117 research outputs found
From nonwetting to prewetting: the asymptotic behavior of 4He drops on alkali substrates
We investigate the spreading of 4He droplets on alkali surfaces at zero
temperature, within the frame of Finite Range Density Functional theory. The
equilibrium configurations of several 4He_N clusters and their asymptotic trend
with increasing particle number N, which can be traced to the wetting behavior
of the quantum fluid, are examined for nanoscopic droplets. We discuss the size
effects, inferring that the asymptotic properties of large droplets correspond
to those of the prewetting film
Stability of the monoclinic phase in the ferroelectric perovskite PbZr(1-x)TixO3
Recent structural studies of ferroelectric PbZr(1-x)TixO3 (PZT) with x= 0.48,
have revealed a new monoclinic phase in the vicinity of the morphotropic phase
boundary (MPB), previously regarded as the the boundary separating the
rhombohedral and tetragonal regions of the PZT phase diagram. In the present
paper, the stability region of all three phases has been established from high
resolution synchrotron x-ray powder diffraction measurements on a series of
highly homogeneous samples with 0.42 <=x<= 0.52. At 20K the monoclinic phase is
stable in the range 0.46 <=x<= 0.51, and this range narrows as the temperature
is increased. A first-order phase transition from tetragonal to rhombohedral
symmetry is observed only for x= 0.45. The MPB, therefore, corresponds not to
the tetragonal-rhombohedral phase boundary, but instead to the boundary between
the tetragonal and monoclinic phases for 0.46 <=x<= 0.51. This result provides
important insight into the close relationship between the monoclinic phase and
the striking piezoelectric properties of PZT; in particular, investigations of
poled samples have shown that the monoclinic distortion is the origin of the
unusually high piezoelectric response of PZT.Comment: REVTeX file, 7 figures embedde
Monte Carlo Methods for Estimating Interfacial Free Energies and Line Tensions
Excess contributions to the free energy due to interfaces occur for many
problems encountered in the statistical physics of condensed matter when
coexistence between different phases is possible (e.g. wetting phenomena,
nucleation, crystal growth, etc.). This article reviews two methods to estimate
both interfacial free energies and line tensions by Monte Carlo simulations of
simple models, (e.g. the Ising model, a symmetrical binary Lennard-Jones fluid
exhibiting a miscibility gap, and a simple Lennard-Jones fluid). One method is
based on thermodynamic integration. This method is useful to study flat and
inclined interfaces for Ising lattices, allowing also the estimation of line
tensions of three-phase contact lines, when the interfaces meet walls (where
"surface fields" may act). A generalization to off-lattice systems is described
as well.
The second method is based on the sampling of the order parameter
distribution of the system throughout the two-phase coexistence region of the
model. Both the interface free energies of flat interfaces and of (spherical or
cylindrical) droplets (or bubbles) can be estimated, including also systems
with walls, where sphere-cap shaped wall-attached droplets occur. The
curvature-dependence of the interfacial free energy is discussed, and estimates
for the line tensions are compared to results from the thermodynamic
integration method. Basic limitations of all these methods are critically
discussed, and an outlook on other approaches is given
Comparative Analysis of Calcineurin Inhibitor-Based Methotrexate and Mycophenolate Mofetil-Containing Regimens for Prevention of Graft-versus-Host Disease after Reduced-Intensity Conditioning Allogeneic Transplantation
The combination of a calcineurin inhibitor (CNI) such as tacrolimus (TAC) or cyclosporine (CYSP) with methotrexate (MTX) or with mycophenolate mofetil (MMF) has been commonly used for graft-versus-host disease (GVHD) prophylaxis after reduced-intensity conditioning (RIC) allogeneic hematopoietic cell transplantation (alloHCT), but there are limited data comparing efficacy of the 2 regimens. We evaluated 1564 adult patients who underwent RIC alloHCT for acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), and myelodysplastic syndrome (MDS) from 2000 to 2013 using HLA-identical sibling (matched related donor [MRD]) or unrelated donor (URD) peripheral blood graft and received CYSP or TAC with MTX or MMF for GVHD prophylaxis. Primary outcomes of the study were acute and chronic GVHD and overall survival (OS). The study divided the patient population into 4 cohorts based on regimen: MMF-TAC, MMF-CYSP, MTX-TAC, and MTX-CYSP. In the URD group, MMF-CYSP was associated with increased risk of grade II to IV acute GVHD (relative risk [RR], 1.78; P <.001) and grade III to IV acute GVHD (RR, 1.93; P =.006) compared with MTX-TAC. In the URD group, use of MMF-TAC (versus MTX-TAC) lead to higher nonrelapse mortality. (hazard ratio, 1.48; P =.008). In either group, no there was no difference in chronic GVHD, disease-free survival, and OS among the GVHD prophylaxis regimens. For RIC alloHCT using MRD, there are no differences in outcomes based on GVHD prophylaxis. However, with URD RIC alloHCT, MMF-CYSP was inferior to MTX-based regimens for acute GVHD prevention, but all the regimens were equivalent in terms of chronic GVHD and OS. Prospective studies, targeting URD recipients are needed to confirm these results
Analysis of shared heritability in common disorders of the brain
ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders
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