1,358 research outputs found

    Running of Fermion Observables in Non-Supersymmetric SO(10) Models

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    We investigate the complete renormalization group running of fermion observables in two different realistic non-supersymmetric models based on the gauge group SO(10)\textrm{SO}(10) with intermediate symmetry breaking for both normal and inverted neutrino mass orderings. Contrary to results of previous works, we find that the model with the more minimal Yukawa sector of the Lagrangian fails to reproduce the measured values of observables at the electroweak scale, whereas the model with the more extended Yukawa sector can do so if the neutrino masses have normal ordering. The difficulty in finding acceptable fits to measured data is a result of the added complexity from the effect of an intermediate symmetry breaking as well as tension in the value of the leptonic mixing angle θ23\theta^\ell_{23}.Comment: 15 pages, 3 figures, 4 tables. Final version published in JHE

    Fits to Non-Supersymmetric SO(10) Models with Type I and II Seesaw Mechanisms Using Renormalization Group Evolution

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    We consider numerical fits to non-supersymmetric SO(10)\mathrm{SO}(10)-based models in which neutrino mass is generated by the type-I or type-II seesaw mechanism or a combination of both. The fits are performed with a sophisticated top-down procedure, taking into account the renormalization group equations of the gauge and Yukawa couplings, integrating out relevant degrees of freedom at their corresponding mass scales, and using recent data for the Standard Model observables. We find acceptable fits for normal neutrino mass ordering only and with neutrino mass generated by either type-I seesaw only or a combination of types I and II seesaw in which type-I seesaw is dominant. Furthermore, we find predictions from the best fit regarding the small neutrino masses, the effective neutrinoless double beta decay mass, and the leptonic CP-violating phase. Finally, we show that the fits are rather insensitive to the chosen value of the unification scale.Comment: 22 pages, 3 figures, 3 tables. Final version published in JHE

    Realizing unification in two different SO(10) models with one intermediate breaking scale

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    We derive the threshold corrections in SO(10)\mathrm{SO}(10) grand unified models with the intermediate symmetry being flipped SU(5)×U(1)\mathrm{SU}(5)\times\mathrm{U}(1) or SU(3)×SU(2)×U(1)×U(1)\mathrm{SU}(3)\times\mathrm{SU}(2)\times\mathrm{U}(1)\times\mathrm{U}(1), with the masses of the scalar fields set by the survival hypothesis. These models do not achieve gauge coupling unification if the matching conditions do not take threshold corrections into account. We present results showing the required size of threshold corrections for any value of the intermediate and unification scales. In particular, our results demonstrate that both of these models are disfavored since they require large threshold corrections to allow for unification with a predicted proton lifetime above current experimental bounds.Comment: 6 pages, 5 figures. Final version published in Eur. Phys. J.

    Long-term impact of postconditioning on infarct size and left ventricular ejection fraction in patients with ST-elevation myocardial infarction

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    Background: Ischemic postconditioning (PostC), reperfusion in brief cycles, is known to induce short-term reduction in infarct size in patients with ST elevation myocardial infarction (STEMI), especially among those with large myocardium at risk (MaR). The aim of the present study was to investigate the long-term effect of PostC on infarct size and left ventricular ejection fraction (LVEF). Methods: Sixty-eight patients with a first STEMI were randomised to primary percutaneous coronary intervention (PCI) (n = 35) or PCI followed by PostC (n = 33). MaR was determined as abnormally contracting segments on left ventricular angiogram. Cardiac magnetic resonance was performed at 3 and 12 months for the determination of infarct size and LVEF. Results: Overall there was no difference in infarct size expressed in percentage of MaR between patients randomised to the control (31%; 23, 41) and PostC (31%; 23, 43) groups at 12 months. Likewise there was no difference in LVEF between control (49%; 41, 55) and PostC (52%; 45, 55). In contrast, patients in the PostC group with MaR in the upper quartile had a significantly smaller infarct size (29%; 18, 38) than those in the control group (40%; 34, 48; p < 0.05) at 12 months. In these patients LVEF was higher in the PostC (47%; 43, 50) compared to the control group (38%; 34, 42; p < 0.01). Conclusions: In this long-term follow-up study PostC did not reduce infarct size in relation to MaR or improved LVEF in the overall study population. However, the present data suggest that PostC exerts long-term beneficial effects in patients with large MaR thereby extending previously published short-term observations

