110 research outputs found
Specht modules and semisimplicity criteria for Brauer and Birman--Murakami--Wenzl Algebras
A construction of bases for cell modules of the Birman--Murakami--Wenzl (or
B--M--W) algebra by lifting bases for cell modules of
is given. By iterating this procedure, we produce cellular bases for B--M--W
algebras on which a large abelian subalgebra, generated by elements which
generalise the Jucys--Murphy elements from the representation theory of the
Iwahori--Hecke algebra of the symmetric group, acts triangularly. The
triangular action of this abelian subalgebra is used to provide explicit
criteria, in terms of the defining parameters and , for B--M--W algebras
to be semisimple. The aforementioned constructions provide generalisations, to
the algebras under consideration here, of certain results from the Specht
module theory of the Iwahori--Hecke algebra of the symmetric group
Hecke algebras of finite type are cellular
Let \cH be the one-parameter Hecke algebra associated to a finite Weyl
group , defined over a ground ring in which ``bad'' primes for are
invertible. Using deep properties of the Kazhdan--Lusztig basis of \cH and
Lusztig's \ba-function, we show that \cH has a natural cellular structure
in the sense of Graham and Lehrer. Thus, we obtain a general theory of ``Specht
modules'' for Hecke algebras of finite type. Previously, a general cellular
structure was only known to exist in types and .Comment: 14 pages; added reference
Higher algebraic -groups and -split sequences
In this paper, we use -split sequences and derived equivalences
to provide formulas for calculation of higher algebraic -groups (or mod-
-groups) of certain matrix subrings which cover tiled orders, rings related
to chains of Glaz-Vasconcelos ideals, and some other classes of rings. In our
results, we do not assume any homological requirements on rings and ideals
under investigation, and therefore extend sharply many existing results of this
type in the algebraic -theory literature to a more general context.Comment: 20 page
Generation of maximum spin entanglement induced by cavity field in quantum-dot systems
Equivalent-neighbor interactions of the conduction-band electron spins of
quantum dots in the model of Imamoglu et al. [Phys. Rev. Lett. 83, 4204 (1999)]
are analyzed. Analytical solution and its Schmidt decomposition are found and
applied to evaluate how much the initially excited dots can be entangled to the
remaining dots if all of them are initially disentangled. It is demonstrated
that the perfect maximally entangled states (MES) can only be generated in the
systems of up to 6 dots with a single dot initially excited. It is also shown
that highly entangled states, approximating the MES with a good accuracy, can
still be generated in systems of odd number of dots with almost half of them
being excited. A sudden decrease of entanglement is observed by increasing the
total number of dots in a system with a fixed number of excitations.Comment: 6 pages, 7 figures, to appear in Phys. Rev.
The Cerenkov effect revisited: from swimming ducks to zero modes in gravitational analogs
We present an interdisciplinary review of the generalized Cerenkov emission
of radiation from uniformly moving sources in the different contexts of
classical electromagnetism, superfluid hydrodynamics, and classical
hydrodynamics. The details of each specific physical systems enter our theory
via the dispersion law of the excitations. A geometrical recipe to obtain the
emission patterns in both real and wavevector space from the geometrical shape
of the dispersion law is discussed and applied to a number of cases of current
experimental interest. Some consequences of these emission processes onto the
stability of condensed-matter analogs of gravitational systems are finally
illustrated.Comment: Lecture Notes at the IX SIGRAV School on "Analogue Gravity" in Como,
Italy from May 16th-21th, 201
JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma
Chromosome 17q21-ter is commonly gained in neuroblastoma, but it is unclear which gene in the region is important for tumorigenesis. The JMJD6 gene at 17q21-ter activates gene transcription. Here we show that JMJD6 forms protein complexes with N-Myc and BRD4, and is important for E2F2, N-Myc and c-Myc transcription. Knocking down JMJD6 reduces neuroblastoma cell proliferation and survival in vitro and tumor progression in mice, and high levels of JMJD6 expression in human neuroblastoma tissues independently predict poor patient prognosis. In addition, JMJD6 gene is associated with transcriptional super-enhancers. Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Our findings therefore identify JMJD6 as a neuroblastoma tumorigenesis factor, and the combination therapy as a treatment strategy
Partial Wave Analysis of
BES data on are presented. The
contribution peaks strongly near threshold. It is fitted with a
broad resonance with mass MeV, width MeV. A broad resonance peaking at 2020 MeV is also required
with width MeV. There is further evidence for a component
peaking at 2.55 GeV. The non- contribution is close to phase
space; it peaks at 2.6 GeV and is very different from .Comment: 15 pages, 6 figures, 1 table, Submitted to PL
Nucleosomes in gene regulation: theoretical approaches
This work reviews current theoretical approaches of biophysics and
bioinformatics for the description of nucleosome arrangements in chromatin and
transcription factor binding to nucleosomal organized DNA. The role of
nucleosomes in gene regulation is discussed from molecular-mechanistic and
biological point of view. In addition to classical problems of this field,
actual questions of epigenetic regulation are discussed. The authors selected
for discussion what seem to be the most interesting concepts and hypotheses.
