151 research outputs found
Ultraviolet Fixed Points in Gauge and SUSY Field Theories in Extra Dimensions
We consider gauge field theories in following the Wilson RG approach
and show that they possess the ultraviolet fixed points where the gauge
coupling is dimensionless in any space-time dimension. At the fixed point the
anomalous dimensions of the field and vertex operators are known exactly. These
fixed points are nonperturbative and correspond to conformal invariant
theories. The same phenomenon also happens in supersymmetric theories with the
Yukawa type interactions.Comment: LaTeX, 10pp. v2: Comments and references adde
Geometric Phase, Curvature, and Extrapotentials in Constrained Quantum Systems
We derive an effective Hamiltonian for a quantum system constrained to a
submanifold (the constraint manifold) of configuration space (the ambient
space) by an infinite restoring force. We pay special attention to how this
Hamiltonian depends on quantities which are external to the constraint
manifold, such as the external curvature of the constraint manifold, the
(Riemannian) curvature of the ambient space, and the constraining potential. In
particular, we find the remarkable fact that the twisting of the constraining
potential appears as a gauge potential in the constrained Hamiltonian. This
gauge potential is an example of geometric phase, closely related to that
originally discussed by Berry. The constrained Hamiltonian also contains an
effective potential depending on the external curvature of the constraint
manifold, the curvature of the ambient space, and the twisting of the
constraining potential. The general nature of our analysis allows applications
to a wide variety of problems, such as rigid molecules, the evolution of
molecular systems along reaction paths, and quantum strip waveguides.Comment: 27 pages with 1 figure, submitted to Phys. Rev.
N=1* in 5 dimensions: Dijkgraaf-Vafa meets Polchinski-Strassler
One of the powerful techniques to analyze the 5 dimensional Super Yang Mills
theory with a massive hypermultiplet (N=1*) is provided by the AdS/CFT
correspondence. It predicts that, for certain special values of the
hypermultiplet mass, this theory develops nonperturbative branches of the
moduli space as well as new light degrees of freedom.
We use the higher dimensional generalization of the matrix model/gauge theory
correspondence and recover all the prediction of the supergravity analysis. We
construct the map between the four dimensional holomorphic superpotential and
the five dimensional action and explicitly show that the superpotential is flat
along the nonperturbative branches. This is the first instance in which the
Dijkgraaf-Vafa method is used to analyze intrinsically higher dimensional
phenomena.Comment: 28 pages, Late
Amyloid and tau pathology associations with personality traits, neuropsychiatric symptoms, and cognitive lifestyle in the preclinical phases of sporadic and autosomal dominant Alzheimer’s disease
Background
Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits.
Methods
A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle.
Results
In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology.
Conclusions
In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression
Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study
The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10−8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10−8). The top IBC association for SBP was rs2012318 (P= 6.4 × 10−6) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10−6) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexit
Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study.
The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10(-8)) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10(-8)). The top IBC association for SBP was rs2012318 (P= 6.4 × 10(-6)) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10(-6)) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexity
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