    Myocardium at risk by magnetic resonance imaging: head-to-head comparison of T2-weighted imaging and early gadolinium enhanced steady state free precession

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    AIMS: To determine the myocardial salvage index, the extent of infarction needs to be related to the myocardium at risk (MaR). Thus, the ability to assess both infarct size and MaR is of central clinical and scientific importance. The aim of the present study was to explore the relationship between T2-weighted cardiac magnetic resonance (CMR) and contrast-enhanced steady-state free precession (CE-SSFP) CMR for the determination of MaR in patients with acute myocardial infarction. METHODS AND RESULTS: Twenty-one prospectively included patients with first-time ST-elevation myocardial infarction underwent CMR 1 week after primary percutaneous coronary intervention. For the assessment of MaR, T2-weighted images were acquired before and CE-SSFP images were acquired after the injection of a gadolinium-based contrast agent. For the assessment of infarct size, late gadolinium enhancement images were acquired. The MaR by T2-weighted imaging and CE-SSFP was 29 ± 11 and 32 ± 12% of the left ventricle, respectively. Thus, the MaR with T2-weighted imaging was slightly smaller than that by CE-SSFP (-3.0 ± 4.0%; P < 0.01). There was a significant correlation between the two MaR measures (r(2)= 0.89, P < 0.01), independent of the time after contrast agent administration at which the CE-SSFP was commenced (2-8 min). CONCLUSION: There is a good agreement between the MaR assessed by T2-weighted imaging and that assessed by CE-SSFP in patients with reperfused acute myocardial infarction 1 week after the acute event. Thus, both methods can be used to determine MaR and myocardial salvage at this point in time

    Neuromuscular responses to mild-muscle damaging eccentric exercise in a low glycogen state.

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    The aim of this study was to examine the effect of low muscle glycogen on the neuromuscular responses to maximal eccentric contractions. Fourteen healthy men (22±3years) performed single-leg cycling (20min at ∼75% maximal oxygen uptake (V̇O2 max); eight 90 s sprints at a 1:1 work-to-rest ratio (5% decrements from 90% to 55% V̇O2 max until exhaustion) the evening before 100 eccentric (1.57rads(-1)) with reduced (RED) and normal glycogen (NORM). Neuromuscular responses were measured during and up to 48h after with maximal voluntary and involuntary (twitch, 20Hz and 50Hz) isometric contractions. During eccentric contractions, peak torque decreased (RED: -16.1±2.5%; NORM: -6.2±5.1%) and EMG frequency increased according to muscle length. EMG activity decreased for RED only. After eccentric contractions, maximal isometric force was reduced up to 24h for NORM (-13.5±5.8%) and 48h for RED (-7.4±10.9%). Twelve hours after eccentric contractions, twitch force and the 20:50Hz ratio were decreased for RED but not for NORM. Immediate involuntary with prolonged voluntary force loss suggests that reduced glycogen is associated with increased susceptibility to mild muscle-damaging eccentric exercise with contributions of peripheral and central mechanisms to be different during recovery

    A minimal non-supersymmetric SO(10) model with Peccei–Quinn symmetry

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    Publisher's version (útgefin grein)We present a minimal non-supersymmetric SO(10) GUT breaking directly to the Standard Model gauge group. Precise gauge coupling unification is achieved due to the presence of two color-octet scalars, one of which is accessible to LHC searches. Proton lifetime is predicted to be below 4.5 × 1034 years, which is within the projected five-year sensitivity of the proposed Hyper-Kamiokande experiment. We find that the Standard Model observables are reproduced to a reasonable accuracy in a numerical fit, which also predicts the unknown neutrino parameters. Finally, the two scalar representations stabilize the electroweak vacuum and the dark matter is comprised of axionsS.M.B. thanks the “Roland Gustafssons Stiftelse för teoretisk fysik” for partial financial support. T.O. acknowledges support by the Swedish Research Council (Vetenskapsrådet) through contract No. 2017-03934 and the KTH Royal Institute of Technology for a sabbatical period at the University of Iceland. M.P. thanks “Stiftelsen Olle Engkvist Byggmästare” for financial support through contract No. 2017/85 (179) as well as “Roland Gustafssons Stiftelse för teoretisk fysik”. Numerical computations were performed on resources provided by the Swedish National Infrastructure for Computing (SNIC) at PDC Center for High Performance Computing (PDC-HPC) at KTH Royal Institute of Technology in Stockholm, Sweden under project numbers PDC-2018-49 and SNIC 2018/3-559.Peer Reviewe

