Systematic Low-Energy Effective Theory for Magnons and Charge Carriers in an Antiferromagnet

By electron or hole doping quantum antiferromagnets may turn into high-temperature superconductors. The low-energy dynamics of antiferromagnets are governed by their Nambu-Goldstone bosons -- the magnons -- and are described by an effective field theory analogous to chiral perturbation theory for the pions in strong interaction physics. In analogy to baryon chiral perturbation theory -- the effective theory for pions and nucleons -- we construct a systematic low-energy effective theory for magnons and electrons or holes in an antiferromagnet. The effective theory is universal and makes model-independent predictions for the entire class of antiferromagnetic cuprates. We present a detailed analysis of the symmetries of the Hubbard model and discuss how these symmetries manifest themselves in the effective theory. A complete set of linearly independent leading contributions to the effective action is constructed. The coupling to external electromagnetic fields is also investigated.Comment: 53 pages, no figures, added references, extended the introductio

Nonperturbative renormalization group approach to frustrated magnets

This article is devoted to the study of the critical properties of classical XY and Heisenberg frustrated magnets in three dimensions. We first analyze the experimental and numerical situations. We show that the unusual behaviors encountered in these systems, typically nonuniversal scaling, are hardly compatible with the hypothesis of a second order phase transition. We then review the various perturbative and early nonperturbative approaches used to investigate these systems. We argue that none of them provides a completely satisfactory description of the three-dimensional critical behavior. We then recall the principles of the nonperturbative approach - the effective average action method - that we have used to investigate the physics of frustrated magnets. First, we recall the treatment of the unfrustrated - O(N) - case with this method. This allows to introduce its technical aspects. Then, we show how this method unables to clarify most of the problems encountered in the previous theoretical descriptions of frustrated magnets. Firstly, we get an explanation of the long-standing mismatch between different perturbative approaches which consists in a nonperturbative mechanism of annihilation of fixed points between two and three dimensions. Secondly, we get a coherent picture of the physics of frustrated magnets in qualitative and (semi-) quantitative agreement with the numerical and experimental results. The central feature that emerges from our approach is the existence of scaling behaviors without fixed or pseudo-fixed point and that relies on a slowing-down of the renormalization group flow in a whole region in the coupling constants space. This phenomenon allows to explain the occurence of generic weak first order behaviors and to understand the absence of universality in the critical behavior of frustrated magnets.Comment: 58 pages, 15 PS figure

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Controle de qualidade de fitoterápicos e insumos vegetais no RS : importância e desenvolvimento da indústria farmacêutica regional

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