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We present a first-principles lattice QCD+QED calculation at physical pion mass of the leading-order hadronic vacuum polarization contribution to the muon anomalous magnetic moment. The total contribution of up, down, strange, and charm quarks including QED and strong isospin breaking effects is a_{µ}^{HVP LO}=715.4(18.7)×10^{-10}. By supplementing lattice data for very short and long distances with R-ratio data, we significantly improve the precision to a_{µ}^{HVP LO}=692.5(2.7)×10^{-10}. This is the currently most precise determination of a_{µ}^{HVP LO}.
RESUMO
We report the first lattice QCD calculation of the hadronic vacuum polarization (HVP) disconnected contribution to the muon anomalous magnetic moment at physical pion mass. The calculation uses a refined noise-reduction technique that enables the control of statistical uncertainties at the desired level with modest computational effort. Measurements were performed on the 48^{3}×96 physical-pion-mass lattice generated by the RBC and UKQCD Collaborations. We find the leading-order hadronic vacuum polarization a_{µ}^{HVP(LO)disc}=-9.6(3.3)(2.3)×10^{-10}, where the first error is statistical and the second systematic.
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OBJECTIVE: Perivascular adipose tissue (PVAT) function during aging has not been investigated in detail so far and its effect on vasodilation remains to be fully elucidated. The aim of this study was to investigate endothelium-dependent vasodilation of thoracic aorta in a mouse model of accelerated, selective vascular smooth muscle and PVAT aging, induced by SM22α-Cre-driven genetic deletion of the endonuclease ERCC1 (SMC-KO mice) versus healthy littermates (LM). We hypothesized that PVAT enhances vasodilation in LM, possibly through adiponectin secretion, which might be compromised in SMC-KO animals. METHODS: Thoracic aorta was isolated from SMC-KO animals and LM and segments with and without PVAT were mounted in wire myography setups. The endothelium-dependent vasodilation was assessed via acetylcholine dose-response curves and pathway contribution was studied. Moreover, adiponectin secretion was measured after stimulating the aortic segments with PVAT with acetylcholine. RESULTS: Adiponectin, secreted by PVAT, led to increased NO-contribution to endothelium-dependent vasodilation in healthy LM, although this did not increase maximum relaxation due to loss of EDH. Endothelium-dependent vasodilation was decreased in SMC-KO animals due to reduced NO-contribution and complete EDH loss. Despite strong lipodystrophy the PVAT partially compensated for lost vasodilation in SMC-KO. LM PVAT contained acetylcholinesterase that attenuated acetylcholine responses. This was lost in SMC-KO. CONCLUSIONS: PVAT-derived adiponectin is able to partially compensate for age-related decline in NO-mediated vasodilation, even during strong lipodystrophy, in conditions of absence of compensating EDH. In aorta with healthy PVAT acetylcholinesterase modulates vascular tone, but this is lost during aging, further compensating for decreased acetylcholine responsiveness. Thus, preservation of adiponectin levels, through relatively increased production in lipodystrophic PVAT, and reduction of cholinesterase might be regulatory mechanisms of the PVAT to preserve cholinergic vasodilation during aging.
