Spatial Evolution of the Ferromagnetic Phase Transition in an Exchange Graded Film.

A combination of experiments and numerical modeling was used to study the spatial evolution of the ferromagnetic phase transition in a thin film engineered to have a smooth gradient in exchange strength. Mean-field simulations predict, and experiments confirm, that a 100 nm Ni_{x}Cu_{1-x} alloy film with Ni concentration that varies by 9% as a function of depth behaves predominantly as if composed of a continuum of uncoupled ferromagnetic layers with continuously varying Curie temperatures. A mobile boundary separating ordered and disordered regions emerges as the temperature is increased. We demonstrate continuous control of the boundary position with temperature, and reversible control of the magnetization on both sides of the boundary with the magnetic field.

Progress in the development of phase-sensitive neutron reflectometry methods.

It has been a number of years since phase-sensitive specular neutron reflectometry (PSNR) methods employing reference layers were first introduced to help remove the ambiguity inherent in the reconstruction of scattering length density (SLD) depth profiles (Majkrzak, C. F.; Berk, N. F. Physica B 2003, 336, 27) from specular reflectivity measurements. Although a number of scientific applications of PSNR techniques have now been successfully realized (Majkrzak, C. F.; Berk, N. F.; Perez-Salas, U. A. Langmuir 2003, 19, 7796 and references therein), in certain cases practical difficulties remain. In this article, we describe possible solutions to two specific problems: (1) the need for explicit, detailed knowledge of the SLD profile of a given reference layer of finite thickness; and (2) for a reference layer of finite thickness in which only two density variations are possible, how to identify which of two mathematical solutions corresponds to the true physical structure.

Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery.

BACKGROUND: Aspirin inhibits platelet activation and reduces atherothrombotic complications in patients at risk of myocardial infarction and stroke. However, a sufficient inhibition of platelet function by aspirin is not always achieved. The causes of this aspirin resistance are unknown. METHODS AND RESULTS: Patients undergoing coronary artery bypass grafting (CABG) have a high incidence of aspirin resistance. To evaluate functional and biochemical responses to aspirin, platelet-rich plasma was obtained before and at days 1, 5, and 10 after CABG. Thromboxane formation, aggregation, and alpha-granule secretion were effectively inhibited by 30 or 100 micromol/L aspirin in vitro before CABG, but this inhibition was prevented or attenuated after CABG. Whereas the inhibition of thromboxane formation and aggregation by aspirin in vitro partly recovered at day 10 after CABG, oral aspirin (100 mg/d) remained ineffective. The inducible isoform of cyclooxygenase in platelets, COX-2, has been suggested to confer aspirin resistance. In fact, immunoreactive COX-2 was increased 16-fold in platelets at day 5 after CABG, but the COX-2 selective inhibitor celecoxib did not alter aspirin-resistant thromboxane formation. By contrast, the combined inhibitor of thromboxane synthase and thromboxane receptor antagonist terbogrel equally prevented thromboxane formation of platelets obtained before (control) and after CABG. CONCLUSIONS: Platelet aspirin resistance involves an impairment of both in vivo and in vitro inhibition of platelet functions and is probably due to a disturbed inhibition of platelet COX-1 by aspirin.