Effect of pressure cycling on Iron: Signatures of an electronic instability and unconventional superconductivity

High pressure electrical resistivity and x-ray diffraction experiments have been performed on Fe single crystals. The crystallographic investigation provides direct evidence that in the martensitic $bcc \rightarrow hcp$ transition at 14 GPa the $\lbrace 110\rbrace_{bcc}$ become the $\lbrace 002\rbrace_{hcp}$ directions. During a pressure cycle, resistivity shows a broad hysteresis of 6.5 GPa, whereas superconductivity, observed between 13 and 31 GPa, remains unaffected. Upon increasing pressure an electronic instability, probably a quantum critical point, is observed at around 19 GPa and, close to this pressure, the superconducting $T_{c}$ and the isothermal resistivity ($0<T<300\,$K) attain maximum values. In the superconducting pressure domain, the exponent $n = 5/3$ of the temperature power law of resistivity and its prefactor, which mimics $T_{c}$, indicate that ferromagnetic fluctuations may provide the glue for the Cooper pairs, yielding unconventional superconductivity

Exploring high temperature magnetic order in CeTi_1-xSc_xGe

Most of magnetic transitions related to Ce ordering are found below T_ord~12K. Among the few cases exceeding that temperature, two types of behaviors can be distinguished. One of them is related to the rare cases of Ce binary compounds formed in BCC structures, with a quartet ground state, whose degeneracy is reduced by undergoing different types of transitions mostly structural. The other group shows evidences of itinerant character with the outstanding example of CeRh_3B_2 showing the highest T_ord=115K. The second highest ordering temperature has been reported for CeScGe with T_ord=47K, but the nature of this magnetic state has not been investigated very deeply. In order to shed more light into this unusual high temperature ordering we studied the structural, magnetic, transport and thermal properties of CeTi_1-xSc_xGe alloys in the stability range of the CeScSi-type structure 0.25<x<1 This system presents a rich variety of magnetic behaviors along this concentration range, with the magnetic ordering growing from ferromagnetic (FM) T_C~7K up to an antiferromagnetic (AFM) transition at T_N=47K. The different regions show the following characteristics: i) on the Ti rich side (0.25<x<0.50) it exhibits a FM ground state (GS) with large saturation magnetization values M_sat up to ~1.15 mu_B. ii) Around x=0.60, the first crystal electric field excited doublet starts to contribute to the GS magnetic properties. Furthermore an AFM component with a connected metamagnetic transition appears. iii) At x=0.65 a clear change in the GS nature is associated to a critical point above which the GS properties can be described like for an itinerant system (with decreasing M_sat) and an effective GS degeneracy N_eff=4. iv) For x>0.65, the magnetic phase boundary splits into two transitions, with an intermediate phase presenting incommensurate spin density waves features.Comment: 8 pages, 10 figure

Jagged1 intracellular domain-mediated inhibition of Notch1 signalling regulates cardiac homeostasis in the postnatal heart.

AIMS: Notch1 signalling in the heart is mainly activated via expression of Jagged1 on the surface of cardiomyocytes. Notch controls cardiomyocyte proliferation and differentiation in the developing heart and regulates cardiac remodelling in the stressed adult heart. Besides canonical Notch receptor activation in signal-receiving cells, Notch ligands can also activate Notch receptor-independent responses in signal-sending cells via release of their intracellular domain. We evaluated therefore the importance of Jagged1 (J1) intracellular domain (ICD)-mediated pathways in the postnatal heart. METHODS AND RESULTS: In cardiomyocytes, Jagged1 releases J1ICD, which then translocates into the nucleus and down-regulates Notch transcriptional activity. To study the importance of J1ICD in cardiac homeostasis, we generated transgenic mice expressing a tamoxifen-inducible form of J1ICD, specifically in cardiomyocytes. Using this model, we demonstrate that J1ICD-mediated Notch inhibition diminishes proliferation in the neonatal cardiomyocyte population and promotes maturation. In the neonatal heart, a response via Wnt and Akt pathway activation is elicited as an attempt to compensate for the deficit in cardiomyocyte number resulting from J1ICD activation. In the stressed adult heart, J1ICD activation results in a dramatic reduction of the number of Notch signalling cardiomyocytes, blunts the hypertrophic response, and reduces the number of apoptotic cardiomyocytes. Consistently, this occurs concomitantly with a significant down-regulation of the phosphorylation of the Akt effectors ribosomal S6 protein (S6) and eukaryotic initiation factor 4E binding protein1 (4EBP1) controlling protein synthesis. CONCLUSIONS: Altogether, these data demonstrate the importance of J1ICD in the modulation of physiological and pathological hypertrophy, and reveal the existence of a novel pathway regulating cardiac homeostasis

On the effect of Ti on Oxidation Behaviour of a Polycrystalline Nickel-based Superalloy

Titanium is commonly added to nickel superalloys but has a well-documented detrimental effect on oxidation resistance. The present work constitutes the first atomistic-scale quantitative measurements of grain boundary and bulk compositions in the oxide scale of a current generation polycrystalline nickel superalloy performed through atom probe tomography. Titanium was found to be particularly detrimental to oxide scale growth through grain boundary diffusion

Is pretreatment with Beta-blockers beneficial in patients with acute coronary syndrome?

