51 research outputs found
Electromagnetic corrections in eta --> 3 pi decays
We re-evaluate the electromagnetic corrections to eta --> 3 pi decays at
next-to-leading order in the chiral expansion, arguing that effects of order
e^2(m_u-m_d) disregarded so far are not negligible compared to other
contributions of order e^2 times a light quark mass. Despite the appearance of
the Coulomb pole in eta --> pi+ pi- pi0 and cusps in eta --> 3 pi0, the overall
corrections remain small.Comment: 21 pages, 11 figures; references updated, version published in EPJ
Physics with the KLOE-2 experiment at the upgraded DANE
Investigation at a --factory can shed light on several debated issues
in particle physics. We discuss: i) recent theoretical development and
experimental progress in kaon physics relevant for the Standard Model tests in
the flavor sector, ii) the sensitivity we can reach in probing CPT and Quantum
Mechanics from time evolution of entangled kaon states, iii) the interest for
improving on the present measurements of non-leptonic and radiative decays of
kaons and eta/eta mesons, iv) the contribution to understand the
nature of light scalar mesons, and v) the opportunity to search for narrow
di-lepton resonances suggested by recent models proposing a hidden dark-matter
sector. We also report on the physics in the continuum with the
measurements of (multi)hadronic cross sections and the study of gamma gamma
processes.Comment: 60 pages, 41 figures; added affiliation for one of the authors; added
reference to section
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
Genome-wide analysis of 102,084 migraine cases identifies 123 risk loci and subtype-specific risk alleles
Migraine affects over a billion individuals worldwide but its genetic underpinning remains largely unknown. Here, we performed a genome-wide association study of 102,084 migraine cases and 771,257 controls and identified 123 loci, of which 86 are previously unknown. These loci provide an opportunity to evaluate shared and distinct genetic components in the two main migraine subtypes: migraine with aura and migraine without aura. Stratification of the risk loci using 29,679 cases with subtype information indicated three risk variants that seem specific for migraine with aura (in HMOX2, CACNA1A and MPPED2), two that seem specific for migraine without aura (near SPINK2 and near FECH) and nine that increase susceptibility for migraine regardless of subtype. The new risk loci include genes encoding recent migraine-specific drug targets, namely calcitonin gene-related peptide (CALCA/CALCB) and serotonin 1F receptor (HTR1F). Overall, genomic annotations among migraine-associated variants were enriched in both vascular and central nervous system tissue/cell types, supporting unequivocally that neurovascular mechanisms underlie migraine pathophysiology.publishedVersionPeer reviewe
Genome-wide analysis of 102,084 migraine cases identifies 123 risk loci and subtype-specific risk alleles
Genome-wide association analyses identify 123 susceptibility loci for migraine and implicate neurovascular mechanisms in its pathophysiology. Subtype analyses highlight risk loci specific for migraine with or without aura in addition to shared risk variants.Migraine affects over a billion individuals worldwide but its genetic underpinning remains largely unknown. Here, we performed a genome-wide association study of 102,084 migraine cases and 771,257 controls and identified 123 loci, of which 86 are previously unknown. These loci provide an opportunity to evaluate shared and distinct genetic components in the two main migraine subtypes: migraine with aura and migraine without aura. Stratification of the risk loci using 29,679 cases with subtype information indicated three risk variants that seem specific for migraine with aura (in HMOX2, CACNA1A and MPPED2), two that seem specific for migraine without aura (near SPINK2 and near FECH) and nine that increase susceptibility for migraine regardless of subtype. The new risk loci include genes encoding recent migraine-specific drug targets, namely calcitonin gene-related peptide (CALCA/CALCB) and serotonin 1F receptor (HTR1F). Overall, genomic annotations among migraine-associated variants were enriched in both vascular and central nervous system tissue/cell types, supporting unequivocally that neurovascular mechanisms underlie migraine pathophysiology.Clinical epidemiolog
Plasma lipid profiles discriminate bacterial from viral infection in febrile children
Fever is the most common reason that children present to Emergency Departments. Clinical signs and symptoms suggestive of bacterial infection ar
A novel high throughput technique for identifying monoclonal antibodies capable of death receptor induced apoptosis
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