40 research outputs found
Implications of Electronics Constraints for Solid-State Quantum Error Correction and Quantum Circuit Failure Probability
In this paper we present the impact of classical electronics constraints on a
solid-state quantum dot logical qubit architecture. Constraints due to routing
density, bandwidth allocation, signal timing, and thermally aware placement of
classical supporting electronics significantly affect the quantum error
correction circuit's error rate. We analyze one level of a quantum error
correction circuit using nine data qubits in a Bacon-Shor code configured as a
quantum memory. A hypothetical silicon double quantum dot quantum bit (qubit)
is used as the fundamental element. A pessimistic estimate of the error
probability of the quantum circuit is calculated using the total number of
gates and idle time using a provably optimal schedule for the circuit
operations obtained with an integer program methodology. The micro-architecture
analysis provides insight about the different ways the electronics impact the
circuit performance (e.g., extra idle time in the schedule), which can
significantly limit the ultimate performance of any quantum circuit and
therefore is a critical foundation for any future larger scale architecture
analysis.Comment: 10 pages, 7 figures, 3 table
M-theory Compactifications on Manifolds with G2 Structure
In this paper we study M-theory compactifications on manifolds of G2
structure. By computing the gravitino mass term in four dimensions we derive
the general form for the superpotential which appears in such compactifications
and show that beside the normal flux term there is a term which appears only
for non-minimal G2 structure. We further apply these results to
compactifications on manifolds with weak G2 holonomy and make a couple of
statements regarding the deformation space of such manifolds. Finally we show
that the superpotential derived from fermionic terms leads to the potential
that can be derived from the explicit compactification, thus strengthening the
conjectures we make about the space of deformations of manifolds with weak G2
holonomy.Comment: 34 pages. Minor changes: typos corrected, references added. Version
to appear in Class. Quantum Gra
Type IIA orientifold compactification on SU(2)-structure manifolds
We investigate the effective theory of type IIA string theory on
six-dimensional orientifold backgrounds with SU(2)-structure. We focus on the
case of orientifolds with O6-planes, for which we compute the bosonic effective
action in the supergravity approximation. For a generic SU(2)-structure
background, we find that the low-energy effective theory is a gauged N=2
supergravity where moduli in both vector and hypermultiplets are charged. Since
all these supergravities descend from a corresponding N=4 background, their
scalar target space is always a quotient of a SU(1,1)/U(1) x
SO(6,n)/SO(6)xSO(n) coset, and is therefore also very constrained.Comment: 31 pages; v2: local report number adde
Smeared versus localised sources in flux compactifications
We investigate whether vacuum solutions in flux compactifications that are
obtained with smeared sources (orientifolds or D-branes) still survive when the
sources are localised. This seems to rely on whether the solutions are BPS or
not. First we consider two sets of BPS solutions that both relate to the GKP
solution through T-dualities: (p+1)-dimensional solutions from
spacetime-filling Op-planes with a conformally Ricci-flat internal space, and
p-dimensional solutions with Op-planes that wrap a 1-cycle inside an everywhere
negatively curved twisted torus. The relation between the solution with smeared
orientifolds and the localised version is worked out in detail. We then
demonstrate that a class of non-BPS AdS_4 solutions that exist for IASD fluxes
and with smeared D3-branes (or analogously for ISD fluxes with anti-D3-branes)
does not survive the localisation of the (anti) D3-branes. This casts doubts on
the stringy consistency of non-BPS solutions that are obtained in the limit of
smeared sources.Comment: 23 pages; v2: minor corrections, added references, version published
in JHE
Massive Abelian Gauge Symmetries and Fluxes in F-theory
F-theory compactified on a Calabi-Yau fourfold naturally describes
non-Abelian gauge symmetries through the singularity structure of the elliptic
fibration. In contrast Abelian symmetries are more difficult to study because
of their inherently global nature. We argue that in general F-theory
compactifications there are massive Abelian symmetries, such as the uplift of
the Abelian part of the U(N) gauge group on D7-branes, that arise from
non-Kahler resolutions of the dual M-theory setup. The four-dimensional
F-theory vacuum with vanishing expectation values for the gauge fields
corresponds to the Calabi-Yau limit. We propose that fluxes that are turned on
along these U(1)s are uplifted to non-harmonic four-form fluxes. We derive the