Mathematical approaches are described in a simplified language to attract
attention to the most important directions of this field
Improving Genetic Prediction by Leveraging Genetic Correlations Among Human Diseases and Traits
Genomic prediction has the potential to contribute to precision medicine. However, to date, the utility of such predictors is limited due to low accuracy for most traits. Here theory and simulation study are used to demonstrate that widespread pleiotropy among phenotypes can be utilised to improve genomic risk prediction. We show how a genetic predictor can be created as a weighted index that combines published genome-wide association study (GWAS) summary statistics across many different traits. We apply this framework to predict risk of schizophrenia and bipolar disorder in the Psychiatric Genomics consortium data, finding substantial heterogeneity in prediction accuracy increases across cohorts. For six additional phenotypes in the UK Biobank data, we find increases in prediction accuracy ranging from 0.7 for height to 47 for type 2 diabetes, when using a multi-trait predictor that combines published summary statistics from multiple traits, as compared to a predictor based only on one trait. © 2018 The Author(s)
Genome-wide association study identifies 30 Loci Associated with Bipolar Disorder
This paper is dedicated to the memory of Psychiatric Genomics Consortium (PGC) founding member and Bipolar disorder working group co-chair Pamela Sklar. We thank the participants who donated their time, experiences and DNA to this research, and to the clinical and scientific teams that worked with them. We are deeply indebted to the investigators who comprise the PGC. The views expressed are those of the authors and not necessarily those of any funding or regulatory body. Analyses were carried out on the NL Genetic Cluster Computer (http://www.geneticcluster.org ) hosted by SURFsara, and the Mount Sinai high performance computing cluster (http://hpc.mssm.edu).Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P<1x10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (GWS, p < 5x10-8) in the discovery GWAS were not GWS in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis 30 loci were GWS including 20 novel loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene-sets including regulation of insulin secretion and endocannabinoid signaling. BDI is strongly genetically correlated with schizophrenia, driven by psychosis, whereas BDII is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential new biological mechanisms for BD.This work was funded in part by the Brain and Behavior Research Foundation, Stanley Medical Research Institute, University of Michigan, Pritzker Neuropsychiatric Disorders Research Fund L.L.C., Marriot Foundation and the Mayo Clinic Center for Individualized Medicine, the NIMH Intramural Research Program; Canadian Institutes of Health Research; the UK Maudsley NHS Foundation Trust, NIHR, NRS, MRC, Wellcome Trust; European Research Council; German Ministry for Education and Research, German Research Foundation IZKF of Münster, Deutsche Forschungsgemeinschaft, ImmunoSensation, the Dr. Lisa-Oehler Foundation, University of Bonn; the Swiss National Science Foundation; French Foundation FondaMental and ANR; Spanish Ministerio de EconomÃa, CIBERSAM, Industria y Competitividad, European Regional Development Fund (ERDF), Generalitat de Catalunya, EU Horizon 2020 Research and Innovation Programme; BBMRI-NL; South-East Norway Regional Health Authority and Mrs. Throne-Holst; Swedish Research Council, Stockholm County Council, Söderström Foundation; Lundbeck Foundation, Aarhus University; Australia NHMRC, NSW Ministry of Health, Janette M O'Neil and Betty C Lynch
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