Hour-glass magnetic spectrum in an insulating, hole-doped antiferromagnet

Superconductivity in layered copper-oxide compounds emerges when charge carriers are added to antiferromagnetically-ordered CuO2 layers. The carriers destroy the antiferromagnetic order, but strong spin fluctuations persist throughout the superconducting phase and are intimately linked to super-conductivity. Neutron scattering measurements of spin fluctuations in hole-doped copper oxides have revealed an unusual `hour-glass' feature in the momentum-resolved magnetic spectrum, present in a wide range of superconducting and non-superconducting materials. There is no widely-accepted explanation for this feature. One possibility is that it derives from a pattern of alternating spin and charge stripes, an idea supported by measurements on stripe-ordered La1.875Ba0.125CuO4. However, many copper oxides without stripe order also exhibit an hour-glass spectrum$. Here we report the observation of an hour-glass magnetic spectrum in a hole-doped antiferromagnet from outside the family of superconducting copper oxides. Our system has stripe correlations and is an insulator, which means its magnetic dynamics can conclusively be ascribed to stripes. The results provide compelling evidence that the hour-glass spectrum in the copper-oxide superconductors arises from fluctuating stripes.Comment: 13 pages, 4 figures, to appear in Natur

Signatures of arithmetic simplicity in metabolic network architecture

Metabolic networks perform some of the most fundamental functions in living cells, including energy transduction and building block biosynthesis. While these are the best characterized networks in living systems, understanding their evolutionary history and complex wiring constitutes one of the most fascinating open questions in biology, intimately related to the enigma of life's origin itself. Is the evolution of metabolism subject to general principles, beyond the unpredictable accumulation of multiple historical accidents? Here we search for such principles by applying to an artificial chemical universe some of the methodologies developed for the study of genome scale models of cellular metabolism. In particular, we use metabolic flux constraint-based models to exhaustively search for artificial chemistry pathways that can optimally perform an array of elementary metabolic functions. Despite the simplicity of the model employed, we find that the ensuing pathways display a surprisingly rich set of properties, including the existence of autocatalytic cycles and hierarchical modules, the appearance of universally preferable metabolites and reactions, and a logarithmic trend of pathway length as a function of input/output molecule size. Some of these properties can be derived analytically, borrowing methods previously used in cryptography. In addition, by mapping biochemical networks onto a simplified carbon atom reaction backbone, we find that several of the properties predicted by the artificial chemistry model hold for real metabolic networks. These findings suggest that optimality principles and arithmetic simplicity might lie beneath some aspects of biochemical complexity

Strength of the Spin-Fluctuation-Mediated Pairing Interaction in a High-Temperature Superconductor

Theories based on the coupling between spin fluctuations and fermionic quasiparticles are among the leading contenders to explain the origin of high-temperature superconductivity, but estimates of the strength of this interaction differ widely. Here we analyze the charge- and spin-excitation spectra determined by angle-resolved photoemission and inelastic neutron scattering, respectively, on the same crystals of the high-temperature superconductor YBa2Cu3O6.6. We show that a self-consistent description of both spectra can be obtained by adjusting a single parameter, the spin-fermion coupling constant. In particular, we find a quantitative link between two spectral features that have been established as universal for the cuprates, namely high-energy spin excitations and "kinks" in the fermionic band dispersions along the nodal direction. The superconducting transition temperature computed with this coupling constant exceeds 150 K, demonstrating that spin fluctuations have sufficient strength to mediate high-temperature superconductivity.Comment: 25 pages, 7 figures, including supplementary information, accepted for publication in Nature Physic

Inter-site pair superconductivity: origins and recent validation experiments

The challenge of understanding high-temperature superconductivity has led to a plethora of ideas, but 30 years after its discovery in cuprates, very few have achieved convincing experimental validation. While Hubbard and t-J models were given a lot of attention, a number of recent experiments appear to give decisive support to the model of real-space inter-site pairing and percolative superconductivity in cuprates. Systematic measurements of the doping dependence of the superfluid density show a linear dependence on superfluid density - rather than doping - over the entire phase diagram, in accordance with the model's predictions. The doping-dependence of the anomalous lattice dynamics of in-plane Cu-O mode vibrations observed by inelastic neutron scattering, gives remarkable reciprocal space signature of the inter-site pairing interaction whose doping dependence closely follows the predicted pair density. Symmetry-specific time-domain spectroscopy shows carrier localization, polaron formation, pairing and superconductivity to be distinct processes occurring on distinct timescales throughout the entire superconducting phase diagram. The three diverse experimental results confirm non-trivial predictions made more than a decade ago by the inter-site pairing model in the cuprates, remarkably also confirming some of the fundamental notions mentioned in the seminal paper on the discovery of high-temperature superconductivity in cuprates.Comment: Dedicated to Prof. K. A. Mueller on the Occasion of his 90th Birthda

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.