for d-dimensional mixtures of
parallel hard hypercubes on a simple hypercubic lattice. The one-dimensional
case is exactly solvable and two cases must be distinguished: all the species
with the same lebgth parity (additive mixture), and arbitrary length parity
(nonadditive mixture). At the best of our knowledge, this is the first time
that the latter case is considered. Based on the one-dimensional exact
functional form, we propose the extension to higher dimensions by generalizing
the zero-dimensional cavities method to lattice models. This assures the
functional to have correct dimensional crossovers to any lower dimension,
including the exact zero-dimensional limit. Some applications of the functional
to particular systems are also shown.Comment: 22 pages, 7 figures, needs IOPP LaTeX styles file
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Immunogenicity of chimeric haemagglutinin-based, universal influenza virus vaccine candidates: interim results of a randomised, placebo-controlled, phase 1 clinical trial.
BackgroundInfluenza viruses cause substantial annual morbidity and mortality globally. Current vaccines protect against influenza only when well matched to the circulating strains. However, antigenic drift can cause considerable mismatches between vaccine and circulating strains, substantially reducing vaccine effectiveness. Moreover, current seasonal vaccines are ineffective against pandemic influenza, and production of a vaccine matched to a newly emerging virus strain takes months. Therefore, there is an unmet medical need for a broadly protective influenza virus vaccine. We aimed to test the ability of chimeric H1 haemagglutinin-based universal influenza virus vaccine candidates to induce broadly cross-reactive antibodies targeting the stalk domain of group 1 haemagglutinin-expressing influenza viruses.MethodsWe did a randomised, observer-blinded, phase 1 study in healthy adults in two centres in the USA. Participants were randomly assigned to one of three prime-boost, chimeric haemagglutinin-based vaccine regimens or one of two placebo groups. The vaccine regimens included a chimeric H8/1, intranasal, live-attenuated vaccine on day 1 followed by a non-adjuvanted, chimeric H5/1, intramuscular, inactivated vaccine on day 85; the same regimen but with the inactivated vaccine being adjuvanted with AS03; and an AS03-adjuvanted, chimeric H8/1, intramuscular, inactivated vaccine followed by an AS03-adjuvanted, chimeric H5/1, intramuscular, inactivated vaccine. In this planned interim analysis, the primary endpoints of reactogenicity and safety were assessed by blinded study group. We also assessed anti-H1 haemagglutinin stalk, anti-H2, anti-H9, and anti-H18 IgG antibody titres and plasmablast and memory B-cell responses in peripheral blood. This trial is registered with ClinicalTrials.gov, number NCT03300050.FindingsBetween Oct 10, 2017, and Nov 27, 2017, 65 participants were enrolled and randomly assigned. The adjuvanted inactivated vaccine, but not the live-attenuated vaccine, induced a substantial serum IgG antibody response after the prime immunisation, with a seven times increase in anti-H1 stalk antibody titres on day 29. After boost immunisation, all vaccine regimens induced detectable anti-H1 stalk antibody (2·2-5·6 times induction over baseline), cross-reactive serum IgG antibody, and peripheral blood plasmablast responses. An unsolicited adverse event was reported for 29 (48%) of 61 participants. Solicited local adverse events were reported in 12 (48%) of 25 participants following prime vaccination with intramuscular study product or placebo, in 12 (33%) of 36 after prime immunisation with intranasal study product or placebo, and in 18 (32%) of 56 following booster doses of study product or placebo. Solicited systemic adverse events were reported in 14 (56%) of 25 after prime immunisation with intramuscular study product or placebo, in 22 (61%) of 36 after immunisation with intranasal study product or placebo, and in 21 (38%) of 56 after booster doses of study product or placebo. Disaggregated safety data were not available at the time of this interim analysis.InterpretationThe tested chimeric haemagglutinin-based, universal influenza virus vaccine regimens elicited cross-reactive serum IgG antibodies that targeted the conserved haemagglutinin stalk domain. This is the first proof-of-principle study to show that high anti-stalk titres can be induced by a rationally designed vaccine in humans and opens up avenues for further development of universal influenza virus vaccines. On the basis of the blinded study group, the vaccine regimens were tolerable and no safety concerns were observed.FundingBill & Melinda Gates Foundation
Mutations with epigenetic effects in myeloproliferative neoplasms and recent progress in treatment: Proceedings from the 5th International Post-ASH Symposium
Immediately following the 2010 annual American Society of Hematology (ASH) meeting, the 5th International Post-ASH Symposium on Chronic Myelogenous Leukemia and BCR-ABL1-Negative Myeloproliferative Neoplasms (MPNs) took place on 7–8 December 2010 in Orlando, Florida, USA. During this meeting, the most recent advances in laboratory research and clinical practice, including those that were presented at the 2010 ASH meeting, were discussed among recognized authorities in the field. The current paper summarizes the proceedings of this meeting in BCR-ABL1-negative MPN. We provide a detailed overview of new mutations with putative epigenetic effects (TET oncogene family member 2 (TET2), additional sex comb-like 1 (ASXL1), isocitrate dehydrogenase (IDH) and enhancer of zeste homolog 2 (EZH2)) and an update on treatment with Janus kinase (JAK) inhibitors, pomalidomide, everolimus, interferon-α, midostaurin and cladribine. In addition, the new ‘Dynamic International Prognostic Scoring System (DIPSS)-plus' prognostic model for primary myelofibrosis (PMF) and the clinical relevance of distinguishing essential thrombocythemia from prefibrotic PMF are discussed
How I treat splenomegaly in myelofibrosis
Symptomatic splenomegaly, a frequent manifestation of myelofibrosis (MF), represents a therapeutic challenge. It is frequently accompanied by constitutional symptoms and by anemia or other cytopenias, which make treatment difficult, as the latter are often worsened by most current therapies. Cytoreductive treatment, usually hydroxyurea, is the first-line therapy, being effective in around 40% of the patients, although the effect is often short lived. The immunomodulatory drugs, such as thalidomide or lenalidomide, rarely show a substantial activity in reducing the splenomegaly. Splenectomy can be considered in patients refractory to drug treatment, but the procedure involves substantial morbidity as well as a certain mortality risk and, therefore, patient selection is important. For patients not eligible for splenectomy, transient relief of the symptoms can be obtained with local radiotherapy that, in turn, can induce severe and long-lasting cytopenias. Allogeneic hemopoietic stem cell transplantation is the only treatment with the potential for curing MF but, due to its associated morbidity and mortality, is usually restricted to a minority of patients with poor risk features. A new class of drugs, the JAK2 inhibitors, although also palliative, are promising in the splenomegaly of MF and will probably change the therapeutic algorithm of this disease
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