effective four-dimensional gauged supergravity resulting from F-theory
compactifications in the presence of the Abelian gauge factors including the
effects of possible fluxes on the gauging, tadpoles and matter spectrum.Comment: 49 page
Cytogenetic abnormalities and fragile-x syndrome in Autism Spectrum Disorder
BACKGROUND: Autism is a behavioral disorder with impaired social interaction, communication, and repetitive and stereotypic behaviors. About 5–10 % of individuals with autism have 'secondary' autism in which an environmental agent, chromosome abnormality, or single gene disorder can be identified. Ninety percent have idiopathic autism and a major gene has not yet been identified. We have assessed the incidence of chromosome abnormalities and Fragile X syndrome in a population of autistic patients referred to our laboratory. METHODS: Data was analyzed from 433 patients with autistic traits tested using chromosome analysis and/or fluorescence in situ hybridization (FISH) and/or molecular testing for fragile X syndrome by Southern and PCR methods. RESULTS: The median age was 4 years. Sex ratio was 4.5 males to 1 female [354:79]. A chromosome (cs) abnormality was found in 14/421 [3.33 %] cases. The aberrations were: 4/14 [28%] supernumerary markers; 4/14 [28%] deletions; 1/14 [7%] duplication; 3/14 [21%] inversions; 2/14 [14%] translocations. FISH was performed on 23 cases for reasons other than to characterize a previously identified cytogenetic abnormality. All 23 cases were negative. Fragile-X testing by Southern blots and PCR analysis found 7/316 [2.2 %] with an abnormal result. The mutations detected were: a full mutation (fM) and abnormal methylation in 3 [43 %], mosaic mutations with partial methylation of variable clinical significance in 3 [43%] and a permutation carrier [14%]. The frequency of chromosome and fragile-X abnormalities appears to be within the range in reported surveys (cs 4.8-1.7%, FRAX 2–4%). Limitations of our retrospective study include paucity of behavioral diagnostic information, and a specific clinical criterion for testing. CONCLUSIONS: Twenty-eight percent of chromosome abnormalities detected in our study were subtle; therefore a high resolution cytogenetic study with a scrutiny of 15q11.2q13, 2q37 and Xp23.3 region should be standard practice when the indication is autism. The higher incidence of mosaic fragile-X mutations with partial methylation compared to FRAXA positive population [50% vs 15–40%] suggests that faint bands and variations in the Southern band pattern may occur in autistic patients
Genomic and epigenetic evidence for oxytocin receptor deficiency in autism
<p>Abstract</p> <p>Background</p> <p>Autism comprises a spectrum of behavioral and cognitive disturbances of childhood development and is known to be highly heritable. Although numerous approaches have been used to identify genes implicated in the development of autism, less than 10% of autism cases have been attributed to single gene disorders.</p> <p>Methods</p> <p>We describe the use of high-resolution genome-wide tilepath microarrays and comparative genomic hybridization to identify copy number variants within 119 probands from multiplex autism families. We next carried out DNA methylation analysis by bisulfite sequencing in a proband and his family, expanding this analysis to methylation analysis of peripheral blood and temporal cortex DNA of autism cases and matched controls from independent datasets. We also assessed oxytocin receptor (OXTR) gene expression within the temporal cortex tissue by quantitative real-time polymerase chain reaction (PCR).</p> <p>Results</p> <p>Our analysis revealed a genomic deletion containing the oxytocin receptor gene, <it>OXTR </it>(MIM accession no.: 167055), previously implicated in autism, was present in an autism proband and his mother who exhibits symptoms of obsessive-compulsive disorder. The proband's affected sibling did not harbor this deletion but instead may exhibit epigenetic misregulation of this gene through aberrant gene silencing by DNA methylation. Further DNA methylation analysis of the CpG island known to regulate <it>OXTR </it>expression identified several CpG dinucleotides that show independent statistically significant increases in the DNA methylation status in the peripheral blood cells and temporal cortex in independent datasets of individuals with autism as compared to control samples. Associated with the increase in methylation of these CpG dinucleotides is our finding that <it>OXTR </it>mRNA showed decreased expression in the temporal cortex tissue of autism cases matched for age and sex compared to controls.</p> <p>Conclusion</p> <p>Together, these data provide further evidence for the role of OXTR and the oxytocin signaling pathway in the etiology of autism and, for the first time, implicate the epigenetic regulation of <it>OXTR </it>in the development of the disorder.</p> <p>See the related commentary by Gurrieri and Neri: <url>http://www.biomedcentral.com/1741-7015/7/63</url></p