    Assessment of myocardium at risk with contrast enhanced steady-state free precession cine cardiovascular magnetic resonance compared to single-photon emission computed tomography

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    <p>Abstract</p> <p>Background</p> <p>Final infarct size following coronary occlusion is determined by the duration of ischemia, the size of myocardium at risk (MaR) and reperfusion injury. The reference method for determining MaR, single-photon emission computed tomography (SPECT) before reperfusion, is impractical in an acute setting. The aim of the present study was to evaluate whether MaR can be determined from the contrast enhanced myocardium using steady-state free precession (SSFP) cine cardiovascular magnetic resonance (CMR) performed one week after the acute event in ST-elevation myocardial infarction (STEMI) patients with total coronary occlusion.</p> <p>Results</p> <p>Sixteen patients with STEMI (age 64 ± 8 years) received intravenous 99 m-Tc immediately before primary percutaneous coronary intervention. SPECT was performed within four hours. MaR was defined as the non-perfused myocardial volume derived with SPECT. CMR was performed 7.8 ± 1.2 days after the myocardial infarction using a protocol in which the contrast agent was administered before acquisition of short-axis SSFP cines. MaR was evaluated as the contrast enhanced myocardial volume in the cines by two blinded observers. MaR determined from the enhanced region on cine CMR correlated significantly with that derived with SPECT (r<sup>2 </sup>= 0.78, p < 0.001). The difference in MaR determined by CMR and SPECT was 0.5 ± 5.1% (mean ± SD). The interobserver variability of contrast enhanced cine SSFP measurements was 1.6 ± 3.7% (mean ± SD) of the left ventricle wall volume.</p> <p>Conclusions</p> <p>Contrast enhanced SSFP cine CMR performed one week after acute infarction accurately depicts MaR prior to reperfusion in STEMI patients with total occlusion undergoing primary PCI. This suggests that a single CMR examination might be performed for determination of MaR and infarct size.</p

    Contribution of α2-adrenoceptors and Y1 neuropeptide Y receptors to the blunting of sympathetic vasoconstriction induced by systemic hypoxia in the rat

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    There is evidence that sympathetically evoked vasoconstriction in skeletal muscle is blunted in systemic hypoxia, but the mechanisms underlying this phenomenon are not clear. In Saffan-anaesthetized Wistar rats, we have studied the role of α2-adrenoceptors and neuropeptide Y (NPY) Y1 receptors in mediating vasoconstriction evoked by direct stimulation of the lumbar sympathetic chain by different patterns of impulses in normoxia (N) and systemic hypoxia (H: breathing 8% O2). Patterns comprised 120 impulses delivered in bursts over a 1 min period at 40 or 20 Hz, or continuously at 2 Hz. Hypoxia attenuated the evoked increases in femoral vascular resistance (FVR) by all patterns, the response to 2 Hz being most affected (40 Hz bursts: N = 3.25 ± 0.75 arbitrary resistance units (RU); H = 1.14 ± 0.29 RU). Yohimbine (Yoh, α2-adrenoceptor antagonist) or BIBP 3226 (Y1-receptor antagonist) did not affect baseline FVR. In normoxia, Yoh attenuated the responses evoked by high frequency bursts and 2 Hz, whereas BIBP 3226 only attenuated the response to 40 Hz (40 Hz bursts: N + Yoh = 2.1 ± 0.59 RU; N + BIBP 3226 = 1.9 ± 0.4 RU). In hypoxia, Yoh did not further attenuate the evoked responses, but BIBP 3226 further attenuated the response to 40 Hz bursts. These results indicate that neither α2-adrenoceptors nor Y1 receptors contribute to basal vascular tone in skeletal muscle, but both contribute to constrictor responses evoked by high frequency bursts of sympathetic activity. We propose that in systemic hypoxia, the α2-mediated component represents about 50% of the sympathetically evoked constriction that is blunted, whereas the contribution made by Y1 receptors is resistant. Thus we suggest the importance of NPY in the regulation of FVR and blood pressure increases during challenges such as systemic hypoxia
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