105 research outputs found
Running couplings for the simultaneous decoupling of heavy quarks
Scale-invariant running couplings are constructed for several quarks being
decoupled together, without reference to intermediate thresholds.
Large-momentum scales can also be included. The result is a multi-scale
generalization of the renormalization group applicable to any order.
Inconsistencies in the usual decoupling procedure with a single running
coupling can then be avoided, e.g. when cancelling anomalous corrections from
t,b quarks to the axial charge of the proton.Comment: 12 pages, 1 figure, version to appear in PLB. Pages 8-11 and Fig. 1
are new, with consequent changes to the abstract, page 2, and the references.
We show that our multi-scale renormalization group is needed to achieve
anomaly cancellation in t,b decoupling from the weak neutral current, and
extend it to include large moment
Transverse Momentum in Semi-Inclusive Polarized Deep Inelastic Scattering and the Spin-Flavor Structure of the Proton
The non-valence spin-flavor structure of the nucleon extracted from
semi-inclusive measurements of polarized deep inelastic scattering depends
strongly on the transverse momentum of the detected hadrons which are used to
determine the individual polarized sea distributions. This physics may explain
the recent HERMES observation of a positively polarized strange sea through
semi-inclusive scattering, in contrast to the negative strange sea polarization
deduced from inclusive polarized deep inelastic scattering.Comment: 4 pages, revtex style, 2 figure
Decoupling heavy particles simultaneously
The renormalization group is extended to cases where several heavy particles
are decoupled at the same time. This involves large logarithms which are
scale-invariant and so cannot be eliminated by a change of renormalization
scheme. A set of scale-invariant running couplings, one for each heavy
particle, is constructed without reference to intermediate thresholds. The
entire heavy-quark correction to the axial charge of the weak neutral current
is derived to next-to-leading order, and checked in leading order by evaluating
diagrams explicitly. The mechanism for cancelling contributions from the top
and bottom quarks in the equal-mass limit is surprisingly non-trivial.Comment: 6 pages, 4 figures. Talk presented at the "QCD Down Under" Workshop,
Barossa Valley and Adelaide, Australia, 10-19 March 2004, with ref 8 now
linked to hep-ph/050727
The Multidimensional Study of Viral Campaigns as Branching Processes
Viral campaigns on the Internet may follow variety of models, depending on
the content, incentives, personal attitudes of sender and recipient to the
content and other factors. Due to the fact that the knowledge of the campaign
specifics is essential for the campaign managers, researchers are constantly
evaluating models and real-world data. The goal of this article is to present
the new knowledge obtained from studying two viral campaigns that took place in
a virtual world which followed the branching process. The results show that it
is possible to reduce the time needed to estimate the model parameters of the
campaign and, moreover, some important aspects of time-generations relationship
are presented.Comment: In proceedings of the 4th International Conference on Social
Informatics, SocInfo 201
Crises and collective socio-economic phenomena: simple models and challenges
Financial and economic history is strewn with bubbles and crashes, booms and
busts, crises and upheavals of all sorts. Understanding the origin of these
events is arguably one of the most important problems in economic theory. In
this paper, we review recent efforts to include heterogeneities and
interactions in models of decision. We argue that the Random Field Ising model
(RFIM) indeed provides a unifying framework to account for many collective
socio-economic phenomena that lead to sudden ruptures and crises. We discuss
different models that can capture potentially destabilising self-referential
feedback loops, induced either by herding, i.e. reference to peers, or
trending, i.e. reference to the past, and account for some of the phenomenology
missing in the standard models. We discuss some empirically testable
predictions of these models, for example robust signatures of RFIM-like herding
effects, or the logarithmic decay of spatial correlations of voting patterns.
One of the most striking result, inspired by statistical physics methods, is
that Adam Smith's invisible hand can badly fail at solving simple coordination
problems. We also insist on the issue of time-scales, that can be extremely
long in some cases, and prevent socially optimal equilibria to be reached. As a
theoretical challenge, the study of so-called "detailed-balance" violating
decision rules is needed to decide whether conclusions based on current models
(that all assume detailed-balance) are indeed robust and generic.Comment: Review paper accepted for a special issue of J Stat Phys; several
minor improvements along reviewers' comment
Characterisation of age and polarity at onset in bipolar disorder
Background
Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.
Aims
To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.
Method
Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.
Results
Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.
Conclusions
AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses
New insights into the genetic etiology of Alzheimer's disease and related dementias
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele
- …