Assuntos
Lipodistrofia , Vasodilatação , Camundongos , Animais , Adiponectina/genética , Acetilcolinesterase/metabolismo , Acetilcolinesterase/farmacologia , Acetilcolina/farmacologia , Acetilcolina/metabolismo , Músculo Liso Vascular/metabolismo , Tecido Adiposo/metabolismo , Envelhecimento , Lipodistrofia/metabolismoAssuntos
Arterite , Arterite de Células Gigantes , Fluordesoxiglucose F18 , Arterite de Células Gigantes/complicações , Arterite de Células Gigantes/diagnóstico por imagem , Humanos , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada/métodos , Tomografia por Emissão de PósitronsRESUMO
We review lattice results related to pion, kaon, D- and B-meson physics with the aim of making them easily accessible to the particle-physics community. More specifically, we report on the determination of the light-quark masses, the form factor [Formula: see text], arising in the semileptonic [Formula: see text] transition at zero momentum transfer, as well as the decay constant ratio [Formula: see text] and its consequences for the CKM matrix elements [Formula: see text] and [Formula: see text]. Furthermore, we describe the results obtained on the lattice for some of the low-energy constants of [Formula: see text] and [Formula: see text] Chiral Perturbation Theory. We review the determination of the [Formula: see text] parameter of neutral kaon mixing as well as the additional four B parameters that arise in theories of physics beyond the Standard Model. The latter quantities are an addition compared to the previous review. For the heavy-quark sector, we provide results for [Formula: see text] and [Formula: see text] (also new compared to the previous review), as well as those for D- and B-meson-decay constants, form factors, and mixing parameters. These are the heavy-quark quantities most relevant for the determination of CKM matrix elements and the global CKM unitarity-triangle fit. Finally, we review the status of lattice determinations of the strong coupling constant [Formula: see text].
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The study described the molecular cytogenetic characterization of myeloma cells in 130 patients via interphase fluorescence in situ hybridization. Nine repetitive DNA probes (for chromosomes 3, 7, 9, 11, 15, 17, 18, X, and Y) as well as seven single-copy DNA probes (for chromosomes 13, 17, 21, and two each for chromosomes 5 and 22) were used for the hybridizations. Using this panel of probes, we were able to show aberrations in 86% of patients. Most of them had one to three aberrations. There was a distinct correlation between the number of aberrations per patient and the tumor stage. Thus, the proportion of patients with 8-12 aberrations increased from 16% in stage II to 26% in stage III. There were marked differences among the chromosomes with respect to the prevalence of genomic losses and gains and deletions of gene loci. Chromosomes 3, 5, 7, 9, 11, 15, and 21 showed a preference for genomic gains. Losses were most often found for chromosomes 13 and 17 (locus specific) as well as for the X and Y chromosomes. The frequency of monosomies and trisomies were approximately the same for chromosomes 15 and 18, which indicates a skewed pattern of distribution. We found two specific aberrations that caused distinct changes in the survival rates of the patients: deletion 13q14 (28% of patients) and translocation of the IGH locus 14q32 (79% of 39 patients who were analyzed separately). The results obtained in this study yielded data of extremely relevant prognostic value.
Assuntos
Aberrações Cromossômicas , Hibridização in Situ Fluorescente , Interfase , Mieloma Múltiplo/diagnóstico , Mieloma Múltiplo/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Mieloma Múltiplo/patologia , PrognósticoRESUMO
We review lattice results related to pion, kaon, [Formula: see text]- and [Formula: see text]-meson physics with the aim of making them easily accessible to the particle-physics community. More specifically, we report on the determination of the light-quark masses, the form factor [Formula: see text], arising in semileptonic [Formula: see text] transition at zero momentum transfer, as well as the decay-constant ratio [Formula: see text] of decay constants and its consequences for the CKM matrix elements [Formula: see text] and [Formula: see text]. Furthermore, we describe the results obtained on the lattice for some of the low-energy constants of [Formula: see text] and [Formula: see text] Chiral Perturbation Theory and review the determination of the [Formula: see text] parameter of neutral kaon mixing. The inclusion of heavy-quark quantities significantly expands the FLAG scope with respect to the previous review. Therefore, we focus here on [Formula: see text]- and [Formula: see text]-meson decay constants, form factors, and mixing parameters, since these are most relevant for the determination of CKM matrix elements and the global CKM unitarity-triangle fit. In addition we review the status of lattice determinations of the strong coupling constant [Formula: see text].
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We present the first results for the K13 form factor from simulations with 2+1 flavors of dynamical domain wall quarks. Combining our result, namely, f+(0)=0.964(5) with the latest experimental results for Kl3 decays leads to |V us|=0.2249(14), reducing the uncertaintity in this important parameter. For the O(p6) term in the chiral expansion we obtain Delta f=-0.013(5).