75 research outputs found
Tetracritical behavior in strongly interacting theories
We suggest a tetracritical fixed point to naturally occur in strongly
interacting theories. As a fundamental example we analyze the
temperature--quark chemical potential phase diagram of QCD with fermions in the
adjoint representation of the gauge group (i.e. adjoint QCD). Here we show that
such a non trivial multicritical point exists and is due to the interplay
between the spontaneous breaking of a global U(1) symmetry and the center group
symmetry associated to confinement. Our results demonstrate that taking
confinement into account is essential for understanding the critical behavior
as well as the full structure of the phase diagram of adjoint QCD. This is in
contrast to ordinary QCD where the center group symmetry associated to
confinement is explicitly broken when the quarks are part of the theory.Comment: RevTex, 5 figures. Final version to appear in PR
Critical behavior of weakly-disordered anisotropic systems in two dimensions
The critical behavior of two-dimensional (2D) anisotropic systems with weak
quenched disorder described by the so-called generalized Ashkin-Teller model
(GATM) is studied. In the critical region this model is shown to be described
by a multifermion field theory similar to the Gross-Neveu model with a few
independent quartic coupling constants. Renormalization group calculations are
used to obtain the temperature dependence near the critical point of some
thermodynamic quantities and the large distance behavior of the two-spin
correlation function. The equation of state at criticality is also obtained in
this framework. We find that random models described by the GATM belong to the
same universality class as that of the two-dimensional Ising model. The
critical exponent of the correlation length for the 3- and 4-state
random-bond Potts models is also calculated in a 3-loop approximation. We show
that this exponent is given by an apparently convergent series in
(with the central charge of the Potts model) and
that the numerical values of are very close to that of the 2D Ising
model. This work therefore supports the conjecture (valid only approximately
for the 3- and 4-state Potts models) of a superuniversality for the 2D
disordered models with discrete symmetries.Comment: REVTeX, 24 pages, to appear in Phys.Rev.
Single-particle isomeric states in 121Pd and 117Ru
Neutron-rich nuclei were populated in a relativistic fission of 238U. Gamma-rays with energies of 135 keV and 184 keV were associated with two isomeric states in 121Pd and 117Ru. Half-lives of 0.63(5) microseconds and 2.0(3) micrisecondss were deduced and the isomeric states were interpreted in terms of deformed single-particle states
Grafting of Poly(methyl methacrylate) Brushes from Magnetite Nanoparticles Using a Phosphonic Acid Based Initiator by Ambient Temperature Atom Transfer Radical Polymerization (ATATRP)
Poly(methyl methacrylate) in the brush form is grown from the surface of magnetite nanoparticles by ambient temperature atom transfer radical polymerization (ATATRP) using a phosphonic acid based initiator. The surface initiator was prepared by the reaction of ethylene glycol with 2-bromoisobutyrl bromide, followed by the reaction with phosphorus oxychloride and hydrolysis. This initiator is anchored to magnetite nanoparticles via physisorption. The ATATRP of methyl methacrylate was carried out in the presence of CuBr/PMDETA complex, without a sacrificial initiator, and the grafting density is found to be as high as 0.90 molecules/nm2. The organic–inorganic hybrid material thus prepared shows exceptional stability in organic solvents unlike unfunctionalized magnetite nanoparticles which tend to flocculate. The polymer brushes of various number average molecular weights were prepared and the molecular weight was determined using size exclusion chromatography, after degrafting the polymer from the magnetite core. Thermogravimetric analysis, X-ray photoelectron spectra and diffused reflection FT-IR were used to confirm the grafting reaction
GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium
Decline in muscle strength with aging is an important predictor of health trajectory in the elderly. Several factors, including genetics, are proposed contributors to variability in muscle strength. To identify genetic contributors to muscle strength, a meta-analysis of genomewide association studies of handgrip was conducted. Grip strength was measured using a handheld dynamometer in 27 581 individuals of European descent over 65 years of age from 14 cohort studies. Genomewide association analysis was conducted on ~2.7 million imputed and genotyped variants (SNPs). Replication of the most significant findings was conducted using data from 6393 individuals from three cohorts. GWAS of lower body strength was also characterized in a subset of cohorts. Two genomewide significant (P-value< 5 × 10−8) and 39 suggestive (P-value< 5 × 10−5) associations were observed from meta-analysis of the discovery cohorts. After meta-analysis with replication cohorts, genomewide significant association was observed for rs752045 on chromosome 8 (β = 0.47, SE = 0.08, P-value = 5.20 × 10−10). This SNP is mapped to an intergenic region and is located within an accessible chromatin region (DNase hypersensitivity site) in skeletal muscle myotubes differentiated from the human skeletal muscle myoblasts cell line. This locus alters a binding motif of the CCAAT/enhancer-binding protein-β (CEBPB) that is implicated in muscle repair mechanisms. GWAS of lower body strength did not yield significant results. A common genetic variant in a chromosomal region that regulates myotube differentiation and muscle repair may contribute to variability in grip strength in the elderly. Further studies are needed to uncover the mechanisms that link this genetic variant with muscle strength
A high-quality human reference panel reveals the complexity and distribution of genomic structural variants
Structural variation (SV) represents a major source of differences between individual human genomes and has been linked to disease phenotypes. However, the majority of studies provide neither a global view of the full spectrum of these variants nor integrate them into reference panels of genetic variation. Here, we analyse whole genome sequencing data of 769 individuals from 250 Dutch families, and provide a haplotype-resolved map of 1.9 million genome variants across 9 different variant classes, including novel forms of complex indels, and retrotransposition-mediated insertions of mobile elements and processed RNAs. A large proportion are previously under reported variants sized between 21 and 100 bp. We detect 4 megabases of novel sequence, encoding 11 new transcripts. Finally, we show 191 known, trait-associated SNPs to be in strong linkage disequilibrium with SVs and demonstrate that our panel facilitates accurate imputation of SVs in unrelated individuals
Genome-wide analyses identify a role for SLC17A4 and AADAT in thyroid hormone regulation.
Thyroid dysfunction is an important public health problem, which affects 10% of the general population and increases the risk of cardiovascular morbidity and mortality. Many aspects of thyroid hormone regulation have only partly been elucidated, including its transport, metabolism, and genetic determinants. Here we report a large meta-analysis of genome-wide association studies for thyroid function and dysfunction, testing 8 million genetic variants in up to 72,167 individuals. One-hundred-and-nine independent genetic variants are associated with these traits. A genetic risk score, calculated to assess their combined effects on clinical end points, shows significant associations with increased risk of both overt (Graves' disease) and subclinical thyroid disease, as well as clinical complications. By functional follow-up on selected signals, we identify a novel thyroid hormone transporter (SLC17A4) and a metabolizing enzyme (AADAT). Together, these results provide new knowledge about thyroid hormone physiology and disease, opening new possibilities for therapeutic targets
Novel genetic loci associated with hippocampal volume
The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness
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