170 research outputs found
Emission of gamma rays shifted from resonant absorption by electron-nuclear double transitions in ^{151}Eu^{2+}:CaF_2
We show that the emission of a gamma-ray photon by a nucleus can be
influenced by a microwave magnetic field acting on the atomic electrons. We
study theoretically these electron-nuclear double transitions (ENDTs) for
^{151}Eu nuclei in a CaF_2 lattice at low temperature, in the presence of a
static magnetic field and of a microwave magnetic field. The ENDTs acquire a
significant intensity for certain resonance frequencies. The ENDTs are of
interest for the identification of the position of the lines in complex
M\"{o}ssbauer spectra.Comment: 8 pages; 3 Postscript figures: Fig. 1, Fig. 2(a), Fig. 2(b
Gas phase mean opacities for varying [M/H], N/O, and C/O
We present a set of gas-phase Planck mean and Rosseland mean opacity tables
applicable for simulations of star and planet formation, stellar evolution,
disk modelling at various metallicities in hydrogen-rich environments. The
tables are calculated for gas temperatures between 1000K and 10000K and total
hydrogen number densities between 10^2 cm^-3 and 10^17 cm^-3. The
carbon-to-oxygen ratio is varied from 0.43 to well above 2.0, the
nitrogen-to-oxygen ration between 0.14 and 100.0. The tables are calculated for
a range of metallicities down to [M/H]'= log N_M/N_H=-7.0. We demonstrate how
the mean opacities and the abundances of the opacity species vary with C/O,
N/O, and [M/H]'. We use the element abundances from Grevesse, Asplund & Sauval
(2007), and we provide additional tables for the oxygen-abundance value from
Caffau et al.(2008). All tables will be available online under
http://star-www.st-and.ac.uk/ch80/datasources.htmlComment: 10 pages, accepted for publication in MNRA
Truncation of a 2-dimensional Fermi surface due to quasiparticle gap formation at the saddle points
We study a two-dimensional Fermi liquid with a Fermi surface containing the
saddle points and . Including Cooper and Peierls channel
contributions leads to a one-loop renormalization group flow to strong coupling
for short range repulsive interactions. In a certain parameter range the
characteristics of the fixed point, opening of a spin and charge gap and
dominant pairing correlations are similar to those of a 2-leg ladder at
half-filling. An increase of the electron density we argue leads to a
truncation of the Fermi surface with only 4 disconnected arcs remaining.Comment: Reference added. RevTeX 4 pages incl. 4 ps file
Short-range spin correlations and induced local spin-singlet amplitude in the Hubbard model
In this paper, from the microscopic Hubbard Hamiltonian we extract the local
spin-singlet amplitude due to short-range spin correlations, and quantify its
strength near half-filling. As a first application of the present approach, we
study a problem of the energy dispersion and its d-wave modulation in the
insulating cuprates, SrCuOCl and CaCuOCl.
Without any adjustable parameters, most puzzling issues are naturally and
quantitatively explained within the present approach.Comment: 6 pages, 3 figure
Two-Particle-Self-Consistent Approach for the Hubbard Model
Even at weak to intermediate coupling, the Hubbard model poses a formidable
challenge. In two dimensions in particular, standard methods such as the Random
Phase Approximation are no longer valid since they predict a finite temperature
antiferromagnetic phase transition prohibited by the Mermin-Wagner theorem. The
Two-Particle-Self-Consistent (TPSC) approach satisfies that theorem as well as
particle conservation, the Pauli principle, the local moment and local charge
sum rules. The self-energy formula does not assume a Migdal theorem. There is
consistency between one- and two-particle quantities. Internal accuracy checks
allow one to test the limits of validity of TPSC. Here I present a pedagogical
review of TPSC along with a short summary of existing results and two case
studies: a) the opening of a pseudogap in two dimensions when the correlation
length is larger than the thermal de Broglie wavelength, and b) the conditions
for the appearance of d-wave superconductivity in the two-dimensional Hubbard
model.Comment: Chapter in "Theoretical methods for Strongly Correlated Systems",
Edited by A. Avella and F. Mancini, Springer Verlag, (2011) 55 pages.
