269 research outputs found

    Ratchet effect on a relativistic particle driven by external forces

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    We study the ratchet effect of a damped relativistic particle driven by both asymmetric temporal bi-harmonic and time-periodic piecewise constant forces. This system can be formally solved for any external force, providing the ratchet velocity as a non-linear functional of the driving force. This allows us to explicitly illustrate the functional Taylor expansion formalism recently proposed for this kind of systems. The Taylor expansion reveals particularly useful to obtain the shape of the current when the force is periodic, piecewise constant. We also illustrate the somewhat counterintuitive effect that introducing damping may induce a ratchet effect. When the force is symmetric under time-reversal and the system is undamped, under symmetry principles no ratchet effect is possible. In this situation increasing damping generates a ratchet current which, upon increasing the damping coefficient eventually reaches a maximum and decreases toward zero. We argue that this effect is not specific of this example and should appear in any ratchet system with tunable damping driven by a time-reversible external force.Comment: 1 figur

    Symmetries shape the current in ratchets induced by a bi-harmonic force

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    Equations describing the evolution of particles, solitons, or localized structures, driven by a zero-average, periodic, external force, and invariant under time reversal and a half-period time shift, exhibit a ratchet current when the driving force breaks these symmetries. The bi-harmonic force f(t)=ϵ1cos(qωt+ϕ1)+ϵ2cos(pωt+ϕ2)f(t)=\epsilon_1\cos(q \omega t+\phi_1)+\epsilon_2\cos(p\omega t+\phi_2) does it for almost any choice of ϕ1\phi_{1} and ϕ2\phi_{2}, provided pp and qq are two co-prime integers such that p+qp+q is odd. It has been widely observed, in experiments in Josephson-junctions, photonic crystals, etc., as well as in simulations, that the ratchet current induced by this force has the shape vϵ1pϵ2qcos(pϕ1qϕ2+θ0)v\propto\epsilon_1^p\epsilon_2^q\cos(p \phi_{1} - q \phi_{2} + \theta_0) for small amplitudes, where θ0\theta_0 depends on the damping (θ0=π/2\theta_0=\pi/2 if there is no damping, and θ0=0\theta_0=0 for overdamped systems). We rigorously prove that this precise shape can be obtained solely from the broken symmetries of the system and is independent of the details of the equation describing the system.Comment: 4 page

    State space formulas for a solution of the suboptimal Nehari problem on the unit disc

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    We give state space formulas for a ("central") solution of the suboptimal Nehari problem for functions defined on the unit disc and taking values in the space of bounded operators in separable Hilbert spaces. Instead of assuming exponential stability, we assume a weaker stability concept (the combination of input-, output- and input-output stability), which allows us to solve the problem for general H-infinity functions

    Coprime factorization and robust stabilization for discrete-time infinite-dimensional systems

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    We solve the problem of robust stabilization with respect to right-coprime factor perturbations for irrational discrete-time transfer functions. The key condition is that the associated dynamical system and its dual should satisfy a finite-cost condition so that two optimal cost operators exist. We obtain explicit state space formulas for a robustly stabilizing controller in terms of these optimal cost operators and the generating operators of the realization. Along the way we also obtain state space formulas for Bezout factors

    Circumstantial Evidence for a Critical Behavior in Peripheral Au + Au Collisions at 35 MeV/nucleon

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    The fragmentation resulting from peripheral Au + Au collisions at an incident energy of E = 35 MeV/nucleon is investigated. A power-law charge distribution, AτA^{-\tau} with τ2.2\tau \approx 2.2, and an intermittency signal are observed for events selected in the region of the Campi scatter plot where "critical" behavior is expected.Comment: 11 pages, RevTex file, 4 postscript figures available upon request from [email protected]

    Searching for the Nuclear Liquid-Gas Phase Transition in Au + Au Collisions at 35 MeV/nucleon

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    Within the framework of Classical Molecular Dynamics, we study the collision Au + Au at an incident energy of 35 MeV/nucleon. It is found that the system shows a critical behaviour at peripheral impact parameters, revealed through the analysis of conditional moments of charge distributions, Campi Scatter Plot, and the occurrence of large fluctuations in the region of the Campi plot where this critical behaviour is expected. When applying the experimental filters of the MULTICS-MINIBALL apparatus, it is found that criticality signals can be hidden due to the inefficiency of the experimental apparatus. The signals are then recovered by identifying semi-peripheral and peripheral collisions looking to the velocity distribution of the largest fragment, then by selecting the most complete events.Comment: RevTex file, 21 pages + 19 figures available upon request from [email protected]

    Prevalent and incident anemia in PARADIGM-HF and the effect of sacubitril/valsartan

