5,337 research outputs found
Quiver Structure of Heterotic Moduli
We analyse the vector bundle moduli arising from generic heterotic
compactifications from the point of view of quiver representations. Phenomena
such as stability walls, crossing between chambers of supersymmetry, splitting
of non-Abelian bundles and dynamic generation of D-terms are succinctly encoded
into finite quivers. By studying the Poincar\'e polynomial of the quiver moduli
space using the Reineke formula, we can learn about such useful concepts as
Donaldson-Thomas invariants, instanton transitions and supersymmetry breaking.Comment: 38 pages, 5 figures, 1 tabl
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Evaluation of meaningful change in bowel move frequency for patients with carcinoid syndrome
Heterotic Models from Vector Bundles on Toric Calabi-Yau Manifolds
We systematically approach the construction of heterotic E_8 X E_8 Calabi-Yau
models, based on compact Calabi-Yau three-folds arising from toric geometry and
vector bundles on these manifolds. We focus on a simple class of 101 such
three-folds with smooth ambient spaces, on which we perform an exhaustive scan
and find all positive monad bundles with SU(N), N=3,4,5 structure groups,
subject to the heterotic anomaly cancellation constraint. We find that
anomaly-free positive monads exist on only 11 of these toric three-folds with a
total number of bundles of about 2000. Only 21 of these models, all of them on
three-folds realizable as hypersurfaces in products of projective spaces, allow
for three families of quarks and leptons. We also perform a preliminary scan
over the much larger class of semi-positive monads which leads to about 44000
bundles with 280 of them satisfying the three-family constraint. These 280
models provide a starting point for heterotic model building based on toric
three-folds.Comment: 41 pages, 5 figures. A table modified and a table adde
Heterotic Model Building: 16 Special Manifolds
We study heterotic model building on 16 specific Calabi-Yau manifolds constructed as hypersurfaces in toric four-folds. These 16 manifolds are the only ones among the more than half a billion manifolds in the Kreuzer-Skarke list with a non-trivial first fundamental group. We classify the line bundle models on these manifolds, both for SU(5) and SO(10) GUTs, which lead to consistent supersymmetric string vacua and have three chiral families. A total of about 29000 models is found, most of them corresponding to SO(10) GUTs. These models constitute a starting point for detailed heterotic model building on Calabi-Yau manifolds in the Kreuzer-Skarke list
Heterotic Bundles on Calabi-Yau Manifolds with Small Picard Number
We undertake a systematic scan of vector bundles over spaces from the largest
database of known Calabi-Yau three-folds, in the context of heterotic string
compactification. Specifically, we construct positive rank five monad bundles
over Calabi-Yau hypersurfaces in toric varieties, with the number of Kahler
moduli equal to one, two, and three and extract physically interesting models.
We select models which can lead to three families of matter after dividing by a
freely-acting discrete symmetry and including Wilson lines. About 2000 such
models on two manifolds are found.Comment: 26 pages, 1 figur
Presymptomatic risk assessment for chronic non-communicable diseases
The prevalence of common chronic non-communicable diseases (CNCDs) far
overshadows the prevalence of both monogenic and infectious diseases combined.
All CNCDs, also called complex genetic diseases, have a heritable genetic
component that can be used for pre-symptomatic risk assessment. Common single
nucleotide polymorphisms (SNPs) that tag risk haplotypes across the genome
currently account for a non-trivial portion of the germ-line genetic risk and
we will likely continue to identify the remaining missing heritability in the
form of rare variants, copy number variants and epigenetic modifications. Here,
we describe a novel measure for calculating the lifetime risk of a disease,
called the genetic composite index (GCI), and demonstrate its predictive value
as a clinical classifier. The GCI only considers summary statistics of the
effects of genetic variation and hence does not require the results of
large-scale studies simultaneously assessing multiple risk factors. Combining
GCI scores with environmental risk information provides an additional tool for
clinical decision-making. The GCI can be populated with heritable risk
information of any type, and thus represents a framework for CNCD
pre-symptomatic risk assessment that can be populated as additional risk
information is identified through next-generation technologies.Comment: Plos ONE paper. Previous version was withdrawn to be updated by the
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Combined acoustic radiation force impulse, aminotransferase to platelet ratio index and Forns index assessment for hepatic fibrosis grading in hepatitis B
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A cross-national study on the antecedents of work–life balance from the fit and balance perspective
Drawing on the perceived work–family fit and balance perspective, this study investigates demands and resources as antecedents of work–life balance (WLB) across four countries (New Zealand, France, Italy and Spain), so as to provide empirical cross-national evidence. Using structural equation modelling analysis on a sample of 870 full time employees, we found that work demands, hours worked and family demands were negatively related to WLB, while job autonomy and supervisor support were positively related to WLB. We also found evidence that resources (job autonomy and supervisor support) moderated the relationships between demands and work–life balance, with high resources consistently buffering any detrimental influence of demands on WLB. Furthermore, our study identified additional predictors of WLB that were unique to some national contexts. For example, in France and Italy, overtime hours worked were negatively associated with WLB, while parental status was positively associated with WLB. Overall, the implications for theory and practice are discussed.Peer ReviewedPostprint (author's final draft
Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.
