We present a theory of magnetic anisotropy in III 1Ϫx Mn x V-diluted magnetic semiconductors with carrierinduced ferromagnetism. The theory is based on four-and six-band envelope function models for the valenceband holes and a mean-field treatment of their exchange interactions with Mn ϩϩ ions. We find that easy-axis reorientations can occur as a function of temperature, carrier density p, and strain. The magnetic anisotropy in strain-free samples is predicted to have a p 5/3 hole-density dependence at small p, a p Ϫ1 dependence at large p, and remarkably large values at intermediate densities. An explicit expression, valid at small p, is given for the uniaxial contribution to the magnetic anisotropy due to unrelaxed epitaxial growth lattice-matching strains. Results of our numerical simulations are in agreement with magnetic anisotropy measurements on samples with both compressive and tensile strains. We predict that decreasing the hole density in current samples will lower the ferromagnetic transition temperature, but will increase the magnetic anisotropy energy and the coercivity.

Matrix metalloproteinase inhibition with PG-116800 failed to reduce LV remodeling or improve clinical outcomes after MI.

ES is common and unpredictable in ICD recipients and it is a strong predictor of hospitalization.

No abstract

Background-Depressed left ventricular function (LVF) and low heart rate variability (HRV) identify patients at risk of increased mortality after myocardial infarction (MI). Azimilide, a novel class III antiarrhythmic drug, was investigated for its effects on mortality in patients with depressed LVF after recent MI and in a subpopulation of patients with low HRV. Methods and Results-A total of 3717 post-MI patients with depressed LVF were enrolled in this randomized, placebo-controlled, double-blind study of azimilide 100 mg on all-cause mortality. Placebo patients with low HRV had a significantly higher 1-year mortality than those with high HRV (Ͼ20 U; 15% versus 9.5%, PϽ0.0005) despite nearly identical ejection fractions. No significant differences were observed between the 100-mg azimilide and placebo groups for all-cause mortality in either the "at-risk" patients identified by depressed LVF (12% versus 12%) or the subpopulation of "high-risk" patients identified by low HRV (14% versus 15%) or for total cardiac or arrhythmic mortality. Significantly fewer patients receiving azimilide developed atrial fibrillation than did patients receiving placebo (0.5% versus 1.2%, PϽ0.04). The incidences of torsade de pointes and severe neutropenia (absolute neutrophil count Յ500 cells/L) were slightly higher in the azimilide group than in the placebo group (0.3% versus 0.1% for torsade de pointes and 0.9% versus 0.2% for severe neutropenia). Conclusions-Azimilide