56 research outputs found

    Generalized Global Defect Solutions

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    We investigate the presence of defect structures in generalized models described by real scalar field in (1,1)(1,1) space-time dimensions. We work with two distinct generalizations, one in the form of a product of functions of the field and its derivative, and the other as a sum. We search for static solutions and study the corresponding linear stability on general grounds. We illustrate the results with several examples, where we find stable defect structures of modified profile. In particular, we show how the new defect solutions may give rise to evolutions not present in the standard scenario in higher spatial dimensions.Comment: RevTex, 10 pages, 2 figures; version to appear in EPJ

    Localized D-dimensional global k-defects

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    We explicitly demonstrate the existence of static global defect solutions of arbitrary dimensionality whose energy does not diverge at spatial infinity, by considering maximally symmetric solutions described by an action with non-standard kinetic terms in a D+1 dimensional Minkowski space-time. We analytically determine the defect profile both at small and large distances from the defect centre. We verify the stability of such solutions and discuss possible implications of our findings, in particular for dark matter and charge fractionalization in graphene.Comment: 6 pages, published versio

    Chronic treatment with ivabradine does not affect cardiovascular autonomic control in rats

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    A low resting heart rate (HR) would be of great benefit in cardiovascular diseases. Ivabradine-a novel selective inhibitor of hyperpolarization-activated cyclic nucleotide gated (HCN) channels- has emerged as a promising HR lowering drug. Its effects on the autonomic HR control are little known. This study assessed the effects of chronic treatment with ivabradine on the modulatory, reflex and tonic cardiovascular autonomic control and on the renal sympathetic nerve activity (RSNA). Male Wistar rats were divided in 2 groups, receiving intraperitoneal injections of vehicle (VEH) or ivabradine (IVA) during 7 or 8 consecutive days. Rats were submitted to vessels cannulation to perform arterial blood pressure (AP) and HR recordings in freely moving rats. Time series of resting pulse interval and systolic AP were used to measure cardiovascular variability parameters. We also assessed the baroreflex, chemoreflex and the Bezold-Jarish reflex sensitivities. To better evaluate the effects of ivabradine on the autonomic control of the heart, we performed sympathetic and vagal autonomic blockade. As expected, ivabradine-treated rats showed a lower resting (VEH: 362 \ufffd 16 bpm vs. IVA: 260 \ufffd 14 bpm, p = 0.0005) and intrinsic HR (VEH: 369 \ufffd 9 bpm vs. IVA: 326 \ufffd 11 bpm, p = 0.0146). However, the chronic treatment with ivabradine did not change normalized HR spectral parameters LF (nu) (VEH: 24.2 \ufffd 4.6 vs. IVA: 29.8 \ufffd 6.4; p > 0.05); HF (nu) (VEH: 75.1 \ufffd 3.7 vs. IVA: 69.2 \ufffd 5.8; p > 0.05), any cardiovascular reflexes, neither the tonic autonomic control of the HR (tonic sympathovagal index; VEH: 0.91\ufffd 0.02 vs. IVA: 0.88 \ufffd 0.03, p = 0.3494). We performed the AP, HR and RSNA recordings in urethane-anesthetized rats. The chronic treatment with ivabradine reduced the resting HR (VEH: 364 \ufffd 12 bpm vs. IVA: 207 \ufffd 11 bpm, p < 0.0001), without affecting RSNA (VEH: 117 \ufffd 16 vs. IVA: 120 \ufffd 9 spikes/s, p = 0.9100) and mean arterial pressure (VEH: 70 \ufffd 4 vs. IVA: 77 \ufffd 6 mmHg, p = 0.3293). Our results suggest that, in health rats, the long-term treatment with ivabradine directly reduces the HR without changing the RSNA modulation and the reflex and tonic autonomic control of the heart

    Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.

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    BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362
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