182 research outputs found
Unidirectional conduction block caused by variations in pathway geometry: A new mechanism for reentry
Optimal Renormalization Scale and Scheme for Exclusive Processes
We use the BLM method to fix the renormalization scale of the QCD coupling in
exclusive hadronic amplitudes such as the pion form factor and the
photon-to-pion transition form factor at large momentum transfer.
Renormalization-scheme-independent commensurate scale relations are established
which connect the hard scattering subprocess amplitudes that control exclusive
processes to other QCD observables such as the heavy quark potential and the
electron-positron annihilation cross section. The commensurate scale relation
connecting the heavy quark potential, as determined from lattice gauge theory,
to the photon-to-pion transition form factor is in excellent agreement with
data assuming that the pion distribution amplitude is
close to its asymptotic form . We also reproduce the
scaling and normalization of the data at large
momentum transfer. Because the renormalization scale is small, we argue that
the effective coupling is nearly constant, thus accounting for the nominal
scaling behavior of the data. However, the normalization of the space-like pion
form factor obtained from electroproduction experiments is
somewhat higher than that predicted by the corresponding commensurate scale
relation. This discrepancy may be due to systematic errors introduced by the
extrapolation of the electroproduction data to the
pion pole.Comment: 22 pages, Latex, 7 Latex figures. Several references added,
discussion of scale fixing revised for clarity. Final version to appear in
Phys. Rev.
Effects of a Novel Nitroxyl Donor in Acute Heart Failure The STAND-UP AHF Study
Objectives:
The primary objective was to identify well-tolerated doses of cimlanod in patients with acute heart failure (AHF). Secondary objectives were to identify signals of efficacy, including biomarkers, symptoms, and clinical events.
Background:
Nitroxyl (HNO) donors have vasodilator, inotropic and lusitropic effects. Bristol-Myers Squibb-986231 (cimlanod) is an HNO donor being developed for acute heart failure (AHF).
Methods:
This was a phase IIb, double-blind, randomized, placebo-controlled trial of 48-h treatment with cimlanod compared with placebo in patients with left ventricular ejection fraction ≤40% hospitalized for AHF. In part I, patients were randomized in a 1:1 ratio to escalating doses of cimlanod or matching placebo. In part II, patients were randomized in a 1:1:1 ratio to either of the 2 highest tolerated doses of cimlanod from part I or placebo. The primary endpoint was the rate of clinically relevant hypotension (systolic blood pressure <90 mm Hg or patients became symptomatic).
Results:
In part I (n = 100), clinically relevant hypotension was more common with cimlanod than placebo (20% vs. 8%; relative risk [RR]: 2.45; 95% confidence interval [CI]: 0.83 to 14.53). In part II (n = 222), the incidence of clinically relevant hypotension was 18% for placebo, 21% for cimlanod 6 μg/kg/min (RR: 1.15; 95% CI: 0.58 to 2.43), and 35% for cimlanod 12 μg/kg/min (RR: 1.9; 95% CI: 1.04 to 3.59). N-terminal pro–B-type natriuretic peptide and bilirubin decreased during infusion of cimlanod treatment compared with placebo, but these differences did not persist after treatment discontinuation.
Conclusions:
Cimlanod at a dose of 6 μg/kg/min was reasonably well-tolerated compared with placebo. Cimlanod reduced markers of congestion, but this did not persist beyond the treatment period. (Evaluate the Safety and Efficacy of 48-Hour Infusions of HNO (Nitroxyl) Donor in Hospitalized Patients With Heart Failure [STANDUP AHF]; NCT03016325
Probing Charge-Symmetry-Violating Quark Distributions in Semi-Inclusive Leptoproduction of Hadrons
Recent experiments by the HERMES group at HERA are measuring semi-inclusive
electroproduction of pions from deuterium. We point out that by comparing the
production of and from an isoscalar target, it is possible, in
principle, to measure charge symmetry violation in the valence quark
distributions of the nucleons. It is also possible in the same experiments to
obtain an independent measurement of the quark fragmentation functions. We
review the information which can be deduced from such experiments and show the
``signature'' for charge symmetry violation in such experiments. Finally, we
predict the magnitude of the charge symmetry violation, from both the valence
quark distributions and the pion fragmentation function, which might be
expected in these experiments.Comment: 19 pages plus 5 figures, used eps
A high-quality bonobo genome refines the analysis of hominid evolution
The divergence of chimpanzee and bonobo provides one of the few examples of recent hominid speciation1,2. Here we describe a fully annotated, high-quality bonobo genome assembly, which was constructed without guidance from reference genomes by applying a multiplatform genomics approach. We generate a bonobo genome assembly in which more than 98% of genes are completely annotated and 99% of the gaps are closed, including the resolution of about half of the segmental duplications and almost all of the full-length mobile elements. We compare the bonobo genome to those of other great apes1,3,4,5 and identify more than 5,569 fixed structural variants that specifically distinguish the bonobo and chimpanzee lineages. We focus on genes that have been lost, changed in structure or expanded in the last few million years of bonobo evolution. We produce a high-resolution map of incomplete lineage sorting and estimate that around 5.1% of the human genome is genetically closer to chimpanzee or bonobo and that more than 36.5% of the genome shows incomplete lineage sorting if we consider a deeper phylogeny including gorilla and orangutan. We also show that 26% of the segments of incomplete lineage sorting between human and chimpanzee or human and bonobo are non-randomly distributed and that genes within these clustered segments show significant excess of amino acid replacement compared to the rest of the genome
Systems genetics identifies a role for Cacna2d1 regulation in elevated intraocular pressure and glaucoma susceptibility
Glaucoma is a multi-factorial blinding disease in which genetic factors play an important role. Elevated intraocular pressure is a highly heritable risk factor for primary open angle glaucoma and currently the only target for glaucoma therapy. Our study helps to better understand underlying genetic and molecular mechanisms that regulate intraocular pressure, and identifies a new candidate gene, Cacna2d1, that modulates intraocular pressure and a promising therapeutic, pregabalin, which binds to CACNA2D1 protein and lowers intraocular pressure significantly. Because our study utilizes a genetically diverse population of mice with kno
Fracture Toughness and Adhesion of Transparent Al:ZnO Films Deposited on Glass Substrates
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