Misprint in Eq.(23) corrected (thanks D. Bergeron
X-exome sequencing of 405 unresolved families identifies seven novel intellectual disability genes
X-linked intellectual disability (XLID) is a clinically and genetically heterogeneous disorder. During the past two decades in excess of 100 X-chromosome ID genes have been identified. Yet, a large number of families mapping to the X-chromosome remained unresolved suggesting that more XLID genes or loci are yet to be identified. Here, we have investigated 405 unresolved families with XLID. We employed massively parallel sequencing of all X-chromosome exons in the index males. The majority of these males were previously tested negative for copy number variations and for mutations in a subset of known XLID genes by Sanger sequencing. In total, 745 X-chromosomal genes were screened. After stringent filtering, a total of 1297 non-recurrent exonic variants remained for prioritization. Co-segregation analysis of potential clinically relevant changes revealed that 80 families (20%) carried pathogenic variants in established XLID genes. In 19 families, we detected likely causative protein truncating and missense variants in 7 novel and validated XLID genes (CLCN4, CNKSR2, FRMPD4, KLHL15, LAS1L, RLIM and USP27X) and potentially deleterious variants in 2 novel candidate XLID genes (CDK16 and TAF1). We show that the CLCN4 and CNKSR2 variants impair protein functions as indicated by electrophysiological studies and altered differentiation of cultured primary neurons from Clcn4−/− mice or after mRNA knock-down. The newly identified and candidate XLID proteins belong to pathways and networks with established roles in cognitive function and intellectual disability in particular. We suggest that systematic sequencing of all X-chromosomal genes in a cohort of patients with genetic evidence for X-chromosome locus involvement may resolve up to 58% of Fragile X-negative cases
Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation
Advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs) have a pathogenetic role in the development and progression of different oxidative-based diseases including diabetes, atherosclerosis, and neurological disorders. AGEs and ALEs represent a quite complex class of compounds that are formed by different mechanisms, by heterogeneous precursors and that can be formed either exogenously or endogenously. There is a wide interest in AGEs and ALEs involving different aspects of research which are essentially focused on set-up and application of analytical strategies (1) to identify, characterize, and quantify AGEs and ALEs in different pathophysiological conditions ; (2) to elucidate the molecular basis of their biological effects ; and (3) to discover compounds able to inhibit AGEs/ALEs damaging effects not only as biological tools aimed at validating AGEs/ALEs as drug target, but also as promising drugs. All the above-mentioned research stages require a clear picture of the chemical formation of AGEs/ALEs but this is not simple, due to the complex and heterogeneous pathways, involving different precursors and mechanisms. In view of this intricate scenario, the aim of the present review is to group the main AGEs and ALEs and to describe, for each of them, the precursors and mechanisms of formation
The Nanostructure of Myoendothelial Junctions Contributes to Signal Rectification between Endothelial and Vascular Smooth Muscle Cells
Micro-anatomical structures in tissues have potential physiological effects. In arteries and arterioles smooth muscle cells and endothelial cells are separated by the internal elastic lamina, but the two cell layers often make contact through micro protrusions called myoendothelial junctions. Cross talk between the two cell layers is important in regulating blood pressure and flow. We have used a spatiotemporal mathematical model to investigate how the myoendothelial junctions affect the information flow between the two cell layers. The geometry of the model mimics the structure of the two cell types and the myoendothelial junction. The model is implemented as a 2D axi-symmetrical model and solved using the finite element method. We have simulated diffusion of Ca2+ and IP3 between the two cell types and we show that the micro-anatomical structure of the myoendothelial junction in itself may rectify a signal between the two cell layers. The rectification is caused by the asymmetrical structure of the myoendothelial junction. Because the head of the myoendothelial junction is separated from the cell it is attached to by a narrow neck region, a signal generated in the neighboring cell can easily drive a concentration change in the head of the myoendothelial protrusion. Subsequently the signal can be amplified in the head, and activate the entire cell. In contrast, a signal in the cell from which the myoendothelial junction originates will be attenuated and delayed in the neck region as it travels into the head of the myoendothelial junction and the neighboring cell
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