To gain insight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths. We found repeat length-dependent transcriptional signatures to be prominent in the striatum, less so in cortex, and minimal in the liver. Coexpression network analyses revealed 13 striatal and 5 cortical modules that correlated highly with CAG length and age, and that were preserved in HD models and sometimes in patients. Top striatal modules implicated mHtt CAG length and age in graded impairment in the expression of identity genes for striatal medium spiny neurons and in dysregulation of cyclic AMP signaling, cell death and protocadherin genes. We used proteomics to confirm 790 genes and 5 striatal modules with CAG length-dependent dysregulation at the protein level, and validated 22 striatal module genes as modifiers of mHtt toxicities in vivo
Epigenetic alterations differ in phenotypically distinct human neuroblastoma cell lines
<p>Abstract</p> <p>Background</p> <p>Epigenetic aberrations and a CpG island methylator phenotype have been shown to be associated with poor outcomes in children with neuroblastoma (NB). Seven cancer related genes (<it>THBS-1, CASP8, HIN-1, TIG-1, BLU, SPARC</it>, and <it>HIC-1</it>) that have been shown to have epigenetic changes in adult cancers and play important roles in the regulation of angiogenesis, tumor growth, and apoptosis were analyzed to investigate the role epigenetic alterations play in determining NB phenotype.</p> <p>Methods</p> <p>Two NB cell lines (tumorigenic LA1-55n and non-tumorigenic LA1-5s) that differ in their ability to form colonies in soft agar and tumors in nude mice were used. Quantitative RNA expression analyses were performed on seven genes in LA1-5s, LA1-55n and 5-Aza-dC treated LA1-55n NB cell lines. The methylation status around <it>THBS-1, HIN-1, TIG-1 </it>and <it>CASP8 </it>promoters was examined using methylation specific PCR. Chromatin immunoprecipitation assay was used to examine histone modifications along the <it>THBS-1 </it>promoter. Luciferase assay was used to determine <it>THBS-1 </it>promoter activity. Cell proliferation assay was used to examine the effect of 5-Aza-dC on NB cell growth. The soft agar assay was used to determine the tumorigenicity.</p> <p>Results</p> <p>Promoter methylation values for <it>THBS-1</it>, <it>HIN-1</it>, <it>TIG-1</it>, and <it>CASP8 </it>were higher in LA1-55n cells compared to LA1-5s cells. Consistent with the promoter methylation status, lower levels of gene expression were detected in the LA1-55n cells. Histone marks associated with repressive chromatin states (H3K9Me3, H3K27Me3, and H3K4Me3) were identified in the <it>THBS-1 </it>promoter region in the LA1-55n cells, but not the LA1-5s cells. In contrast, the three histone codes associated with an active chromatin state (acetyl H3, acetyl H4, and H3K4Me3) were present in the <it>THBS-1 </it>promoter region in LA1-5s cells, but not the LA1-55n cells, suggesting that an accessible chromatin structure is important for <it>THBS-1 </it>expression. We also show that 5-Aza-dC treatment of LA1-55n cells alters the DNA methylation status and the histone code in the <it>THBS-1 </it>promoter modifies cell morphology, and inhibits their ability to form colonies in soft agar.</p> <p>Conclusion</p> <p>Our results suggest that epigenetic aberrations contribute to NB phenotype, and that tumorigenic properties can be inhibited by reversing the epigenetic changes with 5-Aza-dC.</p
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