OBJECTIVES: The role of beta-blockers in the treatment of hypertension is discussed controversially and the data showing a clear benefit in acute coronary syndromes (ACS) were obtained in the thrombolysis era. The goal of this study was to analyze the role of pretreatment with beta-blockers in patients with ACS. METHODS: Using data from the Acute Myocardial Infarction in Switzerland (AMIS Plus) registry, we analyzed outcomes of patients with beta-blocker pretreatment in whom they were continued during hospitalization (group A), those without beta-blocker pretreatment but with administration after admission (group B) and those who never received them (group C). Major adverse cardiac events defined as composed endpoint of re-infarction and stroke (during hospitalization) and/or in-hospital death were compared between the groups. RESULTS: A total of 24,709 patients were included in the study (6,234 in group A, 12,344 in group B, 6,131 in group C). Patients of group B were younger compared to patients of group A and C (62.5, 67.6 and 68.4, respectively). In the multivariate analysis, odds ratio for major adverse cardiac events was 0.59 (CI 0.47-0.74) for group A and 0.66 (CI 0.55-0.83) for group B, while group C was taken as a reference. CONCLUSIONS: beta-Blocker therapy is beneficial in ACS and they should be started in those who are not pretreated and continued in stable patients who had been on chronic beta-blocker therapy before

The effect of manganese and silicon additions on the corrosion resistance of a polycrystalline nickel-based superalloy

The service lives of nickel superalloys are often limited by environmental degradation. The present study compares oxidation, sulfidation and hot corrosion at 750C of three variants of a polycrystalline superalloy: a baseline alloy, a variant containing 1wt% Mn and one containing 0.5wt% Si. Mn reduced the oxidation rate without changing the scale morphology. The MnCr2O4 scale formed proved more protective against sulfidation and hot corrosion, but internal sulfides extended the damage depth. Si modified the oxide morphology to a continuous Cr2O3-Al2O3 dual layer. This provided improved protection, reducing the sulfidation depth by 2/3 and the hot corrosion depth by 1/2.Comment: 21 page

Ischemic postconditioning protects remodeled myocardium via the PI3K-PKB/Akt reperfusion injury salvage kinase pathway

OBJECTIVE: We tested whether ischemic postconditioning (IPostC) is protective in remodeled myocardium. METHODS: Post-myocardial infarct (MI)-remodeled hearts after permanent coronary artery ligation and one kidney one clip (1K1C) hypertensive hearts of male Wistar rats were exposed to 40 min of ischemia followed by 90 min of reperfusion. IPostC was induced by six cycles of 10 s reperfusion interspersed by 10 s of no-flow ischemia. Activation of reperfusion injury salvage kinases was measured using Western blotting and in vitro kinase activity assays. RESULTS: IPostC prevented myocardial damage in both MI-remodeled and 1K1C hearts, as measured by decreased infarct size and lactate dehydrogenase release, and improved function. The reduction in infarct size and the recovery of left ventricular contractility achieved by IPostC was less in 1K1C hearts, but was unchanged in MI-remodeled hearts when compared to healthy hearts. In contrast, the recovery of inotropy was unaffected in 1K1C hearts, but was less in MI-remodeled hearts. Inhibition of the phosphatidylinositol 3-kinase (PI3K) pathway with LY294002 abolished the protective effects of IPostC on both disease models and healthy hearts. Western blot analysis in conjunction with in vitro kinase activity assays identified protein kinase B (PKB)/Akt but not p42/p44 extracellular-signal regulated kinase 1/2 (ERK1/2) as the predominant kinase in IPostC-mediated cardioprotection in remodeled hearts. IPostC increased phosphorylation of the PKB/Akt downstream targets eNOS, GSK3beta, and p70S6K in remodeled hearts. CONCLUSION: Our results offer evidence that IPostC mediates cardioprotection in the remodeled rat myocardium primarily via activation of the PI3K-PKB/Akt reperfusion injury salvage kinase pathwa