Surface magnetism of non-ideal iron borate single crystal

Considered is the influence of crystalline structure imperfections in near-surface layer of easy-plane weak ferromagnet iron borate, FeB0₃, on the effects of surface magnetism observed therein. It is shown that the surface reconstruction and point defects therein change the surface magnetic properties of the crystal very considerably.Розглянуто вплив недосконалості кристалічної структури приповерхневого шару легкоплощинного слабкого феромагнетика борату заліза FeB0₃ на ефекти поверхневого магнетизму, що спостерігається у ньому. Показано, що реконструкція поверхні і наявність в ній точкових дефектів значно змінюють поверхневі магнітні властивості цього кристала.Рассмотрено влияние несовершенств кристаллической структуры приповерхностного слоя легкоплоскостного слабого ферромагнетика бората железа, FeB0₃, на эффекты наблюдаемого в нем поверхностного магнетизма. Показано, что реконструкция поверхности и наличие в ней точечных дефектов весьма значительно изменяют поверхностные магнитные свойства этого кристалла

Structure of near-surface magnetic layer in iron borate

Magnetic structure of inhomogeneously magnetized near-surface magnetic layer for non-basal baces of FeBO₃ single crystals has been calculated. That layer has macroscopic thickness and can be observed in easy-plane weak ferromagnets. The calculation in based on our theory of Iron Borate surface magnetism

Angular dependence of magnetization in axially stressed FeBO₃ single crystals

Magnetization processes in easy-plane weak ferromagnetic FeBO3 under magnetic field H and axial pressure P applied simultaneously in basal plane of the crystal have been investigated. The absence of expected orientational phase transition on the experimental curve MH(P) has been interpreted as degeneration of two magnetic phases into one in case of no parallelism between magnetic field and the pressure. Experimental curves MH(H) at fixed pressure for different values of angle between magnetic field and pressure directions have been constructed. Correlation between the theory and the experiment one can observe in this case as well

Features of acoustic resonance in iron borate

Acoustic resonance in a weak-ferromagnetic iron borate monocrystal was investigated. It was shown that observed field dependence of positions and magnitudes of the resonance peaks can be explained within framework of the developed theory of magnetic birefringence of sound in the inhomogeneous magnetized sample

Fitting MAS NMR spectra in crystals with local disorder: Czjzek's vs. Maurer's model for 11 B and 71 Ga in polycrystalline gallium borate

A comparative analysis of the Czjzek's and Maurer's models of the joint distribution density of NMR quadrupole parameters has been carried out in view of their application to account for spectra broadening induced by local disorder in crystals. As an example of such an application, we have considered Magic Angle Spinning NMR of 11 B and 71 Ga isotopes in polycrystalline gallium borate. Computer simulations carried out using both models unambiguously show that in the case of low local disorder the Maurer's model, in contrast to the Czjzek's model, provides satisfactory fits to experimental NMR spectra

11B MAS NMR study of Ga1−xFexBO3 mixed crystals

11 B MAS NMR Local structure Local disorder. a b s t r a c t : Mixed iron-gallium borate crystals Ga 1-x Fe x BO 3 have been studied by Magic Angle Spinning (MAS) NMR of 11 B isotope. Experimental MAS NMR spectra have been computer simulated using a laboratory-developed code. The quadrupole parameters and isotropic chemical shift for 11 B are consistent with threefold-coordination of boron atoms. A detailed fitting to the experimental NMR spectra reveals the existence of a certain local disorder in Ga 1-x Fe x BO 3 crystals

Lattice-Mediated Optical Control of Magnetic Anisotropy in FeBO3

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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. Copyright © 2017 Massachusetts Medical Society