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    Background: Anemia is common in patients with heart failure with reduced ejection fraction and is associated with poor clinical outcomes. Renin-angiotensin system blockers lower hemoglobin and may induce anemia. Objectives: The authors investigated whether concomitant neprilysin inhibition might ameliorate this effect of renin-angiotensin system blockers in PARADIGM-HF (Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure). Methods: Anemia was defined as hemoglobin <120 g/L in women and <130 g/L in men at screening. The authors investigated the effect of randomized treatment on clinical outcomes according to anemia status, change in hemoglobin from baseline, and the incidence of anemia. Results: Of 8,239 participants with a baseline hemoglobin measurement, 1,677 (20.4%) were anemic. Patients with anemia had a more severe heart failure profile, worse kidney function, greater neurohormonal derangement, and worse clinical outcomes. Sacubitril/valsartan, compared with enalapril, decreased the risk of cardiovascular death or heart failure hospitalization similarly in patients with (HR: 0.84; 95% CI: 0.71-1.00) and without anemia (HR: 0.78 [95% CI: 0.71-0.87]; P value for interaction = 0.478). Between baseline and 12 months, hemoglobin decreased by 1.5 g/L (95% CI: 1.2-1.7 g/L) with sacubitril/valsartan compared with 2.3 g/L (95% CI: 2.0-2.6 g/L) with enalapril: mean difference 0.8 g/L (95% CI: 0.5-1.2 g/L; P < 0.001). Patients assigned to sacubitril/valsartan were less likely to develop anemia at 12 months (321 of 2,806 [11.4%]) compared with patients randomized to enalapril (440 of 2,824 [15.6%]) (odds ratio [OR]: 0.70 [95% CI: 0.60-0.81]; P < 0.001). These findings were similar in PARAGON-HF (Prospective Comparison of ARNI with ARB Global Outcomes in HF with Preserved Ejection Fraction) (sacubitril/valsartan vs valsartan). There was biomarker evidence of increased iron utilization with sacubitril/valsartan. Conclusions: Irrespective of anemia status, sacubitril/valsartan compared with enalapril, decreased mortality and hospitalization. Hemoglobin decreased less with sacubitril/valsartan and the incidence of new anemia was lower with sacubitril/valsartan. (This study will evaluate the Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure [PARADIGM-HF] trial; NCT01035255)

    Variation in The Vitamin D Receptor Gene is Associated With Multiple Sclerosis in an Australian Population

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    Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) resulting in accumulating neurological disability. The disorder is more prevalent at higher latitudes. To investigate VDR gene variation using three intragenic restriction fragment length polymorphisms (Apa I, Taq I and Fok I) in an Australian MS case-control population, one hundred and four Australian MS patients were studied with patients classified clinically as Relapsing Remitting MS (RR-MS), Secondary Progressive MS (SP-MS) or Primary Progressive MS (PP-MS). Also, 104 age-, sex-, and ethnicity-matched controls were investigated as a comparative group. Our results show a significant difference of genotype distribution frequency between the case and control groups for the functional exon 9 VDR marker Taq I (p_Gen = 0.016) and interestingly, a stronger difference for the allelic frequency (p_All = 0.0072). The Apa I alleles were also found to be associated with MS (p_All = 0.04) but genotype frequencies were not significantly different from controls (p_Gen = 0.1). The Taq and Apa variants are in very strong and significant linkage disequilibrium (D' = 0.96, P < 0.0001). The genotypic associations are strongest for the progressive forms of MS (SP-MS and PP-MS). Our results support a role for the VDR gene increasing

    The primary headaches: genetics, epigenetics and a behavioural genetic model

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    The primary headaches, migraine with (MA) and without aura (MO) and cluster headache, all carry a substantial genetic liability. Familial hemiplegic migraine (FHM), an autosomal dominant mendelian disorder classified as a subtype of MA, is due to mutations in genes encoding neural channel subunits. MA/MO are considered multifactorial genetic disorders, and FHM has been proposed as a model for migraine aetiology. However, a review of the genetic studies suggests that the FHM genes are not involved in the typical migraines and that FHM should be considered as a syndromic migraine rather than a subtype of MA. Adopting the concept of syndromic migraine could be useful in understanding migraine pathogenesis. We hypothesise that epigenetic mechanisms play an important role in headache pathogenesis. A behavioural model is proposed, whereby the primary headaches are construed as behaviours, not symptoms, evolutionarily conserved for their adaptive value and engendered out of a genetic repertoire by a network of pattern generators present in the brain and signalling homeostatic imbalance. This behavioural model could be incorporated into migraine genetic research
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